pre-miRNA Information | |
---|---|
pre-miRNA | hsa-mir-29b-1 |
Genomic Coordinates | chr7: 130877459 - 130877539 |
Synonyms | MIRN29B1, miRNA29B1, MIR29B1 |
Description | Homo sapiens miR-29b-1 stem-loop |
Comment | Mourelatos et al. identified two copies of this sequence mapping to chromosome 7, and assigned the names mir-102-7.1 and mir-102-7.2 . Subsequent genome assemblies suggest the presence of only one miR-102 locus on chromosome 7. Human miR-102 is a homologue of mouse miR-29b (MIR:MI0000143) and so has been renamed here for consistency. |
RNA Secondary Structure | |
Associated Diseases | |
pre-miRNA | hsa-mir-29b-2 |
Genomic Coordinates | chr1: 207802443 - 207802523 |
Synonyms | MIRN29B2, mir-29b-2, MIR29B2 |
Description | Homo sapiens miR-29b-2 stem-loop |
Comment | This sequence was named mir-102-1 in reference . Human miR-102 is a homologue of mouse miR-29b (MIR:MI0000143) and so has been renamed here for consistency. |
RNA Secondary Structure | |
Associated Diseases |
Mature miRNA Information | ||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Mature miRNA | hsa-miR-29b-3p | |||||||||||||||||||||
Sequence | 52| UAGCACCAUUUGAAAUCAGUGUU |74 | |||||||||||||||||||||
Evidence | Experimental | |||||||||||||||||||||
Experiments | Cloned | |||||||||||||||||||||
Editing Events in miRNAs |
|
|||||||||||||||||||||
SNPs in miRNA |
|
|||||||||||||||||||||
Putative Targets |
miRNA Expression profile | |
---|---|
Human miRNA Tissue Atlas | |
miRNAs in Extracellular Vesicles |
|
Circulating MicroRNA Expression Profiling |
Gene Information | |||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Gene Symbol | MCL1 | ||||||||||||||||||||
Synonyms | BCL2L3, EAT, MCL1-ES, MCL1L, MCL1S, Mcl-1, TM, bcl2-L-3, mcl1/EAT | ||||||||||||||||||||
Description | MCL1, BCL2 family apoptosis regulator | ||||||||||||||||||||
Transcript | NM_021960 | ||||||||||||||||||||
Other Transcripts | NM_182763 | ||||||||||||||||||||
Expression | |||||||||||||||||||||
Putative miRNA Targets on MCL1 | |||||||||||||||||||||
3'UTR of MCL1 (miRNA target sites are highlighted) |
>MCL1|NM_021960|3'UTR 1 CCTTACTGTAAGTGCAATAGTTGACTTTTAACCAACCACCACCACCACCAAAACCAGTTTATGCAGTTGGACTCCAAGCT 81 GTAACTTCCTAGAGTTGCACCCTAGCAACCTAGCCAGAAAAGCAAGTGGCAAGAGGATTATGGCTAACAAGAATAAATAC 161 ATGGGAAGAGTGCTCCCCATTGATTGAAGAGTCACTGTCTGAAAGAAGCAAAGTTCAGTTTCAGCAACAAACAAACTTTG 241 TTTGGGAAGCTATGGAGGAGGACTTTTAGATTTAGTGAAGATGGTAGGGTGGAAAGACTTAATTTCCTTGTTGAGAACAG 321 GAAAGTGGCCAGTAGCCAGGCAAGTCATAGAATTGATTACCCGCCGAATTCATTAATTTACTGTAGTGTTAAGAGAAGCA 401 CTAAGAATGCCAGTGACCTGTGTAAAAGTTACAAGTAATAGAACTATGACTGTAAGCCTCAGTACTGTACAAGGGAAGCT 481 TTTCCTCTCTCTAATTAGCTTTCCCAGTATACTTCTTAGAAAGTCCAAGTGTTCAGGACTTTTATACCTGTTATACTTTG 561 GCTTGGTTTCCATGATTCTTACTTTATTAGCCTAGTTTATCACCAATAATACTTGACGGAAGGCTCAGTAATTAGTTATG 641 AATATGGATATCCTCAATTCTTAAGACAGCTTGTAAATGTATTTGTAAAAATTGTATATATTTTTACAGAAAGTCTATTT 721 CTTTGAAACGAAGGAAGTATCGAATTTACATTAGTTTTTTTCATACCCTTTTGAACTTTGCAACTTCCGTAATTAGGAAC 801 CTGTTTCTTACAGCTTTTCTATGCTAAACTTTGTTCTGTTCAGTTCTAGAGTGTATACAGAACGAATTGATGTGTAACTG 881 TATGCAGACTGGTTGTAGTGGAACAAATCTGATAACTATGCAGGTTTAAATTTTCTTATCTGATTTTGGTAAGTATTCCT 961 TAGATAGGTTTTTCTTTGAAAACCTGGGATTGAGAGGTTGATGAATGGAAATTCTTTCACTTCATTATATGCAAGTTTTC 1041 AATAATTAGGTCTAAGTGGAGTTTTAAGGTTACTGATGACTTACAAATAATGGGCTCTGATTGGGCAATACTCATTTGAG 1121 TTCCTTCCATTTGACCTAATTTAACTGGTGAAATTTAAAGTGAATTCATGGGCTCATCTTTAAAGCTTTTACTAAAAGAT 1201 TTTCAGCTGAATGGAACTCATTAGCTGTGTGCATATAAAAAGATCACATCAGGTGGATGGAGAGACATTTGATCCCTTGT 1281 TTGCTTAATAAATTATAAAATGATGGCTTGGAAAAGCAGGCTAGTCTAACCATGGTGCTATTATTAGGCTTGCTTGTTAC 1361 ACACACAGGTCTAAGCCTAGTATGTCAATAAAGCAAATACTTACTGTTTTGTTTCTATTAATGATTCCCAAACCTTGTTG 1441 CAAGTTTTTGCATTGGCATCTTTGGATTTCAGTCTTGATGTTTGTTCTATCAGACTTAACCTTTTATTTCCTGTCCTTCC 1521 TTGAAATTGCTGATTGTTCTGCTCCCTCTACAGATATTTATATCAATTCCTACAGCTTTCCCCTGCCATCCCTGAACTCT 1601 TTCTAGCCCTTTTAGATTTTGGCACTGTGAAACCCCTGCTGGAAACCTGAGTGACCCTCCCTCCCCACCAAGAGTCCACA 1681 GACCTTTCATCTTTCACGAACTTGATCCTGTTAGCAGGTGGTAATACCATGGGTGCTGTGACACTAACAGTCATTGAGAG 1761 GTGGGAGGAAGTCCCTTTTCCTTGGACTGGTATCTTTTCAACTATTGTTTTATCCTGTCTTTGGGGGCAATGTGTCAAAA 1841 GTCCCCTCAGGAATTTTCAGAGGAAAGAACATTTTATGAGGCTTTCTCTAAAGTTTCCTTTGTATAGGAGTATGCTCACT 1921 TAAATTTACAGAAAGAGGTGAGCTGTGTTAAACCTCAGAGTTTAAAAGCTACTGATAAACTGAAGAAAGTGTCTATATTG 2001 GAACTAGGGTCATTTGAAAGCTTCAGTCTCGGAACATGACCTTTAGTCTGTGGACTCCATTTAAAAATAGGTATGAATAA 2081 GATGACTAAGAATGTAATGGGGAAGAACTGCCCTGCCTGCCCATCTCAGAGCCATAAGGTCATCTTTGCTAGAGCTATTT 2161 TTACCTATGTATTTATCGTTCTTGATCATAAGCCGCTTATTTATATCATGTATCTCTAAGGACCTAAAAGCACTTTATGT 2241 AGTTTTTAATTAATCTTAAGATCTGGTTACGGTAACTAAAAAAGCCTGTCTGCCAAATCCAGTGGAAACAAGTGCATAGA 2321 TGTGAATTGGTTTTTAGGGGCCCCACTTCCCAATTCATTAGGTATGACTGTGGAAATACAGACAAGGATCTTAGTTGATA 2401 TTTTGGGCTTGGGGCAGTGAGGGCTTAGGACACCCCAAGTGGTTTGGGAAAGGAGGAGGGGAGTGGTGGGTTTATAGGGG 2481 GAGGAGGAGGCAGGTGGTCTAAGTGCTGACTGGCTACGTAGTTCGGGCAAATCCTCCAAAAGGGAAAGGGAGGATTTGCT 2561 TAGAAGGATGGCGCTCCCAGTGACTACTTTTTGACTTCTGTTTGTCTTACGCTTCTCTCAGGGAAAAACATGCAGTCCTC 2641 TAGTGTTTCATGTACATTCTGTGGGGGGTGAACACCTTGGTTCTGGTTAAACAGCTGTACTTTTGATAGCTGTGCCAGGA 2721 AGGGTTAGGACCAACTACAAATTAATGTTGGTTGTCAAATGTAGTGTGTTTCCCTAACTTTCTGTTTTTCCTGAGAAAAA 2801 AAAATAAATCTTTTATTCAAATACAGGGAAAAAAAAAAAAAAAAAA Target sites
Provided by authors
Predicted by miRanda
DRVs
SNPs
DRVs & SNPs
|
||||||||||||||||||||
miRNA-target interactions (Predicted by miRanda) |
|
||||||||||||||||||||
DRVs in gene 3'UTRs | |||||||||||||||||||||
SNPs in gene 3'UTRs |
Experimental Support 1 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | HeLa |
Disease | 4170.0; |
Location of target site | 3'UTR |
Tools used in this research | miRanda |
Original Description (Extracted from the article) |
...
"when the mir-29 target site from the Mcl-1 3芒鈧鈩UTR is inserted into the luciferase construct
... - Mott JL; Kobayashi S; Bronk SF; Gores GJ, 2007, Oncogene. |
Article |
- Mott JL; Kobayashi S; Bronk SF; Gores GJ - Oncogene, 2007
Cellular expression of Mcl-1, an anti-apoptotic Bcl-2 family member, is tightly regulated. Recently, Bcl-2 expression was shown to be regulated by microRNAs, small endogenous RNA molecules that regulate protein expression through sequence-specific interaction with messenger RNA. By analogy, we reasoned that Mcl-1 expression may also be regulated by microRNAs. We chose human immortalized, but non-malignant, H69 cholangiocyte and malignant KMCH cholangiocarcinoma cell lines for these studies, because Mcl-1 is dysregulated in cells with the malignant phenotype. By in silico analysis, we identified a putative target site in the Mcl-1 mRNA for the mir-29 family, and found that mir-29b was highly expressed in cholangiocytes. Interestingly, mir-29b was downregulated in malignant cells, consistent with Mcl-1 protein upregulation. Enforced mir-29b expression reduced Mcl-1 protein expression in KMCH cells. This effect was direct, as mir-29b negatively regulated the expression of an Mcl-1 3' untranslated region (UTR)-based reporter construct. Enforced mir-29b expression reduced Mcl-1 cellular protein levels and sensitized the cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) cytotoxicity. Transfection of non-malignant cells (that express high levels of mir-29) with a locked-nucleic acid antagonist of mir-29b increased Mcl-1 levels and reduced TRAIL-mediated apoptosis. Thus mir-29 is an endogenous regulator of Mcl-1 protein expression, and thereby, apoptosis.
LinkOut: [PMID: 17404574]
|
Experimental Support 2 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Article |
- Mraz M; Pospisilova S; Malinova K; Slapak et al. - Leukemia & lymphoma, 2009
MicroRNAs (miRNAs) are short, non-coding RNAs, which function as evolutionary conserved regulators of a gene expression. They have essential roles in development, cell differentiation, proliferation, apoptosis and chromosome structure. MiRNAs constitute about 3-5% of predicted genes in the human genome (i.e. about 1000); and 20-30% of the protein-coding genes are estimated to be regulated by the miRNAs. The primary evidence that miRNAs possibly act as a novel class of oncogenes/tumor-suppressors comes from the discovery of the miR-15a and miR-16-1 in 13q14 region deleted in chronic lymphocytic leukemia (CLL). Moreover, miRNA signatures have been used to classify tumor types. There have recently been several reports on the miRNAs role in CLL pathogenesis and disease subtypes (according to IgV(H) mutation status). In this report, we will review the published observations and present our miRNA profiling data in aggressive CLL with TP53 abnormalities (deletion and/or mutation of p53 gene). We have identified a deregulated miRNA expression pattern (down regulation of miR-34a, miR-29 and miR-17-5p) in these samples, compared to cells with wild-type TP53. It has previously been shown that miR-34a is directly regulated by p53 and targets BCL-2, miR-29c regulates the MCL-1 and TCL-1 proto-oncogenes and the miR-17-5p targets important cell cycle regulatory molecules. Consequently, these three miRNAs could potentially play important roles in the pathogenesis of aggressive CLL.
LinkOut: [PMID: 19347736]
|
Experimental Support 3 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | K562 |
Disease | MIMAT0000100; |
Location of target site | 3'UTR |
Tools used in this research | TargetScan |
Original Description (Extracted from the article) |
...
"A marked reduction in the luciferase/Renilla ratio was seen for MCL-1
... - Garzon R; Heaphy CE; Havelange V; Fabbri M; et al., 2009, Blood. |
Article |
- Garzon R; Heaphy CE; Havelange V; Fabbri M; et al. - Blood, 2009
MicroRNAs (miRNAs) are associated with cytogenetics and molecular subtypes of acute myelogeneous leukemia (AML), but their impact on AML pathogenesis is poorly understood. We have previously shown that miR-29b expression is deregulated in primary AML blasts. In this work, we investigated the functional role of miR-29b in leukemogenesis. Restoration of miR-29b in AML cell lines and primary samples induces apoptosis and dramatically reduces tumorigenicity in a xenograft leukemia model. Transcriptome analysis after ectopic transfection of synthetic miR-29b into leukemia cells indicates that miR-29b target apoptosis, cell cycle, and proliferation pathways. A significant enrichment for apoptosis genes, including MCL-1, was found among the mRNAs inversely correlated with miR-29b expression in 45 primary AML samples. Together, the data support a tumor suppressor role for miR-29 and provide a rationale for the use of synthetic miR-29b oligonucleotides as a novel strategy to improve treatment response in AML.
LinkOut: [PMID: 19850741]
|
Experimental Support 4 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | HEK293T |
Location of target site | 3'UTR |
Tools used in this research | miRanda , TargetScan |
Original Description (Extracted from the article) |
...
Bcl-2 and Mcl-1 Are Direct Targets of miR-29.
... - Xiong Y; Fang JH; Yun JP; Yang J; Zhang Y; et al., 2010, Hepatology (Baltimore, Md.). |
Article |
- Xiong Y; Fang JH; Yun JP; Yang J; Zhang Y; et al. - Hepatology (Baltimore, Md.), 2010
UNLABELLED: Based on microarray data, we have previously shown a significant down-regulation of miR-29 in hepatocellular carcinoma (HCC) tissues. To date, the role of miR-29 deregulation in hepatocarcinogenesis and the signaling pathways by which miR-29 exerts its function and modulates the malignant phenotypes of HCC cells remain largely unknown. In this study, we confirmed that reduced expression of miR-29 was a frequent event in HCC tissues using both Northern blot and real-time quantitative reverse-transcription polymerase chain reaction. More interestingly, we found that miR-29 down-regulation was significantly associated with worse disease-free survival of HCC patients. Both gain- and loss-of-function studies revealed that miR-29 could sensitize HCC cells to apoptosis that was triggered by either serum starvation and hypoxia or chemotherapeutic drugs, which mimicked the tumor growth environment in vivo and the clinical treatment. Moreover, introduction of miR-29 dramatically repressed the ability of HCC cells to form tumor in nude mice. Subsequent investigation characterized two antiapoptotic molecules, Bcl-2 and Mcl-1, as direct targets of miR-29. Furthermore, silencing of Bcl-2 and Mcl-1 phenocopied the proapoptotic effect of miR-29, whereas overexpression of these proteins attenuated the effect of miR-29. In addition, enhanced expression of miR-29 resulted in the loss of mitochondrial potential and the release of cytochrome c to cytoplasm, suggesting that miR-29 may promote apoptosis through a mitochondrial pathway that involves Mcl-1 and Bcl-2. CONCLUSION: Our data highlight an important role of miR-29 in the regulation of apoptosis and in the molecular etiology of HCC, and implicate the potential application of miR-29 in prognosis prediction and in cancer therapy.
LinkOut: [PMID: 20041405]
|
Experimental Support 5 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | HEK293 |
Location of target site | 3'UTR |
Tools used in this research | TargetScan , miRTarCLIP , Piranha |
Original Description (Extracted from the article) |
...
PAR-CLIP data was present in GSM545212. RNA binding protein: AGO1. Condition:Control
PAR-CLIP data was present in GSM545214. RNA binding protein: AGO3. Condition:Control
PAR-CLIP data was present in GSM545215. RNA binding protein: AGO4. Condition:Control
PAR-CLIP data was present in GSM545216. RNA binding protein: AGO2. Condition:miR-124 transfection
PAR-CLIP data was present in GSM545217. RNA binding protein: AGO2. Condition:miR-7 transfection
... - Hafner M; Landthaler M; Burger L; Khorshid et al., 2010, Cell. |
Article |
- Hafner M; Landthaler M; Burger L; Khorshid et al. - Cell, 2010
RNA transcripts are subject to posttranscriptional gene regulation involving hundreds of RNA-binding proteins (RBPs) and microRNA-containing ribonucleoprotein complexes (miRNPs) expressed in a cell-type dependent fashion. We developed a cell-based crosslinking approach to determine at high resolution and transcriptome-wide the binding sites of cellular RBPs and miRNPs. The crosslinked sites are revealed by thymidine to cytidine transitions in the cDNAs prepared from immunopurified RNPs of 4-thiouridine-treated cells. We determined the binding sites and regulatory consequences for several intensely studied RBPs and miRNPs, including PUM2, QKI, IGF2BP1-3, AGO/EIF2C1-4 and TNRC6A-C. Our study revealed that these factors bind thousands of sites containing defined sequence motifs and have distinct preferences for exonic versus intronic or coding versus untranslated transcript regions. The precise mapping of binding sites across the transcriptome will be critical to the interpretation of the rapidly emerging data on genetic variation between individuals and how these variations contribute to complex genetic diseases.
LinkOut: [PMID: 20371350]
|
Experimental Support 6 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | artificial tissues |
Location of target site | 3'UTR |
Original Description (Extracted from the article) |
...
miR-29 family resulted in decreased levels of its targets DNMT3a and MCL1.
... - Kovalchuk O; Zemp FJ; Filkowski JN; et al., 2010, Carcinogenesis. |
Article |
- Kovalchuk O; Zemp FJ; Filkowski JN; et al. - Carcinogenesis, 2010
The radiation-induced bystander effect (RIBE) is a phenomenon whereby unexposed cells exhibit molecular symptoms of stress exposure when adjacent or nearby cells are traversed by ionizing radiation (IR). Recent data suggest that RIBE may be epigenetically mediated by microRNAs (miRNAs), which are small regulatory molecules that target messenger RNA transcripts for translational inhibition. Here, we analyzed microRNAome changes in bystander tissues after alpha-particle microbeam irradiation of three-dimensional artificial human tissues using miRNA microarrays. Our results indicate that IR leads to a deregulation of miRNA expression in bystander tissues. We report that major bystander end points, including apoptosis, cell cycle deregulation and DNA hypomethylation, may be mediated by altered expression of miRNAs. Specifically, c-MYC-mediated upregulation of the miR-17 family was associated with decreased levels of E2F1 and RB1, suggesting a switch to a proliferative state in bystander tissues, while priming these cells for impending death signals. Upregulation of the miR-29 family resulted in decreased levels of its targets DNMT3a and MCL1, consequently affecting DNA methylation and apoptosis. Altered expression of miR-16 led to changes in expression of BCL2, suggesting modulation of apoptosis. Thus, our data clearly show that miRNAs play a profound role in the manifestation of late RIBE end points. In summary, this study creates a roadmap for understanding the role of microRNAome in RIBE and for developing novel RIBE biomarkers.
LinkOut: [PMID: 20643754]
|
Experimental Support 7 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | PC3 , DU145 |
Disease | prostate cancer |
Location of target site | 3'UTR |
Tools used in this research | TargetScan |
Original Description (Extracted from the article) |
...
miR-29b inhibits McI-I in PC3 cells
... - Steele R; Mott JL; Ray RB, 2010, Genes & cancer. |
Article |
- Steele R; Mott JL; Ray RB - Genes & cancer, 2010
c-myc promoter binding protein (MBP-1) is a multi-functional protein known to regulate expression of targets involved in the malignant phenotype. We have previously demonstrated that exogenous expression of MBP-1 inhibits prostate tumor growth, although the mechanism of growth inhibition is not well understood. We hypothesized that MBP-1 may modulate microRNA (miRNA) expression for regulation of prostate cancer cell growth. In this study, we demonstrated that exogenous MBP-1 upregulates miR-29b by 5-9 fold in prostate cancer cells as measured by real-time quantitative reverse transcription-PCR. Subsequent studies indicated that exogenous expression of miR-29b inhibited Mcl-1, COL1A1, and COL4A1. Further, a novel target with potential implications for invasion and metastasis, matrix metallopeptidase-2 (MMP-2), was identified and confirmed to be a miR-29b target in prostate cancer cells. Together our results demonstrated that exogenous expression of miR-29b regulates prostate cancer cell growth by modulating anti-apoptotic and pro-metastatic matrix molecules, implicating therapeutic potential of miR-29b for prostate cancer inhibition.
LinkOut: [PMID: 20657750]
|
Experimental Support 8 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | HEK293 |
Disease | 4170.0 |
Location of target site | 3'UTR |
Tools used in this research | TargetScan , miRTarCLIP , Piranha |
Original Description (Extracted from the article) |
...
"PAR-CLIP data was present in GSM714644. RNA binding protein: AGO2. Condition:completeT1
"PAR-CLIP data was present in GSM714645. RNA binding protein: AGO2. Condition:completeT1
... - Kishore S; Jaskiewicz L; Burger L; Hausser et al., 2011, Nature methods. |
Article |
- Kishore S; Jaskiewicz L; Burger L; Hausser et al. - Nature methods, 2011
Cross-linking and immunoprecipitation (CLIP) is increasingly used to map transcriptome-wide binding sites of RNA-binding proteins. We developed a method for CLIP data analysis, and applied it to compare CLIP with photoactivatable ribonucleoside-enhanced CLIP (PAR-CLIP) and to uncover how differences in cross-linking and ribonuclease digestion affect the identified sites. We found only small differences in accuracies of these methods in identifying binding sites of HuR, which binds low-complexity sequences, and Argonaute 2, which has a complex binding specificity. We found that cross-link-induced mutations led to single-nucleotide resolution for both PAR-CLIP and CLIP. Our results confirm the expectation from original CLIP publications that RNA-binding proteins do not protect their binding sites sufficiently under the denaturing conditions used during the CLIP procedure, and we show that extensive digestion with sequence-specific RNases strongly biases the recovered binding sites. This bias can be substantially reduced by milder nuclease digestion conditions.
LinkOut: [PMID: 21572407]
|
Experimental Support 9 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | HEK293 |
Disease | 4170.0 |
Location of target site | 3'UTR |
Tools used in this research | TargetScan , miRTarCLIP , Piranha |
Original Description (Extracted from the article) |
...
"PAR-CLIP data was present in GSM1065668. RNA binding protein: AGO1. Condition:4-thiouridine
"PAR-CLIP data was present in GSM1065669. RNA binding protein: AGO1. Condition:4-thiouridine
"PAR-CLIP data was present in GSM1065670. RNA binding protein: AGO2. Condition:4-thiouridine
... - Memczak S; Jens M; Elefsinioti A; Torti F; et al., 2013, Nature. |
Article |
- Memczak S; Jens M; Elefsinioti A; Torti F; et al. - Nature, 2013
Circular RNAs (circRNAs) in animals are an enigmatic class of RNA with unknown function. To explore circRNAs systematically, we sequenced and computationally analysed human, mouse and nematode RNA. We detected thousands of well-expressed, stable circRNAs, often showing tissue/developmental-stage-specific expression. Sequence analysis indicated important regulatory functions for circRNAs. We found that a human circRNA, antisense to the cerebellar degeneration-related protein 1 transcript (CDR1as), is densely bound by microRNA (miRNA) effector complexes and harbours 63 conserved binding sites for the ancient miRNA miR-7. Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript. Together, our data provide evidence that circRNAs form a large class of post-transcriptional regulators. Numerous circRNAs form by head-to-tail splicing of exons, suggesting previously unrecognized regulatory potential of coding sequences.
LinkOut: [PMID: 23446348]
|
Experimental Support 10 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | Fresh human primary pDCs |
Location of target site | 3'UTR |
Tools used in this research | RNAhybrid , TargetScan |
Article |
- Hong Y; Wu J; Zhao J; Wang H; Liu Y; Chen et al. - PloS one, 2013
Glucocorticoids (GCs) are frequently used to treat many of the acute disease manifestations associated with inflammatory and autoimmune disorders. However, Toll-like receptor (TLR) pathway-activated plasmacytoid dendritic cells (pDCs) are resistant to GC-induced apoptosis, which leads to the inefficiency of GCs in the treatment of type I interferon-related autoimmune diseases, such as systemic lupus erythematosus (SLE). Therefore, compounds promoting pDC apoptosis may be helpful for improving the efficacy of GCs. In this study, we performed screening to identify microRNAs (miRNAs) involved in TLR-inhibited GC-induced pDC apoptosis and found an array of miRNAs that may regulate pDC apoptosis. Among those demonstrating altered expression, 6 miRNAs were inhibited in TLR-activated pDCs. Bioinformatics analysis and functional studies indicated that miR-29b and miR-29c were 2 key miRNAs involved in TLR-inhibited GC-induced pDC apoptosis. Furthermore, both of these miRNAs promoted pDC apoptosis by directly targeting Mcl-1 and Bcl-2 in human primary pDCs. Our findings provide new targets that could improve the efficacy of GCs for the treatment of SLE.
LinkOut: [PMID: 23894561]
|
Experimental Support 11 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | GN1C |
Location of target site | 3'UTR |
Tools used in this research | MicroCosm , miRanda , PicTar , PITA , TargetScan |
Original Description (Extracted from the article) |
...
miR-29a and miR-29b targeted MCL1 mRNA in GICs and increased apoptosis
... - Aldaz B; Sagardoy A; Nogueira L; Guruceaga et al., 2013, PloS one. |
Article |
- Aldaz B; Sagardoy A; Nogueira L; Guruceaga et al. - PloS one, 2013
Glioblastoma multiforme (GBM)-initiating cells (GICs) represent a tumor subpopulation with neural stem cell-like properties that is responsible for the development, progression and therapeutic resistance of human GBM. We have recently shown that blockade of NFkappaB pathway promotes terminal differentiation and senescence of GICs both in vitro and in vivo, indicating that induction of differentiation may be a potential therapeutic strategy for GBM. MicroRNAs have been implicated in the pathogenesis of GBM, but a high-throughput analysis of their role in GIC differentiation has not been reported. We have established human GIC cell lines that can be efficiently differentiated into cells expressing astrocytic and neuronal lineage markers. Using this in vitro system, a microarray-based high-throughput analysis to determine global expression changes of microRNAs during differentiation of GICs was performed. A number of changes in the levels of microRNAs were detected in differentiating GICs, including over-expression of hsa-miR-21, hsa-miR-29a, hsa-miR-29b, hsa-miR-221 and hsa-miR-222, and down-regulation of hsa-miR-93 and hsa-miR-106a. Functional studies showed that miR-21 over-expression in GICs induced comparable cell differentiation features and targeted SPRY1 mRNA, which encodes for a negative regulator of neural stem-cell differentiation. In addition, miR-221 and miR-222 inhibition in differentiated cells restored the expression of stem cell markers while reducing differentiation markers. Finally, miR-29a and miR-29b targeted MCL1 mRNA in GICs and increased apoptosis. Our study uncovers the microRNA dynamic expression changes occurring during differentiation of GICs, and identifies miR-21 and miR-221/222 as key regulators of this process.
LinkOut: [PMID: 24155920]
|
Experimental Support 12 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | MCF7 |
Location of target site | 3'UTR |
Tools used in this research | TargetScan , miRTarCLIP , Piranha |
Original Description (Extracted from the article) |
...
PAR-CLIP data was present in SRR1045082. RNA binding protein: AGO2. Condition:Untreated
... - Farazi TA; Ten Hoeve JJ; Brown M; et al., 2014, Genome biology. |
Article |
- Farazi TA; Ten Hoeve JJ; Brown M; et al. - Genome biology, 2014
BACKGROUND: Various microRNAs (miRNAs) are up- or downregulated in tumors. However, the repression of cognate miRNA targets responsible for the phenotypic effects of this dysregulation in patients remains largely unexplored. To define miRNA targets and associated pathways, together with their relationship to outcome in breast cancer, we integrated patient-paired miRNA-mRNA expression data with a set of validated miRNA targets and pathway inference. RESULTS: To generate a biochemically-validated set of miRNA-binding sites, we performed argonaute-2 photoactivatable-ribonucleoside-enhanced crosslinking and immunoprecipitation (AGO2-PAR-CLIP) in MCF7 cells. We then defined putative miRNA-target interactions using a computational model, which ranked and selected additional TargetScan-predicted interactions based on features of our AGO2-PAR-CLIP binding-site data. We subselected modeled interactions according to the abundance of their constituent miRNA and mRNA transcripts in tumors, and we took advantage of the variability of miRNA expression within molecular subtypes to detect miRNA repression. Interestingly, our data suggest that miRNA families control subtype-specific pathways; for example, miR-17, miR-19a, miR-25, and miR-200b show high miRNA regulatory activity in the triple-negative, basal-like subtype, whereas miR-22 and miR-24 do so in the HER2 subtype. An independent dataset validated our findings for miR-17 and miR-25, and showed a correlation between the expression levels of miR-182 targets and overall patient survival. Pathway analysis associated miR-17, miR-19a, and miR-200b with leukocyte transendothelial migration. CONCLUSIONS: We combined PAR-CLIP data with patient expression data to predict regulatory miRNAs, revealing potential therapeutic targets and prognostic markers in breast cancer.
LinkOut: [PMID: 24398324]
|
Experimental Support 13 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | ES2 |
Location of target site | 3'UTR |
Tools used in this research | unspecified |
Original Description (Extracted from the article) |
...
"mimic significantly suppressed luciferase activity of a reporter gene containing the Mcl-1 mRNA 3芒鈧虏-UTR (Fig. 5C). Moreover
... - Sugio A; Iwasaki M; Habata S; Mariya T; et al., 2014, Gynecologic oncology. |
Article |
- Sugio A; Iwasaki M; Habata S; Mariya T; et al. - Gynecologic oncology, 2014
OBJECTIVE: Ovarian cancer is the leading cause of death from gynecologic cancer, reflecting its often late diagnosis and its chemoresistance. We identified a set of microRNAs whose expression is altered upon BAG3 knockdown. Our primary objective was to examine the relationships between BAG3, miR-29b and Mcl-1, an antiapoptotic Bcl-2 family protein, in ovarian cancer cells. METHODS: Ovarian cancer cells were cultured and their responsiveness to paclitaxel was tested. Microarray analysis was performed to identify microRNAs differentially expressed in ES2 BAG3 knockdown ovarian cancer cells and their control cells. Primary ovarian cancer tissues were obtained from 56 patients operated on for ovarian cancer. The patients' clinical and pathological data were obtained from their medical records. RESULTS: BAG3 knockdown increased the chemosensitivity to paclitaxel of ES2 ovarian clear cell carcinoma cells to a greater degree than AMOC2 serous adenocarcinoma cells. qRT-PCR analysis showed that miR-29b expression was significantly upregulated in primary cancer tissue expressing low levels of BAG3, as compared to tissue expressing high levels. Moreover, levels of miR-29b correlated significantly with progression-free survival. Upregulation of miR-29b also reduced levels of Mcl-1 and sensitized ES2 cells to low-dose paclitaxel. CONCLUSIONS: BAG3 knockdown appears to downregulate expression of Mcl-1 through upregulation of miR-29b, thereby increasing the chemosensitivity of ovarian clear cell carcinoma cells. This suggests that BAG3 is a key determinant of the responsiveness of ovarian cancer cells, especially clear cell carcinoma, to paclitaxel and that BAG3 may be a useful therapeutic target for the treatment of ovarian cancer.
LinkOut: [PMID: 24992675]
|
Experimental Support 14 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Tools used in this research | previous_study |
Original Description (Extracted from the article) |
...
"A negative expression correlation level for miR-29a and the two target genes (Bcl-2: rs = 芒藛鈥0.572
... - Xu L; Xu Y; Jing Z; Wang X; Zha X; Zeng C; et al., 2014, Experimental hematology & oncology. |
Article |
- Xu L; Xu Y; Jing Z; Wang X; Zha X; Zeng C; et al. - Experimental hematology & oncology, 2014
OBJECTIVES: The miR-29 family have been demonstrated acting as vital tumor suppressor in multiple cancers as well as regulators in the adaptive immune system. Little is known about their role in leukemogenesis. The purpose of this study is to analyze the expression pattern of miR-29a/29b and its target genes Mcl-1 (myeloid cell leukemia sequence 1) and B-cell lymphoma 2 (Bcl-2) in myeloid leukemia. METHODS: Quantitative real-time PCR was used for detecting genes expression level in peripheral blood mononuclear cells (PBMCs) from 10 cases with newly diagnosed, untreated acute myeloid leukemia (AML) and 14 cases with newly diagnosed, untreated chronic myeloid leukemia (CML) in chronic phase, and 14 healthy individual (HI) served as controls. Correlation between the relative expression levels of different genes have been analyzed. RESULTS: Significant lower expression of miR-29a/29b and higher expression level of two potential target genes Bcl-2 and Mcl-1 were found in PBMCs from AML and CML patients compared with HI group. In addtion, miR-29a expression in AML was significantly lower than that in CML. Moreover, negative correlation between miR-29a/29b and its target genes have been found. While, positive correlation between relative expression level of miR-29a and miR-29b or Bcl-2 and Mcl-1 were presented in the total 38 research objects. CONCLUSION: Down-regulated miR-29a and miR-29b, and accompanying up-regulated Bcl-2 and Mcl-1 are the common feature in myeloid leukemias. These data further support the role for miR-29a/29b dysregulation in myeloid leukemogenesis and the therapeutic promise of regulating miR-29a/29b expression for myeloid leukemia in the future.
LinkOut: [PMID: 25006537]
|
Experimental Support 15 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | Peripheral blood mononuclear cells |
Disease | MIMAT0000100 |
Tools used in this research | PicTar and PITA |
Original Description (Extracted from the article) |
...
"we determined that MCL-1 and JAK3 expression levels in T cells were counter-regulated by miR-29b and miR-198
... - Gigante M; Pontrelli P; Herr W; Gigante M; et al., 2016, Journal of translational medicine. |
Article |
- Gigante M; Pontrelli P; Herr W; Gigante M; et al. - Journal of translational medicine, 2016
BACKGROUND: Mammalian microRNAs (miR) regulate the expression of genes relevant for the development of adaptive and innate immunity against cancer. Since T cell dysfunction has previously been reported in patients with renal cell carcinoma (RCC; clear cell type), we aimed to analyze these immune cells for genetic and protein differences when compared to normal donor T cells freshly after isolation and 35 days after in vitro stimulation (IVS) with HLA-matched RCC tumor cells. METHODS: We investigated gene expression profiles of tumor-reactive CD8(+) T cells obtained from RCC patient and compared with their HLA-matched healthy sibling donors using a microarray approach. In addition, miRNAs analysis was performed in a validation cohort of peripheral blood CD8(+) T cells from 25 RCC patients compared to 15 healthy volunteers. RESULTS: We observed that CD8(+) T cells from RCC patients expressed reduced levels of anti-apoptotic and proliferation-associated gene products when compared with normal donor T cells both pre- and post-IVS. In particular, JAK3 and MCL-1 were down-regulated in patient CD8(+) T cells versus their normal counterparts, likely due to defective suppressor activity of miR-29b and miR-198 in RCC CD8(+) T cells. Indeed, specific inhibition of miR-29b or miR-198 in peripheral blood mononuclear cells (PBMCs) isolated from RCC patients, resulted in the up-regulation of JAK3 and MCL-1 proteins and significant improvement of cell survival in vitro. CONCLUSIONS: Our results suggest that miR-29b and miR-198 dysregulation in RCC patient CD8(+) T cells is associated with dysfunctional immunity and foreshadow the development of miR-targeted therapeutics to correct such T cell defects in vivo.
LinkOut: [PMID: 27063186]
|
Experimental Support 16 for Functional miRNA-Target Interaction | |
---|---|
miRNA:Target | ---- |
Validation Method |
|
Conditions | HCT116 , DLD-1 , HT55 , HT29 , SW837 , VACO4S |
Disease | Crohn's disease fibrosis |
Original Description (Extracted from the article) |
...
We propose that an anti-fibrotic miR-29b/IL-6 IL8/MCL-1L axis may influence intestinal fibrosis in CD
... - Nijhuis A; Curciarello R; Mehta S; Feakins et al., 2017, Cell and tissue research. |
Article |
- Nijhuis A; Curciarello R; Mehta S; Feakins et al. - Cell and tissue research, 2017
The miR-29 family is involved in fibrosis in multiple organs, including the intestine where miR-29b facilitates TGF-beta-mediated up-regulation of collagen in mucosal fibroblasts from Crohn's disease (CD) patients. Myeloid cell leukemia-1 (MCL-1), a member of the B-cell CLL/Lymphoma 2 (BCL-2) apoptosis family, is involved in liver fibrosis and is targeted by miR-29b via its 3'-UTR in cultured cell lines. We investigate the role of MCL-1 and miR-29b in primary intestinal fibroblasts and tissue from stricturing CD patients. Transfection of CD intestinal fibroblasts with pre-miR-29b resulted in a significant increase in the mRNA expression of MCL-1 isoforms [MCL-1Long (L)/Extra Short (ES) and MCL-1Short (S)], although MCL-1S was expressed at significantly lower levels. Western blotting predominantly detected the anti-apoptotic MCL-1L isoform, and immunofluorescence showed that staining was localised in discrete nuclear foci. Transfection with pre-miR-29b or anti-miR-29b resulted in a significant increase or decrease, respectively, in MCL-1L foci. CD fibroblasts treated with IL-6 and IL-8, inflammatory cytokines upstream of MCL-1, increased the total mass of MCL-1L-positive foci. Furthermore, transfection of intestinal fibroblasts with pre-miR-29b resulted in an increase in mRNA and protein levels of IL-6 and IL-8. Finally, immunohistochemistry showed reduced MCL-1 protein expression in fibrotic CD samples compared to non-stricturing controls. Together, our findings suggest that induction of MCL-1 by IL-6/IL-8 may surmount any direct down-regulation by miR-29b via its 3'-UTR. We propose that an anti-fibrotic miR-29b/IL-6 IL-8/MCL-1L axis may influence intestinal fibrosis in CD. In the future, therapeutic modulation of this pathway might contribute to the management of fibrosis in CD.
LinkOut: [PMID: 28190086]
|
CLIP-seq Support 1 for dataset GSM545212 | |
---|---|
Method / RBP | PAR-CLIP / AGO1 |
Cell line / Condition | HEK293 / Control |
Location of target site | ENST00000369026.2 | 3UTR | UCUAACCAUGGUGCUAUUAUUA |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 20371350 / GSE21578 |
CLIP-seq Viewer | Link |
CLIP-seq Support 2 for dataset GSM545214 | |
---|---|
Method / RBP | PAR-CLIP / AGO3 |
Cell line / Condition | HEK293 / Control |
Location of target site | ENST00000369026.2 | 3UTR | UCUAACCAUGGUGCUAUUAUUAG |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 20371350 / GSE21578 |
CLIP-seq Viewer | Link |
CLIP-seq Support 3 for dataset GSM545215 | |
---|---|
Method / RBP | PAR-CLIP / AGO4 |
Cell line / Condition | HEK293 / Control |
Location of target site | ENST00000369026.2 | 3UTR | UCUAACCAUGGUGCUAUUAU |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 20371350 / GSE21578 |
CLIP-seq Viewer | Link |
CLIP-seq Support 4 for dataset GSM545216 | |
---|---|
Method / RBP | PAR-CLIP / AGO2 |
Cell line / Condition | HEK293 / miR-124 transfection |
Location of target site | ENST00000369026.2 | 3UTR | CAGGCUAGUCUAACCAUGGUGCUAUUAUUAG |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 20371350 / GSE21578 |
CLIP-seq Viewer | Link |
CLIP-seq Support 5 for dataset GSM545217 | |
---|---|
Method / RBP | PAR-CLIP / AGO2 |
Cell line / Condition | HEK293 / miR-7 transfection |
Location of target site | ENST00000369026.2 | 3UTR | UCUAACCAUGGUGCUAUUAUU |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 20371350 / GSE21578 |
CLIP-seq Viewer | Link |
CLIP-seq Support 6 for dataset GSM714644 | |
---|---|
Method / RBP | PAR-CLIP / AGO2 |
Cell line / Condition | HEK293 / completeT1, repA |
Location of target site | ENST00000369026.2 | 3UTR | CAGGCUAGUCUAACCAUGGUGCUAUUAUUAGGCUUG |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 21572407 / GSE28865 |
CLIP-seq Viewer | Link |
CLIP-seq Support 7 for dataset GSM714645 | |
---|---|
Method / RBP | PAR-CLIP / AGO2 |
Cell line / Condition | HEK293 / completeT1, repB |
Location of target site | ENST00000369026.2 | 3UTR | UCUAACCAUGGUGCUAUUAUUAG |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 21572407 / GSE28865 |
CLIP-seq Viewer | Link |
CLIP-seq Support 8 for dataset GSM1065668 | |
---|---|
Method / RBP | PAR-CLIP / AGO1 |
Cell line / Condition | HEK293 / 4-thiouridine, ML_MM_7 |
Location of target site | ENST00000369026.2 | 3UTR | GCUAGUCUAACCAUGGUGCUAUUAU |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 23446348 / GSE43573 |
CLIP-seq Viewer | Link |
CLIP-seq Support 9 for dataset GSM1065669 | |
---|---|
Method / RBP | PAR-CLIP / AGO1 |
Cell line / Condition | HEK293 / 4-thiouridine, ML_MM_8 |
Location of target site | ENST00000369026.2 | 3UTR | UCUAACCAUGGUGCUAUUAUUAG |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 23446348 / GSE43573 |
CLIP-seq Viewer | Link |
CLIP-seq Support 10 for dataset GSM1065670 | |
---|---|
Method / RBP | PAR-CLIP / AGO2 |
Cell line / Condition | HEK293 / 4-thiouridine, 3_ML_LG |
Location of target site | ENST00000369026.2 | 3UTR | CAGGCUAGUCUAACCAUGGUGCUAUUAUUAGGCU |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 23446348 / GSE43573 |
CLIP-seq Viewer | Link |
CLIP-seq Support 11 for dataset SRR1045082 | |
---|---|
Method / RBP | PAR-CLIP / AGO2 |
Cell line / Condition | MCF7 / Untreated |
Location of target site | ENST00000369026.2 | 3UTR | UCUAACCAUGGUGCUAUUAUUAG |
Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
Article / Accession Series | PMID: 24398324 / SRX388831 |
CLIP-seq Viewer | Link |
MiRNA-Target Expression Profile | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
MiRNA-Target Expression Profile (TCGA) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
ID | Target | Description | Validation methods | |||||||||
Strong evidence | Less strong evidence | |||||||||||
MIRT000095 | TGFB3 | transforming growth factor beta 3 | 2 | 1 | ||||||||
MIRT000096 | HDAC4 | histone deacetylase 4 | 4 | 4 | ||||||||
MIRT000097 | CTNNBIP1 | catenin beta interacting protein 1 | 4 | 4 | ||||||||
MIRT000098 | COL5A3 | collagen type V alpha 3 chain | 2 | 2 | ||||||||
MIRT000099 | COL4A2 | collagen type IV alpha 2 chain | 2 | 2 | ||||||||
MIRT000100 | COL1A1 | collagen type I alpha 1 chain | 8 | 8 | ||||||||
MIRT000101 | ACVR2A | activin A receptor type 2A | 1 | 1 | ||||||||
MIRT000445 | SP1 | Sp1 transcription factor | 5 | 6 | ||||||||
MIRT000684 | CDK6 | cyclin dependent kinase 6 | 6 | 5 | ||||||||
MIRT000930 | BACE1 | beta-secretase 1 | 3 | 1 | ||||||||
MIRT002310 | SFPQ | splicing factor proline and glutamine rich | 3 | 1 | ||||||||
MIRT002316 | DNAJB11 | DnaJ heat shock protein family (Hsp40) member B11 | 3 | 1 | ||||||||
MIRT003026 | DNMT3B | DNA methyltransferase 3 beta | 4 | 7 | ||||||||
MIRT003029 | DNMT3A | DNA methyltransferase 3 alpha | 5 | 9 | ||||||||
MIRT003287 | MCL1 | MCL1, BCL2 family apoptosis regulator | 7 | 20 | ||||||||
MIRT003290 | BCL2 | BCL2, apoptosis regulator | 4 | 3 | ||||||||
MIRT003661 | DNMT1 | DNA methyltransferase 1 | 4 | 2 | ||||||||
MIRT003736 | S100B | S100 calcium binding protein B | 3 | 1 | ||||||||
MIRT003813 | VEGFA | vascular endothelial growth factor A | 9 | 9 | ||||||||
MIRT004308 | ESR1 | estrogen receptor 1 | 2 | 1 | ||||||||
MIRT004312 | NCOA3 | nuclear receptor coactivator 3 | 2 | 1 | ||||||||
MIRT004419 | TET1 | tet methylcytosine dioxygenase 1 | 4 | 2 | ||||||||
MIRT004510 | TCL1A | T-cell leukemia/lymphoma 1A | 5 | 4 | ||||||||
MIRT005381 | Mmp15 | matrix metallopeptidase 15 | 3 | 1 | ||||||||
MIRT005383 | MMP15 | matrix metallopeptidase 15 | 2 | 1 | ||||||||
MIRT005385 | MMP24 | matrix metallopeptidase 24 | 4 | 2 | ||||||||
MIRT005387 | Mmp24 | matrix metallopeptidase 24 | 2 | 1 | ||||||||
MIRT005486 | GRN | granulin precursor | 4 | 1 | ||||||||
MIRT005522 | FGG | fibrinogen gamma chain | 2 | 1 | ||||||||
MIRT005533 | FGA | fibrinogen alpha chain | 2 | 1 | ||||||||
MIRT005534 | FGB | fibrinogen beta chain | 2 | 1 | ||||||||
MIRT005567 | COL3A1 | collagen type III alpha 1 chain | 5 | 4 | ||||||||
MIRT005568 | COL4A1 | collagen type IV alpha 1 chain | 7 | 9 | ||||||||
MIRT005570 | MMP2 | matrix metallopeptidase 2 | 5 | 8 | ||||||||
MIRT005614 | BBC3 | BCL2 binding component 3 | 2 | 2 | ||||||||
MIRT005667 | ADAM12 | ADAM metallopeptidase domain 12 | 5 | 3 | ||||||||
MIRT005669 | NID1 | nidogen 1 | 4 | 1 | ||||||||
MIRT006054 | HMGA2 | high mobility group AT-hook 2 | 3 | 1 | ||||||||
MIRT006058 | TGFB2 | transforming growth factor beta 2 | 3 | 2 | ||||||||
MIRT006059 | TGFB1 | transforming growth factor beta 1 | 2 | 1 | ||||||||
MIRT006060 | BMP1 | bone morphogenetic protein 1 | 3 | 2 | ||||||||
MIRT006098 | PTEN | phosphatase and tensin homolog | 7 | 3 | ||||||||
MIRT006251 | NASP | nuclear autoantigenic sperm protein | 2 | 1 | ||||||||
MIRT006486 | PPP1R13B | protein phosphatase 1 regulatory subunit 13B | 2 | 1 | ||||||||
MIRT006488 | CDC42 | cell division cycle 42 | 4 | 2 | ||||||||
MIRT006753 | GSK3B | glycogen synthase kinase 3 beta | 1 | 1 | ||||||||
MIRT006815 | PIK3CG | phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma | 3 | 1 | ||||||||
MIRT006915 | NKIRAS2 | NFKB inhibitor interacting Ras like 2 | 5 | 3 | ||||||||
MIRT007011 | RAX | retina and anterior neural fold homeobox | 2 | 1 | ||||||||
MIRT007033 | TBX21 | T-box 21 | 1 | 1 | ||||||||
MIRT007034 | IFNG | interferon gamma | 1 | 1 | ||||||||
MIRT007102 | DUSP2 | dual specificity phosphatase 2 | 3 | 3 | ||||||||
MIRT007254 | FOS | Fos proto-oncogene, AP-1 transcription factor subunit | 3 | 3 | ||||||||
MIRT027237 | PIK3R1 | phosphoinositide-3-kinase regulatory subunit 1 | 2 | 2 | ||||||||
MIRT027238 | IMPDH1 | inosine monophosphate dehydrogenase 1 | 2 | 2 | ||||||||
MIRT027239 | MYCN | MYCN proto-oncogene, bHLH transcription factor | 3 | 3 | ||||||||
MIRT048359 | SCAF8 | SR-related CTD associated factor 8 | 1 | 1 | ||||||||
MIRT048360 | CLDN1 | claudin 1 | 1 | 1 | ||||||||
MIRT048361 | MRPS35 | mitochondrial ribosomal protein S35 | 1 | 1 | ||||||||
MIRT048362 | RSL24D1 | ribosomal L24 domain containing 1 | 1 | 1 | ||||||||
MIRT048363 | LRP10 | LDL receptor related protein 10 | 1 | 1 | ||||||||
MIRT048364 | HP1BP3 | heterochromatin protein 1 binding protein 3 | 1 | 1 | ||||||||
MIRT048365 | B4GALT5 | beta-1,4-galactosyltransferase 5 | 1 | 1 | ||||||||
MIRT048366 | KIAA1671 | KIAA1671 | 1 | 1 | ||||||||
MIRT048367 | NNT | nicotinamide nucleotide transhydrogenase | 1 | 1 | ||||||||
MIRT048368 | IFIH1 | interferon induced with helicase C domain 1 | 1 | 1 | ||||||||
MIRT048369 | TPT1 | tumor protein, translationally-controlled 1 | 1 | 1 | ||||||||
MIRT048370 | RUNDC3B | RUN domain containing 3B | 1 | 1 | ||||||||
MIRT048371 | CECR2 | CECR2, histone acetyl-lysine reader | 1 | 1 | ||||||||
MIRT048372 | TPD52L2 | tumor protein D52 like 2 | 1 | 1 | ||||||||
MIRT048373 | NUS1 | NUS1 dehydrodolichyl diphosphate synthase subunit | 1 | 1 | ||||||||
MIRT048374 | CIT | citron rho-interacting serine/threonine kinase | 1 | 1 | ||||||||
MIRT048375 | GNB2L1 | receptor for activated C kinase 1 | 1 | 1 | ||||||||
MIRT048376 | SMARCC1 | SWI/SNF related, matrix associated, actin dependent regulator of chromatin subfamily c member 1 | 1 | 1 | ||||||||
MIRT048377 | PRKAA1 | protein kinase AMP-activated catalytic subunit alpha 1 | 1 | 1 | ||||||||
MIRT048378 | PIGN | phosphatidylinositol glycan anchor biosynthesis class N | 1 | 1 | ||||||||
MIRT048379 | RPS4X | ribosomal protein S4, X-linked | 1 | 1 | ||||||||
MIRT048380 | CCSAP | centriole, cilia and spindle associated protein | 1 | 1 | ||||||||
MIRT048381 | CALU | calumenin | 1 | 1 | ||||||||
MIRT048382 | NREP | neuronal regeneration related protein | 1 | 1 | ||||||||
MIRT048383 | MKI67 | marker of proliferation Ki-67 | 1 | 1 | ||||||||
MIRT053293 | TDG | thymine DNA glycosylase | 5 | 5 | ||||||||
MIRT053581 | CCND2 | cyclin D2 | 5 | 3 | ||||||||
MIRT053738 | COL4A5 | collagen type IV alpha 5 chain | 1 | 1 | ||||||||
MIRT053739 | COL7A1 | collagen type VII alpha 1 chain | 1 | 1 | ||||||||
MIRT053740 | COL15A1 | collagen type XV alpha 1 chain | 1 | 1 | ||||||||
MIRT053741 | COL2A1 | collagen type II alpha 1 chain | 1 | 1 | ||||||||
MIRT053742 | COL4A6 | collagen type IV alpha 6 chain | 1 | 1 | ||||||||
MIRT053743 | CSGALNACT2 | chondroitin sulfate N-acetylgalactosaminyltransferase 2 | 1 | 1 | ||||||||
MIRT053744 | SOX12 | SRY-box 12 | 1 | 1 | ||||||||
MIRT053745 | MAP2K6 | mitogen-activated protein kinase kinase 6 | 1 | 1 | ||||||||
MIRT053746 | TGIF2 | TGFB induced factor homeobox 2 | 1 | 1 | ||||||||
MIRT053747 | SERPINH1 | serpin family H member 1 | 2 | 2 | ||||||||
MIRT053748 | NOTCH2 | notch 2 | 4 | 1 | ||||||||
MIRT053749 | PPARD | peroxisome proliferator activated receptor delta | 1 | 1 | ||||||||
MIRT054045 | SNAI3 | snail family transcriptional repressor 3 | 2 | 1 | ||||||||
MIRT054192 | AKT2 | AKT serine/threonine kinase 2 | 4 | 2 | ||||||||
MIRT054574 | PER1 | period circadian clock 1 | 3 | 1 | ||||||||
MIRT060983 | LAMC1 | laminin subunit gamma 1 | 3 | 1 | ||||||||
MIRT061662 | BTG2 | BTG anti-proliferation factor 2 | 2 | 4 | ||||||||
MIRT067385 | TMTC3 | transmembrane and tetratricopeptide repeat containing 3 | 2 | 4 | ||||||||
MIRT079942 | RNF138 | ring finger protein 138 | 2 | 2 | ||||||||
MIRT080798 | SH3GLB1 | SH3 domain containing GRB2 like, endophilin B1 | 2 | 4 | ||||||||
MIRT081893 | KCTD15 | potassium channel tetramerization domain containing 15 | 2 | 8 | ||||||||
MIRT082515 | CALM3 | calmodulin 3 | 2 | 2 | ||||||||
MIRT085293 | CCNT2 | cyclin T2 | 2 | 6 | ||||||||
MIRT102856 | INSIG1 | insulin induced gene 1 | 2 | 2 | ||||||||
MIRT207249 | TET3 | tet methylcytosine dioxygenase 3 | 2 | 2 | ||||||||
MIRT207755 | VHL | von Hippel-Lindau tumor suppressor | 2 | 4 | ||||||||
MIRT210969 | TET2 | tet methylcytosine dioxygenase 2 | 1 | 1 | ||||||||
MIRT211650 | ABCE1 | ATP binding cassette subfamily E member 1 | 2 | 2 | ||||||||
MIRT213230 | REST | RE1 silencing transcription factor | 2 | 10 | ||||||||
MIRT225103 | GOLGA7 | golgin A7 | 2 | 2 | ||||||||
MIRT250481 | MAZ | MYC associated zinc finger protein | 2 | 2 | ||||||||
MIRT264266 | FAM102B | family with sequence similarity 102 member B | 2 | 2 | ||||||||
MIRT267090 | ZFP91 | ZFP91 zinc finger protein | 2 | 2 | ||||||||
MIRT303363 | MXD1 | MAX dimerization protein 1 | 2 | 1 | ||||||||
MIRT316344 | ULBP2 | UL16 binding protein 2 | 2 | 2 | ||||||||
MIRT401476 | AIM1 | crystallin beta-gamma domain containing 1 | 2 | 1 | ||||||||
MIRT437369 | LAMC2 | laminin subunit gamma 2 | 3 | 1 | ||||||||
MIRT437372 | ITGA6 | integrin subunit alpha 6 | 3 | 2 | ||||||||
MIRT437552 | COL5A2 | collagen type V alpha 2 chain | 1 | 1 | ||||||||
MIRT437553 | COL10A1 | collagen type X alpha 1 chain | 1 | 1 | ||||||||
MIRT437554 | SPARC | secreted protein acidic and cysteine rich | 1 | 1 | ||||||||
MIRT437555 | FBN1 | fibrillin 1 | 1 | 1 | ||||||||
MIRT437556 | LOX | lysyl oxidase | 2 | 2 | ||||||||
MIRT437557 | PDGFRB | platelet derived growth factor receptor beta | 2 | 2 | ||||||||
MIRT437710 | PHACTR2 | phosphatase and actin regulator 2 | 2 | 1 | ||||||||
MIRT437713 | TUBB2A | tubulin beta 2A class IIa | 2 | 1 | ||||||||
MIRT437716 | EMP1 | epithelial membrane protein 1 | 2 | 1 | ||||||||
MIRT437719 | SNX24 | sorting nexin 24 | 2 | 1 | ||||||||
MIRT437722 | AMFR | autocrine motility factor receptor | 2 | 1 | ||||||||
MIRT437725 | RIOK3 | RIO kinase 3 | 2 | 1 | ||||||||
MIRT437728 | WDR26 | WD repeat domain 26 | 4 | 3 | ||||||||
MIRT437731 | DSC2 | desmocollin 2 | 2 | 1 | ||||||||
MIRT437870 | IL32 | interleukin 32 | 1 | 1 | ||||||||
MIRT438911 | GATA3 | GATA binding protein 3 | 2 | 1 | ||||||||
MIRT438912 | PDGFRA | platelet derived growth factor receptor alpha | 2 | 1 | ||||||||
MIRT438913 | PDGFC | platelet derived growth factor C | 2 | 1 | ||||||||
MIRT438914 | PDGFB | platelet derived growth factor subunit B | 2 | 1 | ||||||||
MIRT438915 | PDGFA | platelet derived growth factor subunit A | 2 | 1 | ||||||||
MIRT438916 | MMP9 | matrix metallopeptidase 9 | 2 | 1 | ||||||||
MIRT438917 | LOXL4 | lysyl oxidase like 4 | 2 | 1 | ||||||||
MIRT438918 | LOXL2 | lysyl oxidase like 2 | 2 | 1 | ||||||||
MIRT438919 | ITGB1 | integrin subunit beta 1 | 2 | 1 | ||||||||
MIRT438920 | ANGPTL4 | angiopoietin like 4 | 2 | 1 | ||||||||
MIRT454812 | NEDD9 | neural precursor cell expressed, developmentally down-regulated 9 | 2 | 2 | ||||||||
MIRT456827 | MORF4L2 | mortality factor 4 like 2 | 2 | 8 | ||||||||
MIRT462151 | RPL22 | ribosomal protein L22 | 2 | 2 | ||||||||
MIRT465314 | TRAM2 | translocation associated membrane protein 2 | 2 | 2 | ||||||||
MIRT467808 | SLC2A14 | solute carrier family 2 member 14 | 2 | 2 | ||||||||
MIRT467829 | SLC29A2 | solute carrier family 29 member 2 | 2 | 2 | ||||||||
MIRT467971 | SLC16A1 | solute carrier family 16 member 1 | 2 | 4 | ||||||||
MIRT468225 | SGK1 | serum/glucocorticoid regulated kinase 1 | 2 | 2 | ||||||||
MIRT469448 | REL | REL proto-oncogene, NF-kB subunit | 2 | 2 | ||||||||
MIRT469723 | RAB40C | RAB40C, member RAS oncogene family | 2 | 2 | ||||||||
MIRT469841 | R3HDM4 | R3H domain containing 4 | 2 | 2 | ||||||||
MIRT472643 | NAA40 | N(alpha)-acetyltransferase 40, NatD catalytic subunit | 2 | 2 | ||||||||
MIRT474209 | LEPRE1 | prolyl 3-hydroxylase 1 | 1 | 1 | ||||||||
MIRT474576 | KLHDC3 | kelch domain containing 3 | 2 | 2 | ||||||||
MIRT475837 | HDGF | heparin binding growth factor | 2 | 4 | ||||||||
MIRT476721 | FRK | fyn related Src family tyrosine kinase | 2 | 4 | ||||||||
MIRT477473 | ELMSAN1 | ELM2 and Myb/SANT domain containing 1 | 2 | 2 | ||||||||
MIRT478668 | CTC1 | CST telomere replication complex component 1 | 2 | 14 | ||||||||
MIRT478710 | CSRNP2 | cysteine and serine rich nuclear protein 2 | 2 | 2 | ||||||||
MIRT478985 | COMMD2 | COMM domain containing 2 | 2 | 2 | ||||||||
MIRT479826 | CCNA2 | cyclin A2 | 2 | 8 | ||||||||
MIRT479901 | CCDC117 | coiled-coil domain containing 117 | 2 | 2 | ||||||||
MIRT480066 | CAND1 | cullin associated and neddylation dissociated 1 | 2 | 2 | ||||||||
MIRT482012 | AMER1 | APC membrane recruitment protein 1 | 2 | 8 | ||||||||
MIRT489024 | C1QTNF6 | C1q and TNF related 6 | 5 | 2 | ||||||||
MIRT492513 | RAET1L | retinoic acid early transcript 1L | 2 | 2 | ||||||||
MIRT493825 | FSCN1 | fascin actin-bundling protein 1 | 2 | 2 | ||||||||
MIRT495936 | SLC7A5P2 | solute carrier family 7 member 5 pseudogene 2 | 2 | 2 | ||||||||
MIRT496358 | PPY | pancreatic polypeptide | 2 | 2 | ||||||||
MIRT496662 | TMEM237 | transmembrane protein 237 | 2 | 2 | ||||||||
MIRT497644 | GLDN | gliomedin | 2 | 2 | ||||||||
MIRT501878 | MORF4L1 | mortality factor 4 like 1 | 2 | 8 | ||||||||
MIRT502932 | CDC42SE1 | CDC42 small effector 1 | 2 | 4 | ||||||||
MIRT506750 | LDOC1L | retrotransposon Gag like 6 | 2 | 6 | ||||||||
MIRT507168 | GAS2L3 | growth arrest specific 2 like 3 | 2 | 2 | ||||||||
MIRT514918 | MDM2 | MDM2 proto-oncogene | 2 | 6 | ||||||||
MIRT523962 | DYNLT1 | dynein light chain Tctex-type 1 | 2 | 4 | ||||||||
MIRT527675 | CASP8 | caspase 8 | 2 | 2 | ||||||||
MIRT536936 | HECW1 | HECT, C2 and WW domain containing E3 ubiquitin protein ligase 1 | 2 | 2 | ||||||||
MIRT537359 | FJX1 | four jointed box 1 | 2 | 2 | ||||||||
MIRT537687 | ENPP2 | ectonucleotide pyrophosphatase/phosphodiesterase 2 | 2 | 2 | ||||||||
MIRT538124 | DDX6 | DEAD-box helicase 6 | 2 | 2 | ||||||||
MIRT538813 | C21orf91 | chromosome 21 open reading frame 91 | 2 | 2 | ||||||||
MIRT546938 | PTP4A1 | protein tyrosine phosphatase type IVA, member 1 | 2 | 2 | ||||||||
MIRT547104 | PLAG1 | PLAG1 zinc finger | 2 | 2 | ||||||||
MIRT547823 | ISG20L2 | interferon stimulated exonuclease gene 20 like 2 | 2 | 2 | ||||||||
MIRT548237 | FEM1B | fem-1 homolog B | 2 | 2 | ||||||||
MIRT550036 | WWTR1 | WW domain containing transcription regulator 1 | 2 | 2 | ||||||||
MIRT552619 | ZBTB5 | zinc finger and BTB domain containing 5 | 2 | 2 | ||||||||
MIRT556562 | LIMS1 | LIM zinc finger domain containing 1 | 2 | 2 | ||||||||
MIRT558857 | CDC23 | cell division cycle 23 | 2 | 2 | ||||||||
MIRT565485 | SPRTN | SprT-like N-terminal domain | 2 | 2 | ||||||||
MIRT568205 | CBX6 | chromobox 6 | 2 | 2 | ||||||||
MIRT576774 | Tmem127 | transmembrane protein 127 | 2 | 2 | ||||||||
MIRT576958 | Pigs | phosphatidylinositol glycan anchor biosynthesis, class S | 2 | 3 | ||||||||
MIRT610003 | PIGS | phosphatidylinositol glycan anchor biosynthesis class S | 2 | 3 | ||||||||
MIRT616511 | COX7A2L | cytochrome c oxidase subunit 7A2 like | 2 | 2 | ||||||||
MIRT640887 | ENTPD1 | ectonucleoside triphosphate diphosphohydrolase 1 | 2 | 2 | ||||||||
MIRT641350 | RAB11FIP1 | RAB11 family interacting protein 1 | 2 | 2 | ||||||||
MIRT642978 | TESPA1 | thymocyte expressed, positive selection associated 1 | 2 | 2 | ||||||||
MIRT643634 | YY2 | YY2 transcription factor | 2 | 2 | ||||||||
MIRT644386 | ZNF286A | zinc finger protein 286A | 2 | 2 | ||||||||
MIRT650749 | YAE1D1 | Yae1 domain containing 1 | 2 | 2 | ||||||||
MIRT661585 | EPHX2 | epoxide hydrolase 2 | 2 | 2 | ||||||||
MIRT664287 | RNMTL1 | mitochondrial rRNA methyltransferase 3 | 2 | 2 | ||||||||
MIRT689393 | ZNF850 | zinc finger protein 850 | 2 | 2 | ||||||||
MIRT693815 | SEC31A | SEC31 homolog A, COPII coat complex component | 2 | 2 | ||||||||
MIRT694532 | TRIM72 | tripartite motif containing 72 | 2 | 2 | ||||||||
MIRT694628 | ZFPM1 | zinc finger protein, FOG family member 1 | 2 | 2 | ||||||||
MIRT695135 | PRY2 | PTPN13-like, Y-linked 2 | 2 | 2 | ||||||||
MIRT695152 | PRY | PTPN13-like, Y-linked | 2 | 2 | ||||||||
MIRT703640 | FBRS | fibrosin | 2 | 2 | ||||||||
MIRT704551 | CNBP | CCHC-type zinc finger nucleic acid binding protein | 2 | 2 | ||||||||
MIRT704967 | CBX2 | chromobox 2 | 2 | 2 | ||||||||
MIRT705497 | ASXL2 | additional sex combs like 2, transcriptional regulator | 2 | 2 | ||||||||
MIRT707993 | OTUD4 | OTU deubiquitinase 4 | 2 | 2 | ||||||||
MIRT708741 | FAM71F2 | family with sequence similarity 71 member F2 | 2 | 2 | ||||||||
MIRT710621 | COLEC10 | collectin subfamily member 10 | 2 | 2 | ||||||||
MIRT713056 | IFRD1 | interferon related developmental regulator 1 | 2 | 2 | ||||||||
MIRT715515 | MAPKBP1 | mitogen-activated protein kinase binding protein 1 | 2 | 2 | ||||||||
MIRT720770 | FAM193A | family with sequence similarity 193 member A | 2 | 2 | ||||||||
MIRT731925 | AQP4 | aquaporin 4 | 3 | 1 | ||||||||
MIRT732673 | HMGB1 | high mobility group box 1 | 3 | 0 | ||||||||
MIRT734350 | IL6 | interleukin 6 | 1 | 0 | ||||||||
MIRT734351 | TP53 | tumor protein p53 | 1 | 0 | ||||||||
MIRT734565 | BCL2L11 | BCL2 like 11 | 2 | 0 | ||||||||
MIRT734770 | TRIM44 | tripartite motif containing 44 | 2 | 0 | ||||||||
MIRT734771 | CCNE1 | cyclin E1 | 2 | 0 | ||||||||
MIRT735260 | STAT3 | signal transducer and activator of transcription 3 | 6 | 1 | ||||||||
MIRT735414 | HBP1 | HMG-box transcription factor 1 | 3 | 0 | ||||||||
MIRT735537 | HIF3A | hypoxia inducible factor 3 alpha subunit | 3 | 0 | ||||||||
MIRT735639 | HUWE1 | HECT, UBA and WWE domain containing 1, E3 ubiquitin protein ligase | 3 | 0 | ||||||||
MIRT735641 | AKT3 | AKT serine/threonine kinase 3 | 3 | 0 | ||||||||
MIRT735943 | DNM3OS | DNM3 opposite strand/antisense RNA | 4 | 0 | ||||||||
MIRT737493 | SMAD3 | SMAD family member 3 | 1 | 0 | ||||||||
MIRT737577 | SNAI1 | snail family transcriptional repressor 1 | 2 | 0 | ||||||||
MIRT755941 | SLMAP | sarcolemma associated protein | 4 | 1 | ||||||||
MIRT755963 | ROBO1 | roundabout guidance receptor 1 | 5 | 1 | ||||||||
MIRT755964 | SRGAP2 | SLIT-ROBO Rho GTPase activating protein 2 | 5 | 1 | ||||||||
MIRT756271 | YWHAE | tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein epsilon | 3 | 1 | ||||||||
MIRT756364 | LIN7A | lin-7 homolog A, crumbs cell polarity complex component | 2 | 1 | ||||||||
MIRT756474 | COL5A1 | collagen type V alpha 1 chain | 3 | 1 |
miRNA-Drug Associations | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
miRNA-Drug Resistance Associations | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|