| pre-miRNA Information | |
|---|---|
| pre-miRNA | hsa-mir-151b |
| Genomic Coordinates | chr14: 100109419 - 100109514 |
| Description | Homo sapiens miR-151b stem-loop |
| Comment | None |
| RNA Secondary Structure |  |
| Associated Diseases |  |
| Mature miRNA Information | |||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Mature miRNA | hsa-miR-151b | ||||||||||||
| Sequence | 60| UCGAGGAGCUCACAGUCU |77 | ||||||||||||
| Evidence | Experimental | ||||||||||||
| Experiments | RAKE | ||||||||||||
| SNPs in miRNA |
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| Putative Targets | |||||||||||||
| miRNA Expression profile | |
|---|---|
| Human miRNA Tissue Atlas | |
| miRNAs in Extracellular Vesicles |
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| Circulating MicroRNA Expression Profiling | |
| Gene Information | |||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Gene Symbol | SMYD1 | ||||||||||||||||||||
| Synonyms | BOP, KMT3D, ZMYND18, ZMYND22 | ||||||||||||||||||||
| Description | SET and MYND domain containing 1 | ||||||||||||||||||||
| Transcript | NM_198274 | ||||||||||||||||||||
| Expression | |||||||||||||||||||||
| Putative miRNA Targets on SMYD1 | |||||||||||||||||||||
| 3'UTR of SMYD1 (miRNA target sites are highlighted) |
>SMYD1|NM_198274|3'UTR 1 GGACTGCCCAGTGGAGGAGGGGCGATGTGGCTGGGGAGCTAGGGAGAGACTCTGGAGGTGGTGGGTCTCTCGGGAGACCC 81 CTAATGAGGAAGTTGAGGTAATGCTTAACATTGTTGCTGTGAGAATTTACTGCCCTATGTTTCCCAGAGCCATTTTGGCT 161 CAATTCAAGTCTATTCAATTCAAGTTAACTCTAGCCCAGCCCAGATCAACTCCTCCTACAAATATTATTGGATGATAGGC 241 CCTAGAACCCAATAAAGGAGCTCCAAATGTCGTTGGGTGGGGAAGCAAAATGTAGAGAAACATTTAAAGCACACTGTAAT 321 AATAAATGCAATTATAAACTATATGGAGGAGGGTGCAGAGGAGGGAATGTGTCTGGTGTGTGATGTGTGTGTGTGCAGTG 401 GGGGTATCACAGAGAGTATGACATCTGAGTTGAGGGTAGCAGGTGCCTGGAGTCTCAGGTGGCTGCTCACCCATCTGTGC 481 AGGTGTCTCTGGGGCTGCTGGTCTCACCTGTGGTCTGCAGTAGACACAATTGGCTGAGCAGGATATGTGATACTGTGTGG 561 TTGGTGTGGAGTTTTGAAGAAGGGGCTGTGTTTGGGCCACGTAGGCTCTACTCAGAGACCTGAAACCACTTCAGAATGGT 641 GCATATGTCGAAAGAGCTGGCTGGGGGCCTTGCCCAAACCAACTGAGGTCTTAAAGTCCAGGGAAAAAAAGTCTGGGTTC 721 CAACTAGAATTCTAGAAATATTTCTAGAACACACAGAGAGGGAATAAGTCCCTCTATCACCCTTATTACCAAGCCTTGTG 801 GTTCCCTGTGATTTTAGATAATGTCTGATATTTTTCTGGCTATTTGCCTAGTAGGATTTAAAAAATATTTTCAAAGTGAA 881 GCTGAGAGAGAATCTTGGAAACACACATACCTGTTGATCATGGGCCCTGCAGAATTGGCCCTTGGGGGCTTTATTTGGTT 961 ACATGTGCCTGGGTGGTCTTTACCAGCTTAGACTCTATCATGGGCCCCCATGAAGCTCCATTCTCAATACTGAATAATTA 1041 TTACTTCCCTTGTTGAGTTTCTTTTTCTGTCATGCCCTGGGGGCTTCTGCTCTTCTCACCAGAAAGAACATTTGAATCTG 1121 GATTCTTGTACACCTGGGTTAGACCCTGTTCAGAGGTGTGGCCAATTTATCCCGATCTCCTGGAAGGCTGTTGTGATTTC 1201 CATCTAAGAAATGAGGGTCTTGAGAATCAACCAGTCCCAAGATTAGCCTGTTATCCTGTTATCTACTGAGACCCCAAATT 1281 TCTCACCAATGTTTTGGGAGATCCTGGAAAAGATCCCTTCAGTTTGGGGTGTCACCAAGACTTCTACACAACCCAGGACT 1361 ACCATTGACCTCAGAGCTGTACCCCACATCTTGAAGTAAATTGATCCCACCAGGTCCCACGTTTGTTATCTCTGCCTAAA 1441 TGTTAGCTTCTCCATCCTCACCACATGATGACCTGCTGTGTCCCTCTGAGCACTACCCAGTGGCTGAAAACTCTGCAAAT 1521 GGGCCACACTTTTGCAAAATACTTGTATCTGACACTTAGGTCTTGTTTGAAGAATTTCCTTTCTGGAAGGTTTTACAAGA 1601 AGACTGATAGTCTTTCAAGCCCCCACATCACAGGCTTAGGGACGGCACTAACTTTCTCCCAGGGATCTAACTGGCTAGTT 1681 CAAATTATCACTCTTTTACCTTCATATAAAATGTCTCCCCCAAACCTTTTTCCCTTCTTTGTCATTGTTATCTGCTAAGC 1761 CCCTGGTCATTTCCCCATATTCGTAGTCTTTTTTTCCATCCTATCTTTCTAATATTTGTTGTCTTTAACAAACTGTGTTC 1841 TGTGTCTGTGCTCCTCCTTCCCTCTCAGACCACTGGAATGCAAGTCCTTCTTCCCTTTGGAATGTACTCTGGATCCCTTC 1921 CCCTGCTTTGACCCCCAGACTTTGCTCCATCTATTATTGCTTCTCCATCCTGGATCCTTGACATTTGTCACCCCACTGGC 2001 CTTCTCAGGTGCAATCAGTAAAAATGCTGAGAACTCTTGGATCTTAATCTTCATGACTGAGTTTTTTTTAGTTGTATAGT 2081 TATCATCTGCCTTTCTTCACTTTGCATTTCTTCTTGAATCCATTGCAGATTGACTTCCACTCCCACTCCTTCACTAAAAG 2161 GGCTCTTACCAAGATCAAATCTAATGGGTACATTTTAGTTCCTATGTGATTTGGCCTTTCGATGTCAATCATCACTCCCA 2241 GCCATTGATTTTGGTGACCCACTTCCCTGTGATGATCTTCTGATCTAGTTTCTCAGGTTCCTTCGCTGGTCCTTTTTCTT 2321 TCCCTGCCCCTGACATATTGACATTTCCTGGAGTTGGTTTTGTCCTTGATTCATTCTCATGTCATTCTGCACACAGTCTC 2401 TGCATGAACTCAGGCAGACCCTTCATTTAATGACCACCTTAGGGCTGATGATTCTCAAATCTGTATTCCCCGATCTTGCA 2481 TTTGAGCTCCAGCCCCACTCATCCTCTCGGATGTTCTGCAGGCCCAGCAAACTCATCATGTCCAAAGTGAAACTTTTTCT 2561 CTTTCCTGTCTCCTCTCCTCTGATCTGTTCTTTCTTGGAACACCACCCAAGAACGTCACCTCCTCCATCAGATTGTGAGC 2641 TCCTGGAGGGCAGGAGCTGTGTCCTTCTATTCATCTTCCTATCCCCAGAACCTTGCACAGATCCTGGAATGTGGTAGGTG 2721 CTCAGTAAATGTGTGTTGAATAAATGAATGAATGAATGAACAAATGAATGAATTTGCTTACTTCAAGGCAAAAGAACCAT 2801 GAAACTGTATTTTGAGTTTCTATGTTATAGCAGTCAGCAAATCCTATTAAATACTTTGTGTTTCCAAGCAAAAAAAAAAA 2881 AAA Target sites
Provided by authors
Predicted by miRanda
DRVs
SNPs
DRVs & SNPs
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| miRNA-target interactions (Predicted by miRanda) |
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| DRVs in gene 3'UTRs | |||||||||||||||||||||
| SNPs in gene 3'UTRs | |||||||||||||||||||||
| Experimental Support 1 for Functional miRNA-Target Interaction | |||||||
|---|---|---|---|---|---|---|---|
| miRNA:Target | ---- | ||||||
| Validation Method |
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| Conditions | HEK293 | ||||||
| Disease | 150572.0 | ||||||
| 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 GSM714646. RNA binding protein: AGO2. Condition:mildMNase
"PAR-CLIP data was present in GSM714647. RNA binding protein: AGO2. Condition:mildMNase
... - Kishore S; Jaskiewicz L; Burger L; Hausser et al., 2011, Nature methods. |
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| miRNA-target interactions (Provided by authors) |
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| 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]
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| Experimental Support 2 for Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | ---- |
| Validation Method |
|
| Conditions | TZM-bl |
| 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 GSM1462574. RNA binding protein: AGO2. Condition:TZM-bl ami BaL
... - Whisnant AW; Bogerd HP; Flores O; Ho P; et al., 2013, mBio. |
| Article |
- Whisnant AW; Bogerd HP; Flores O; Ho P; et al. - mBio, 2013
UNLABELLED: The question of how HIV-1 interfaces with cellular microRNA (miRNA) biogenesis and effector mechanisms has been highly controversial. Here, we first used deep sequencing of small RNAs present in two different infected cell lines (TZM-bl and C8166) and two types of primary human cells (CD4(+) peripheral blood mononuclear cells [PBMCs] and macrophages) to unequivocally demonstrate that HIV-1 does not encode any viral miRNAs. Perhaps surprisingly, we also observed that infection of T cells by HIV-1 has only a modest effect on the expression of cellular miRNAs at early times after infection. Comprehensive analysis of miRNA binding to the HIV-1 genome using the photoactivatable ribonucleoside-induced cross-linking and immunoprecipitation (PAR-CLIP) technique revealed several binding sites for cellular miRNAs, a subset of which were shown to be capable of mediating miRNA-mediated repression of gene expression. However, the main finding from this analysis is that HIV-1 transcripts are largely refractory to miRNA binding, most probably due to extensive viral RNA secondary structure. Together, these data demonstrate that HIV-1 neither encodes viral miRNAs nor strongly influences cellular miRNA expression, at least early after infection, and imply that HIV-1 transcripts have evolved to avoid inhibition by preexisting cellular miRNAs by adopting extensive RNA secondary structures that occlude most potential miRNA binding sites. IMPORTANCE: MicroRNAs (miRNAs) are a ubiquitous class of small regulatory RNAs that serve as posttranscriptional regulators of gene expression. Previous work has suggested that HIV-1 might subvert the function of the cellular miRNA machinery by expressing viral miRNAs or by dramatically altering the level of cellular miRNA expression. Using very sensitive approaches, we now demonstrate that neither of these ideas is in fact correct. Moreover, HIV-1 transcripts appear to largely avoid regulation by cellular miRNAs by adopting an extensive RNA secondary structure that occludes the ability of cellular miRNAs to interact with viral mRNAs. Together, these data suggest that HIV-1, rather than seeking to control miRNA function in infected cells, has instead evolved a mechanism to become largely invisible to cellular miRNA effector mechanisms.
LinkOut: [PMID: 23592263]
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| Experimental Support 3 for Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | ---- |
| Validation Method |
|
| Conditions | HCT116 |
| 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 ERX177599. RNA binding protein: AGO2. Condition:p53_D_AGO_CLIP_2_1
PAR-CLIP data was present in ERX177611. RNA binding protein: AGO2. Condition:p53_D_AGO_CLIP_3_1
PAR-CLIP data was present in ERX177627. RNA binding protein: AGO2. Condition:p53_D_AGO_CLIP_4_5
PAR-CLIP data was present in ERX177632. RNA binding protein: AGO2. Condition:p53_V_AGO_CLIP_4_10
PAR-CLIP data was present in ERX177603. RNA binding protein: AGO2. Condition:p53_D_AGO_CLIP_2_5
... - Krell J; Stebbing J; Carissimi C; Dabrowska et al., 2016, Genome research. |
| Article |
- Krell J; Stebbing J; Carissimi C; Dabrowska et al. - Genome research, 2016
DNA damage activates TP53-regulated surveillance mechanisms that are crucial in suppressing tumorigenesis. TP53 orchestrates these responses directly by transcriptionally modulating genes, including microRNAs (miRNAs), and by regulating miRNA biogenesis through interacting with the DROSHA complex. However, whether the association between miRNAs and AGO2 is regulated following DNA damage is not yet known. Here, we show that, following DNA damage, TP53 interacts with AGO2 to induce or reduce AGO2's association of a subset of miRNAs, including multiple let-7 family members. Furthermore, we show that specific mutations in TP53 decrease rather than increase the association of let-7 family miRNAs, reducing their activity without preventing TP53 from interacting with AGO2. This is consistent with the oncogenic properties of these mutants. Using AGO2 RIP-seq and PAR-CLIP-seq, we show that the DNA damage-induced increase in binding of let-7 family members to the RISC complex is functional. We unambiguously determine the global miRNA-mRNA interaction networks involved in the DNA damage response, validating them through the identification of miRNA-target chimeras formed by endogenous ligation reactions. We find that the target complementary region of the let-7 seed tends to have highly fixed positions and more variable ones. Additionally, we observe that miRNAs, whose cellular abundance or differential association with AGO2 is regulated by TP53, are involved in an intricate network of regulatory feedback and feedforward circuits. TP53-mediated regulation of AGO2-miRNA interaction represents a new mechanism of miRNA regulation in carcinogenesis.
LinkOut: [PMID: 26701625]
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| Experimental Support 4 for Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | ---- |
| Validation Method |
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| Conditions | Prostate Tissue |
| 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 SRX1760583. RNA binding protein: AGO2. Condition:AGO-CLIP-LNCaP_A
PAR-CLIP data was present in SRX1760591. RNA binding protein: AGO2. Condition:AGO-CLIP-LNCaP_B
PAR-CLIP data was present in SRX1760620. RNA binding protein: AGO2. Condition:AGO-CLIP-LAPC4_A
PAR-CLIP data was present in SRX1760630. RNA binding protein: AGO2. Condition:AGO-CLIP-22RV1_A
PAR-CLIP data was present in SRX1760631. RNA binding protein: AGO2. Condition:AGO-CLIP-22RV1_B
PAR-CLIP data was present in SRX1760638. RNA binding protein: AGO2. Condition:AGO-CLIP-PC3-miR148
PAR-CLIP data was present in SRX1760639. RNA binding protein: AGO2. Condition:AGO-CLIP-LNCaP-MDV_A
PAR-CLIP data was present in SRX1760641. RNA binding protein: AGO2. Condition:AGO-CLIP-LNCaP-MDV_B
PAR-CLIP data was present in SRX1760628. RNA binding protein: AGO2. Condition:AGO-CLIP-LAPC4_B
... - Hamilton MP; Rajapakshe KI; Bader DA; Cerne et al., 2016, Neoplasia (New York, N.Y.). |
| Article |
- Hamilton MP; Rajapakshe KI; Bader DA; Cerne et al. - Neoplasia (New York, N.Y.), 2016
MicroRNA (miRNA) deregulation in prostate cancer (PCa) contributes to PCa initiation and metastatic progression. To comprehensively define the cancer-associated changes in miRNA targeting and function in commonly studied models of PCa, we performed photoactivatable ribonucleoside-enhanced cross-linking immunoprecipitation of the Argonaute protein in a panel of PCa cell lines modeling different stages of PCa progression. Using this comprehensive catalogue of miRNA targets, we analyzed miRNA targeting on known drivers of PCa and examined tissue-specific and stage-specific pathway targeting by miRNAs. We found that androgen receptor is the most frequently targeted PCa oncogene and that miR-148a targets the largest number of known PCa drivers. Globally, tissue-specific and stage-specific changes in miRNA targeting are driven by homeostatic response to active oncogenic pathways. Our findings indicate that, even in advanced PCa, the miRNA pool adapts to regulate continuing alterations in the cancer genome to balance oncogenic molecular changes. These findings are important because they are the first to globally characterize miRNA changes in PCa and demonstrate how the miRNA target spectrum responds to staged tumorigenesis.
LinkOut: [PMID: 27292025]
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| CLIP-seq Support 1 for dataset GSM714646 | |
|---|---|
| Method / RBP | PAR-CLIP / AGO2 |
| Cell line / Condition | HEK293 / mildMNase, repA |
| Location of target site | ENST00000419482.2 | 3UTR | CAUCAGAUUGUGAGCUCCUGGAG |
| Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
| Article / Accession Series | PMID: 21572407 / GSE28865 |
| CLIP-seq Viewer | Link |
| CLIP-seq Support 2 for dataset GSM714647 | |
|---|---|
| Method / RBP | PAR-CLIP / AGO2 |
| Cell line / Condition | HEK293 / mildMNase, repB |
| Location of target site | ENST00000419482.2 | 3UTR | CCAUCAGAUUGUGAGCUCCUGGAG |
| Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
| Article / Accession Series | PMID: 21572407 / GSE28865 |
| CLIP-seq Viewer | Link |
| CLIP-seq Support 3 for dataset GSM1462574 | |
|---|---|
| Method / RBP | PAR-CLIP / AGO2 |
| Cell line / Condition | TZM-bl / TZM-bl ami BaL |
| Location of target site | ENST00000419482.2 | 3UTR | CAUCAGAUUGUGAGCUCCUGGA |
| Tools used in this analysis | TargetScan, miRTarCLIP, and Piranha |
| Article / Accession Series | PMID: 23592263 / GSE59944 |
| CLIP-seq Viewer | Link |
| MiRNA-Target Expression Profile | |||||||
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| MiRNA-Target Expression Profile (TCGA) | |||||||
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25 hsa-miR-151b Target Genes:
Functional analysis:
ID |
Target | Description | Validation methods |
 |
 |
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| Strong evidence | Less strong evidence | |||||||||||
 |
 |
 |
 |
 |
 |
 |
 |
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| MIRT249674 | SLC39A9 | solute carrier family 39 member 9 |  |
|
2 | 4 | ||||||
| MIRT366296 | GDI1 | GDP dissociation inhibitor 1 | |
|
2 | 4 | ||||||
| MIRT451313 | LGALS3BP | galectin 3 binding protein | |
|
2 | 2 | ||||||
| MIRT467467 | SMYD1 | SET and MYND domain containing 1 | |
|
2 | 4 | ||||||
| MIRT477248 | ERGIC2 | ERGIC and golgi 2 | |
|
2 | 2 | ||||||
| MIRT489948 | RFX2 | regulatory factor X2 | |
|
2 | 2 | ||||||
| MIRT490364 | SLC6A1 | solute carrier family 6 member 1 | |
|
2 | 4 | ||||||
| MIRT494531 | BCL7A | BCL tumor suppressor 7A | |
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2 | 2 | ||||||
| MIRT500190 | BARX1 | BARX homeobox 1 | |
|
2 | 4 | ||||||
| MIRT511912 | FKBP1A | FK506 binding protein 1A | |
|
2 | 2 | ||||||
| MIRT524875 | ARHGDIA | Rho GDP dissociation inhibitor alpha | |
|
2 | 6 | ||||||
| MIRT555338 | PPP1R3B | protein phosphatase 1 regulatory subunit 3B | |
|
2 | 4 | ||||||
| MIRT557122 | HOXA3 | homeobox A3 | |
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2 | 2 | ||||||
| MIRT559034 | C20orf24 | chromosome 20 open reading frame 24 | |
|
2 | 4 | ||||||
| MIRT559824 | SLPI | secretory leukocyte peptidase inhibitor | |
|
2 | 2 | ||||||
| MIRT568547 | AKT2 | AKT serine/threonine kinase 2 | |
|
2 | 2 | ||||||
| MIRT568714 | TMEM30B | transmembrane protein 30B | |
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2 | 2 | ||||||
| MIRT569827 | CRMP1 | collapsin response mediator protein 1 | |
|
2 | 2 | ||||||
| MIRT687618 | LYRM4 | LYR motif containing 4 | |
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2 | 2 | ||||||
| MIRT689949 | MANSC1 | MANSC domain containing 1 | |
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2 | 2 | ||||||
| MIRT690433 | FAM71F2 | family with sequence similarity 71 member F2 | |
|
2 | 2 | ||||||
| MIRT694845 | KRT80 | keratin 80 | |
|
2 | 2 | ||||||
| MIRT697594 | YME1L1 | YME1 like 1 ATPase | |
|
2 | 2 | ||||||
| MIRT697848 | UBE2Z | ubiquitin conjugating enzyme E2 Z | |
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2 | 2 | ||||||
| MIRT719553 | CBLB | Cbl proto-oncogene B | |
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2 | 2 | ||||||
| miRNA-Drug Associations | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| miRNA-Drug Resistance Associations | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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