>C3|NM_000064|3'UTR
   1 CCACACCCCCATTCCCCCACTCCAGATAAAGCTTCAGTTATATCTCAAAAAAAAAAAAAAAAA

ID	Duplex structure	Position	Score	MFE
1	miRNA 3' acGGUCGGAGCGGGUcg 5' ||| :|| |||| Target 5' ccCCA--TTCCCCCAct 3'	7 - 21	99.00	-8.70
2	miRNA 3' acggucggagCG-GGUCg 5' || :||| Target 5' tccagataaaGCTTCAGt 3'	21 - 38	72.00	-11.30

Mutant ID	Mutant Position	Mutant Source
COSN30493661	7	COSMIC
COSN30480985	14	COSMIC
COSN30487702	17	COSMIC
COSN30531922	48	COSMIC
COSN30532170	49	COSMIC
COSN28193532	61	COSMIC
COSN26442121	102	COSMIC

Mutant ID	Mutant Position	Mutant Source
rs529117988	2	dbSNP
rs759368543	6	dbSNP
rs751407633	7	dbSNP
rs1157659267	8	dbSNP
rs374414103	9	dbSNP
rs763044103	10	dbSNP
rs1411871899	11	dbSNP
rs1428040767	11	dbSNP
rs1462364473	13	dbSNP
rs1166485735	14	dbSNP
rs943694477	16	dbSNP
rs369677782	17	dbSNP
rs1171555676	18	dbSNP
rs1412185965	19	dbSNP
rs377116496	20	dbSNP
rs371899248	22	dbSNP
rs1479842267	23	dbSNP
rs772285110	25	dbSNP
rs746171602	26	dbSNP
rs779307101	28	dbSNP
rs771420517	31	dbSNP
rs749838591	32	dbSNP
rs1308966716	36	dbSNP
rs1453414586	40	dbSNP
rs751613103	41	dbSNP
rs1222767446	42	dbSNP
rs755597886	46	dbSNP
rs111617932	48	dbSNP
rs113074880	49	dbSNP
rs1209518958	54	dbSNP
rs563213866	55	dbSNP
rs1484278248	74	dbSNP
rs1020127310	85	dbSNP
rs1251475211	89	dbSNP
rs147895142	93	dbSNP
rs11569585	94	dbSNP
rs1366250930	100	dbSNP
rs1236110972	101	dbSNP
rs758259667	103	dbSNP
rs1398184554	108	dbSNP
rs992082211	114	dbSNP
rs1462818599	122	dbSNP
rs1307202089	131	dbSNP
rs563748272	141	dbSNP
rs541279850	147	dbSNP
rs572645448	155	dbSNP
rs11569566	161	dbSNP
rs931663537	165	dbSNP
rs898905154	166	dbSNP
rs1037492810	179	dbSNP

- 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.

- Cell, 2013

The induction of pluripotency or trans-differentiation of one cell type to another can be accomplished with cell-lineage-specific transcription factors. Here, we report that repression of a single RNA binding polypyrimidine-tract-binding (PTB) protein, which occurs during normal brain development via the action of miR-124, is sufficient to induce trans-differentiation of fibroblasts into functional neurons. Besides its traditional role in regulated splicing, we show that PTB has a previously undocumented function in the regulation of microRNA functions, suppressing or enhancing microRNA targeting by competitive binding on target mRNA or altering local RNA secondary structure. A key event during neuronal induction is the relief of PTB-mediated blockage of microRNA action on multiple components of the REST complex, thereby derepressing a large array of neuronal genes, including miR-124 and multiple neuronal-specific transcription factors, in nonneuronal cells. This converts a negative feedback loop to a positive one to elicit cellular reprogramming to the neuronal lineage.

- 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.