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miR-30 microRNA precursor is a small non-coding RNA that regulates gene expression. Animal microRNAs are transcribed as pri-miRNA (primary miRNA) of varying length which in turns are processed in the nucleus by Drosha into ~70 nucleotide stem-loop precursor called pre-miRNA (preliminary miRNA) and subsequently processed by the Dicer enzyme to give a mature ~22 nucleotide product. In this case the mature sequence comes from both the 3' (miR-30) and 5' (mir-97-6) arms of the precursor. The products are thought to have regulatory roles through complementarity to mRNA.
A screen of 17 miRNAs that have been predicted to regulate a number of breast cancer associated genes found variations in the microRNAs miR-17 and miR-30c-1, these patients were noncarriers of BRCA1 or BRCA2 mutations, lending the possibility that familial breast cancer may be caused by variation in these miRNAs.
Members of the miR-30 family have been found to be highly expressed in heart cells.
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miR-30 microRNA precursor is a small non-coding RNA that regulates gene expression. Animal microRNAs are transcribed as pri-miRNA (primary miRNA) of varying length which in turns are processed in the nucleus by Drosha into ~70 nucleotide stem-loop precursor called pre-miRNA (preliminary miRNA) and subsequently processed by the Dicer enzyme to give a mature ~22 nucleotide product. In this case the mature sequence comes from both the 3' (miR-30)[1] and 5' (mir-97-6)[2] arms of the precursor. The products are thought to have regulatory roles through complementarity to mRNA.[3]
A screen of 17 miRNAs that have been predicted to regulate a number of breast cancer associated genes found variations in the microRNAs miR-17 and miR-30c-1, these patients were noncarriers of BRCA1 or BRCA2 mutations, lending the possibility that familial breast cancer may be caused by variation in these miRNAs.[4]
Members of the miR-30 family have been found to be highly expressed in heart cells.[5]
[edit] Targets of miR-30
It has been shown that the integrin ITGB3 and the ubiquitin conjugating E2 enzyme UBC9 are downregulated by miR-30.[6] It has also been suggested that the TP53 protein may be a target of miR-30c and miR-30e. An immunoblot analysis revealed that p53 expression levels were elevated upon knockdown of miR-30c and miR-30e.[7]
[edit] References
- ^ Lagos-Quintana, M; Rauhut R, Lendeckel W, Tuschl T (2001). "Identification of novel genes coding for small expressed RNAs". Science 294 (5543): 853–858. doi:10.1126/science.1064921. PMID 11679670.
- ^ Mourelatos, Z; Dostie J, Paushkin S, Sharma A, Charroux B, Abel L, Rappsilber J, Mann M, Dreyfuss G (2002). "miRNPs: a novel class of ribonucleoproteins containing numerous microRNAs". Genes Dev 16 (6): 720–728. doi:10.1101/gad.974702. PMC 155365. PMID 11914277. //www.ncbi.nlm.nih.gov/pmc/articles/PMC155365/.
- ^ Ambros V (2001). "microRNAs: tiny regulators with great potential". Cell 107 (7): 823–6. doi:10.1016/S0092-8674(01)00616-X. PMID 11779458.
- ^ Shen J, Ambrosone CB, Zhao H (2009). "Novel genetic variants in microRNA genes and familial breast cancer". Int J Cancer 124 (5): 1178–82. doi:10.1002/ijc.24008. PMID 19048628.
- ^ Duisters RF, Tijsen AJ, Schroen B, et al. (January 2009). "miR-133 and miR-30 regulate connective tissue growth factor: implications for a role of microRNAs in myocardial matrix remodeling". Circ. Res. 104 (2): 170–8, 6p following 178. doi:10.1161/CIRCRESAHA.108.182535. PMID 19096030.
- ^ Yu F, Deng H, Yao H, Liu Q, Su F, Song E (July 2010). "Mir-30 reduction maintains self-renewal and inhibits apoptosis in breast tumor-initiating cells". Oncogene 29 (29): 4194–204. doi:10.1038/onc.2010.167. PMID 20498642.
- ^ Li J, Donath S, Li Y, Qin D, Prabhakar BS, Li P (January 2010). McManus, Michael T.. ed. "miR-30 regulates mitochondrial fission through targeting p53 and the dynamin-related protein-1 pathway". PLoS Genet. 6 (1): e1000795. doi:10.1371/journal.pgen.1000795. PMC 2793031. PMID 20062521. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2793031/.
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