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The miR-24 microRNA precursor is a small non-coding RNA molecule that regulates gene expression. microRNAs are transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give a mature ~22 nucleotide product. In this case the mature sequence comes from the 3' arm of the precursor. The mature products are thought to have regulatory roles through complementarity to mRNA. miR-24 is conserved in various species, and is clustered with miR-23 and miR-27, on human chromosome 9 and 19. Recently, miR-24 has been shown to suppress expression of two crucial cell cycle control genes, E2F2 and Myc in hematopoietic differentiation and also to promote keratinocyte differentiation by repressing actin-cytoskeleton regulators PAK4, Tsk5 and ArhGAP19.
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The miR-24 microRNA precursor is a small non-coding RNA molecule that regulates gene expression. microRNAs are transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give a mature ~22 nucleotide product. In this case the mature sequence comes from the 3' arm of the precursor. The mature products are thought to have regulatory roles through complementarity to mRNA. miR-24 is conserved in various species, and is clustered with miR-23 and miR-27, on human chromosome 9 and 19.[1] Recently, miR-24 has been shown to suppress expression of two crucial cell cycle control genes, E2F2 and Myc in hematopoietic differentiation [2] and also to promote keratinocyte differentiation by repressing actin-cytoskeleton regulators PAK4, Tsk5 and ArhGAP19.[3]
[edit] Targets of miR-24
- Lal et al. suggested that miR-24 suppresses the tumor suppressor p16(INK4a).[1]
- Lal et al. reported that mi-24 inhibits cell proliferation by targeting E2F2, MYC via binding to "seedless" 3'UTR microRNA recognition elements.[2]
- Amelio I. et al. suggest that miR-24 regulates keratinocyte differentiation, controlling actin-cytoskeleton dynamics via PAK4, Tsk5 and ArhGAP19 repression.[3]
- Wang et al.. have shown that miR-24 reduces the mRNA and protein levels of human ALK4 by targeting the 3'-untranslated region of mRNA.[4]
- Mishra et al. suggest that miR-24 targets the DHFR gene.[5]
[edit] References
- ^ a b Lal A, Kim HH, Abdelmohsen K, et al (2008). Preiss, Thomas. ed. "p16(INK4a) translation suppressed by miR-24". PLoS ONE 3 (3): e1864. doi:10.1371/journal.pone.0001864. PMC 2274865. PMID 18365017. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2274865/.
- ^ a b Lal A, Navarro F, Maher CA, Maliszewski LE, Yan N, O'Day E, Chowdhury D, Dykxhoorn DM, Tsai P, Hofmann O, Becker KG, Gorospe M, Hide W, Lieberman J. (2009). Preiss, Thomas. ed. "miR-24 Inhibits cell proliferation by targeting E2F2, MYC, and other cell-cycle genes via binding to "seedless" 3'UTR microRNA recognition elements.". Molecular Cell 11 (3): e1864. PMID 19748357.
- ^ a b Amelio I, Lena AM, Viticchiè G, Shalom-Feuerstein R, Terrinoni A, Dinsdale D, Russo G, Fortunato C, Bonanno E, Spagnoli LG, Aberdam D, Knight RA, Candi E, Melino G. (October 2012). "miR-24 triggers epidermal differentiation by controlling actin adhesion and cell migration". The Journal of Cell Biology 104 (33): 13513–8. doi:10.1083/jcb.201203134.. PMID 23071155.
- ^ Wang Q, Huang Z, Xue H, et al (January 2008). "MicroRNA miR-24 inhibits erythropoiesis by targeting activin type I receptor ALK4". Blood 111 (2): 588–95. doi:10.1182/blood-2007-05-092718. PMID 17906079.
- ^ Mishra PJ, Humeniuk R, Mishra PJ, Longo-Sorbello GS, Banerjee D, Bertino JR (August 2007). "A miR-24 microRNA binding-site polymorphism in dihydrofolate reductase gene leads to methotrexate resistance". Proceedings of the National Academy of Sciences of the United States of America 104 (33): 13513–8. doi:10.1073/pnas.0706217104. PMC 1948927. PMID 17686970. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1948927/.
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