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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]
Targets of miR-24[edit]
- 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]
References[edit]
- ^ a b Lal A, Kim HH, Abdelmohsen K, et al (2008). "p16(INK4a) translation suppressed by miR-24". In Preiss, Thomas. PLoS ONE 3 (3): e1864. doi:10.1371/journal.pone.0001864. PMC 2274865. PMID 18365017.
- ^ 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). "miR-24 Inhibits cell proliferation by targeting E2F2, MYC, and other cell-cycle genes via binding to "seedless" 3'UTR microRNA recognition elements.". In Preiss, Thomas. Molecular Cell 11 (3): e1864. doi:10.1016/j.molcel.2009.08.020. 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.
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