| Community annotation |
This text is a summary paragraph taken from the Wikipedia
entry entitled MiR-224. miRBase and Rfam
are facilitating community annotation of microRNA families and entries in Wikipedia. Read more ...
The text in this section is taken from the free, online
encyclopedia, Wikipedia. Anyone can edit a Wikipedia page. We hope
that experts on particular microRNA sequences will use the links to
Wikipedia below to edit the annotation of individual microRNAs, to add
information about function, evolution, discovery, and literature
references, for example. Any changes that you make will be visible in
Wikipedia immediately, and in miRBase within 24 hours.
Editing Wikipedia entries is straightforward. If you haven't
edited a page before, you might like to take a look at the following
Wikipedia help pages:
You can also create new pages at Wikipedia about microRNA families
that do not currently have specific entries there. Please let us know
if you do, so we can incorporate your annotation into miRBase, and
create the appropriate links from miRBase entries to the relevant
Wikipedia pages.
Please note, we're not responsible for the content of Wikipedia pages.
You can read more about miRBase, Wikipedia and community annotation on this blog post.
Please email us for
help or with comments about this community annotation initiative.
miR-224 is a family of microRNA precursors found in mammals, including humans. The ~22 nucleotide mature miRNA sequence is excised from the precursor hairpin by the enzyme Dicer.
Show Wikipedia entry
View @ Wikipedia
Edit Wikipedia entry
miR-224 is a family of microRNA precursors found in mammals, including humans. The ~22 nucleotide mature miRNA sequence is excised from the precursor hairpin by the enzyme Dicer.[1]
[edit] Function
miR-224, being located on the X-chromosome, is thought to be active in mammalian ovaries, and possibly responds to TGF beta 1.[2] A target of miR-224 has been predicted to be SMAD4. Experimental evidence has shown that while the SMAD4 mRNA level is unchanged, increased miR-224 expression decreases concentration of SMDA4 protein in murine granulosa cells.[3] This is consistent with post-transcriptional miRNA regulation.[2]
[edit] Role in cancer
miR-224 has been noted as the most upregulated microRNA in hepatocellular carcinoma.[4] The same study identified a target of mir-224 as apoptosis-inhibitor 5 (API-5).[4]
miR-224 has also been linked with pancreatic ductal carcinoma, where it is thought to repress CD40 expression in cancer cells.[5]
[edit] References
- ^ Ambros, V (2001-12-28). "microRNAs: tiny regulators with great potential.". Cell 107 (7): 823–6. doi:10.1016/S0092-8674(01)00616-X. PMID 11779458.
- ^ a b Christenson, LK (2010-07-01). "MicroRNA control of ovarian function.". Animal reproduction / Colegio Brasileiro de Reproducao Animal 7 (3): 129–133. PMC 3111027. PMID 21666774. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3111027.
- ^ Yao, G; Yin, M, Lian, J, Tian, H, Liu, L, Li, X, Sun, F (2010 Mar). "MicroRNA-224 is involved in transforming growth factor-beta-mediated mouse granulosa cell proliferation and granulosa cell function by targeting Smad4.". Molecular endocrinology (Baltimore, Md.) 24 (3): 540–51. doi:10.1210/me.2009-0432. PMID 20118412.
- ^ a b Wang, Y; Lee, AT, Ma, JZ, Wang, J, Ren, J, Yang, Y, Tantoso, E, Li, KB, Ooi, LL, Tan, P, Lee, CG (2008-05-09). "Profiling microRNA expression in hepatocellular carcinoma reveals microRNA-224 up-regulation and apoptosis inhibitor-5 as a microRNA-224-specific target.". The Journal of Biological Chemistry 283 (19): 13205–15. doi:10.1074/jbc.M707629200. PMID 18319255.
- ^ Mees, ST; Mardin, WA, Sielker, S, Willscher, E, Senninger, N, Schleicher, C, Colombo-Benkmann, M, Haier, J (2009 Aug). "Involvement of CD40 targeting miR-224 and miR-486 on the progression of pancreatic ductal adenocarcinomas.". Annals of Surgical Oncology 16 (8): 2339–50. doi:10.1245/s10434-009-0531-4. PMID 19475450.
|