mir-278 microRNA precursor family

In molecular biology mir-278 microRNA is a short RNA molecule belonging to a class of molecules referred to as microRNAs. These function to regulate the expression levels of other genes by several mechanisms, primarily binding to their target at its 3'UTR.

mir-278
Identifiers
Symbolmir-278
RfamRF00729
miRBase family3
Other data
RNA typemicroRNA
Domain(s)Eukaryota;
PDB structuresPDBe

Mis- and altered expression in Drosophila

miR-278 affects energy metabolism in the Drosophila melanogaster species. Elevated insulin production has been observed in miR-278 mutants, due to insulin resistance in the absence of this microRNA. miR-278 is now known to act through regulation of the expanded gene transcript, and most likely through further miR-278 targets as well.[1]

Misexpression in the developing eye has been found to result in overgrowth, partially through apoptotic inhibition.[2] There is a single base substitution which blocks the gain-of-function phenotype, indicating the acquisition of novel functions by misexpressed miRNAs which bring about unscheduled cell proliferation in vivo. This is reflective of a microRNA potential in the promotion of tumour formation.

gollark: Or, well, less since hammers have balance stuff, but it's still quite fast.
gollark: Ah yes, mining 9 times as fast is soøøøøøøøø useless.
gollark: You put on a Blast Protection suit, and go to the nether roof, and a TNT cannon propels you in the direction you want.
gollark: How about, nether TNT cannon networks?
gollark: Hmm, nether viaduct networks, interesting iðeæ.

See also

References
  1. Teleman AA, Maitra S, Cohen SM (2006). "Drosophila lacking microRNA miR-278 are defective in energy homeostasis". Genes Dev. 20 (4): 417–22. doi:10.1101/gad.374406. PMC 1369043. PMID 16481470.
  2. Nairz K, Rottig C, Rintelen F, Zdobnov E, Moser M, Hafen E (2006). "Overgrowth caused by misexpression of a microRNA with dispensable wild-type function". Dev Biol. 291 (2): 314–24. doi:10.1016/j.ydbio.2005.11.047. PMID 16443211.

Further reading

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