The oncogene JUN is the putative transforming gene of avian sarcoma virus 17; it appears to be derived from a gene of the
chicken genome and has homologs in several other vertebrate species. (The name JUN comes from the Japanese 'ju-nana,'
meaning the number 17.) JUN was thought to be identical to the transcription factor AP1.
Three are at least 3 members of the JUN protooncogene family in the mouse: JUN ,JUNB and JUND.
This gene was found to be regulated by gonadotropins in DNA arrays.
General function
Nucleic acid binding, DNA binding, Transcription factor
Comment
Cellular localization
Nuclear
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Ovarian function
Follicle development
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Expression regulated by
FSH, LH
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Sharma SC, et al 2000 reported the regulation of AP1 (Jun/Fos) Factor expression and activation in ovarian
granulosacells and the relation of JunD and Fra2 to terminal differentiation.
The expression patterns of Jun and Fos family
members in response to hormones(FSH and LH) were distinct. c-Jun, JunB, c-Fos and Fra2 were
rapidly but transiently induced by FSH in immature granulosa cells. JunD and Fra2 were induced by
LH and maintained as granulosa cells terminally differentiated into luteal cells. FSH and forskolin
induced expression of AP1 factors by A-kinase-dependent (Fra2) and A-kinase-independent
mechanisms (c-Fos, JunB), one of which involves p38MAPK. Forskolin and PMA acted
synergistically to enhance transcription of an AP1(-73COL)-luciferase construct. JunD appears to be
one mediator of this effect.