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FOS — GDNF

Text-mined interactions from Literome

Jeon et al., Immunopharmacology 2000 : Treatment of DEX to RAW 264.7 cells induced a dose related inhibition of NF-kappaB/Rel and AP-1 in chloramphenicol acetyltransferase activity, while neither NF-IL6 nor CREB/ATF activation was affected by DEX
Hsu et al., Mol Cell Biol 1992 : LRF-1/c-Jun, c-Fos/c-Jun , and c-Fos/JunB activate specific AP-1 and ATF site containing promoters, and in contrast, LRF-1/JunB potently represses c-Fos- and c-Jun mediated activation of these promoters
Liu et al., Shi Yan Sheng Wu Xue Bao 2005 (Substance Withdrawal Syndrome) : The antisense approach and immunohistochemistry were used to study the effects of different muscarinic receptor ( M ) subtypes and glial cell derived neurotrophic factor ( GDNF ) on the scores of morphine-withdrawal syndrome and the expression of c-Fos in locus coeruleus ( LC )
He et al., Stem Cells 2008 : Gdnf upregulates c-Fos transcription via the Ras/Erk1/2 pathway to promote mouse spermatogonial stem cell proliferation
Yuan et al., Mol Cell Biol 2009 : A chromatin immunoprecipitation assay also revealed that c-Fos expression prevents the binding of c-Jun/ATF2 heterodimers to conserved ATF sites