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FGF2 — PRKCA

Text-mined interactions from Literome

Wang et al., Shi Yan Sheng Wu Xue Bao 1998 (Nasopharyngeal Neoplasms) : The result suggests that PKC-alpha translocation and activation can phosphorylate bFGF in CNE-2 cells and increase bFGF release
Hsia et al., J Cell Biochem 2003 : Using pharmacological inhibitors of specific PKC isozymes, we elucidated a potential mode of regulation whereby PKCalpha mediates the nuclear localization of FGF-2 and PKCdelta inhibits it
Xiao et al., Acta Biochim Biophys Sin (Shanghai) 2008 (Carcinoma, Small Cell...) : FGF-2 also inhibited the release of Smac from mitochondria to the cytoplasm induced by serum starvation and increased PKC alpha translocation from the cytoplasm to the cell membrane
Lee et al., J Biol Chem 1995 (Breast Neoplasms) : Corroborating this observation, overexpression of PKC alpha induced bFGF gene expression in MCF-7 cells
Haller et al., Arterioscler Thromb Vasc Biol 1996 : Thus, tyrosine kinase receptor activation via bFGF induced a rapid association of PKC alpha and epsilon with nuclear structures, while activation of the G protein coupled thrombin receptor increased mostly nuclear PKC zeta
Hrzenjak et al., Recept Signal Transduct 1997 (Prostatic Neoplasms) : FGF-2 promoted rapid activation of rat prostate-cancer-cell PKCalpha and PKCepsilon, as assessed by isozyme translocation from the soluble to particulate cell fraction, and only moderately altered PKCdelta distribution
Haller et al., Acta Physiol Scand 1998 : Thus, tyrosine kinase receptor activation via bFGF induces a rapid association of PKC alpha and epsilon within nuclear structures