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FOS — SOCS1
Text-mined interactions from Literome
Lu et al., FASEB J 2002
(MAP Kinase Signaling System) :
As an intracrine factor, the intracellular function of HPO is to increase c-Jun phosphorylation independent of c-Jun amino-terminal kinase (JNK), extracellular signal regulated kinase ( ERK ) -1 and -2, and leads to potentiation of
JAB1 mediated
AP-1 activation
Chen et al., J Biol Chem 2003
:
HPO site directed mutants ( Cys/Ser ) at active sites, which lost sulfhydryl oxidase activity, could not increase c-Jun phosphorylation and failed to potentiate
JAB1 mediated
AP-1 activation
Wang et al., Acta Biochim Biophys Sin (Shanghai) 2004
:
Protein product encoded by a human novel gene E9730
enhances AP-1 activity through interacting with
Jab1 ... Furthermore, the data indicated that E9730 appeared to enhance
Jab1 induced
AP-1 activity in a concentration dependent manner and Jab1 may be involved in the intracellular signaling transduction from E9730 to AP-1
Tanaka et al., Oncogene 2006
:
These results suggest that the interaction between HBx and
Jab1 enhances HBx mediated
AP-1 activation
Zhang et al., Biochim Biophys Acta 2006
:
Molecular cloning and characterization of human Aph2 gene, involved in
AP-1 regulation by interaction with
JAB1 ... Furthermore, overexpression of hAPH2 could increase apoptosis of COS-7 cells and negatively regulate
JAB1 induced activation of
AP-1 in a concentration dependent manner
Shi et al., FEBS Lett 2008
:
Overexpression of
SOCS-1 in HMCs
inhibited HG-induced JAK2/STAT activation,
c-Fos/c-Jun expression, and increased synthesis of TGF-beta1 and fibronectin