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JUN — SOCS1

Text-mined interactions from Literome

Kleemann et al., Nature 2000 : Jab1 activates c-Jun amino-terminal kinase (JNK) activity and enhances endogenous phospho-c-Jun levels, and MIF inhibits these effects
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
Luo et al., J Biol Chem 2006 : Jab1 , a novel protease activated receptor-2 (PAR-2) interacting protein, is involved in PAR-2 induced activation of activator protein-1 ... Loss-of-function studies, using Jab1 small interfering RNA, demonstrated that Jab1 knockdown blocked PAR-2 induced activator protein-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
Wu et al., Bone 2012 (MAP Kinase Signaling System) : As the result of increased SOCS1 expression, knockdown of miR-155 significantly reduced the JNK/c-Jun activation
Claret et al., Nature 1996 : In vitro, JAB1 specifically stabilizes complexes of c-Jun or JunD with AP-1 sites and does not affect binding of either JunB or v-Jun