Gene interactions and pathways from curated databases and text-mining

◀ Back to JUN

JUN — MAP3K1

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Kim et al., J Biol Chem 2000 : Taken together with previous observations, these results implicate that, for the assembly of an IFN-beta enhanceosome, MEKK1 can induce IRF3 and ATF2/c-JUN through the JNK pathway, whereas it can induce NF-kappaB through the IKK pathway
Xia et al., Proc Natl Acad Sci U S A 2000 : MEK kinase 1 is critically required for c-Jun N-terminal kinase activation by proinflammatory stimuli and growth factor induced cell migration
Dennler et al., J Biol Chem 2000 : Overexpression of constitutively active MEKK1 or MKK4 mutants stabilizes the physical interaction between Smad3 and c-Jun , whereas dominant negative mutants inhibit this interaction
Minet et al., Exp Cell Res 2001 : We also observed that AP-1 transcriptional activity is inhibited by a MEKK1 dominant negative mutant
Yu et al., Mol Pharmacol 2001 : Interestingly, resveratrol had little effect on the induction of AP-1 reporter gene by active Raf-1, MEKK1 , or MKK6, suggesting that it inhibited MAPK pathways by targeting the signaling molecules upstream of Raf-1 or MEKK1
Jahn et al., J Biol Chem 2001 : The inhibitory activity of Grb4 is specific for c-jun/c-fos regulated promoter elements and is located downstream of MEKK1 and JNK because co-expression of Grb4 resulted in down-regulation of MEKK1 induced AP-1 activity without affecting JNK activity
Minamino et al., Proc Natl Acad Sci U S A 2002 (Cardiomegaly...) : In cardiac myocytes derived from embryonic stem cells in culture, homozygous disruption of MEKK1 selectively impaired c-Jun N-terminal kinase activity in the absence or presence of phenlyephrine, a Galphaq dependent agonist
Che et al., Circ Res 2002 : Interestingly, Gab1 inhibited c-Jun transcriptional activity induced by MEKK3 but not MEKK1 and MEK4
Christerson et al., J Cell Physiol 2002 : The reduced activation of AP-1 is dependent on the association of MEKK1 with p115 Rho GAP, because deletion of the Rho GAP SH3 domain, which abrogates their interaction, restores the stimulatory effect of MEKK1 on AP-1 activity
Komoda et al., Int J Oncol 2002 (Carcinoma, Hepatocellular...) : MEKK1 induces c-Jun complexes that act as negative regulators for cell survival and proliferation of HCC cells ... Gel retardation assays indicated that CA-MEKK1 induces c-Jun DNA binding, and luciferase assays exhibited that CA-MEKK1 enhances the transactivating activity of c-Jun in HCC cells
Sánchez-Pérez et al., Mol Biol Cell 2002 : Cell stress and MEKK1 mediated c-Jun activation modulate NFkappaB activity and cell viability
Tu et al., Cell Signal 2003 : Such mutations were also found to impair MEKK1delta induced activation of an AP1 reporter gene
O'Reilly et al., Biochem Biophys Res Commun 2003 : Furthermore full length and C-terminal A20 showed similar regulatory effects on MEKK-1 activation of NF-kappa B and AP-1 and induction of IL-8
Zhang et al., EMBO J 2003 : MEKK1-driven JNK activation is required for actin stress fiber formation, c-Jun phosphorylation and cell migration
Hammaker et al., J Immunol 2004 (Arthritis, Rheumatoid...) : Of interest, MEKK1 immunoprecipitates from IL-1 stimulated FLS appeared to activate c-Jun through the JNK pathway and TAK1 activation of c-Jun was dependent on JNK, ERK, and p38
Zhang et al., Mol Cell Biol 2005 : We found that activins cause the activation of RhoA but not of Rac and CDC42, leading to MEKK1 dependent phosphorylation of JNK and transcription factor c-Jun
Rangaswami et al., J Biol Chem 2005 (Neoplasm Invasiveness) : OPN stimulated both NIK and MEKK1 dependent c-Jun expression, leading to AP-1 activation, whereas NIK dependent AP-1 activation is independent of JNK1
Gallagher et al., Nat Immunol 2007 : Those defects were B cell intrinsic, as MEKK1 was necessary for CD40 mediated activation of the kinases Jnk and p38 and transcription factor c-Jun , as well as for expression of cyclin D2 and activation induced deaminase
Kim et al., Neurosci Lett 2007 (Neuroblastoma...) : Furthermore, SAG inhibits MEKK1 dependent c-Jun transcription activity in SH-SY5Y cells
Rangaswami et al., Oncol Rep 2007 (Lung Neoplasms...) : OPN triggers NIK- and MEKK1 dependent AP-1 activation whereas NIK dependent AP-1 activation is independent of JNK1 that leads to pro-MMP-9 activation
Kim et al., J Biol Chem 2007 (MAP Kinase Signaling System) : We document that c-Jun activation is dependent on the MAPK kinase kinase MEKK1
Das et al., Mol Cell Biochem 2010 : Furthermore, transfection of kinase-dead MEKK1 , an initiating kinase of the JNK pathway inhibited Trx mediated AP-1 transactivation and DNA binding, suggesting that MEKK1 may mediate Trx induced AP-1 activation ... In contrast, wild-type MEKK1 overexpression did not inhibit Trx mediated AP-1 activation
Sun et al., Oncol Rep 2011 : We found that MEKK1/MEKK4 as opposed to ASK1, are responsible for TRAIL induced c-Jun NH2-terminal kinase (JNK) or p38 activation, and that their catalytic activity is repressed by the caspase-8 inhibitor, suggesting that the caspase-8 activation induced by TRAIL is indispensible for MEKK activation
Jin et al., Dev Biol 2013 : Second, MAP3K1 potentiated AP-2a expression and SRF and AP-1 activity, but its target genes were enriched for binding motifs of AP-2a and SRF, and not AP-1, suggesting the existence of novel MAP3K1-AP-2a/SRF modules in gene regulation ... Second, MAP3K1 potentiated AP-2a expression and SRF and AP-1 activity, but its target genes were enriched for binding motifs of AP-2a and SRF, and not AP-1, suggesting the existence of novel MAP3K1-AP-2a/SRF modules in gene regulation
Lu et al., J Biol Chem 1997 : Transient transfection assays demonstrated that JNKK2 potentiated the stimulation of c-Jun transcriptional activity by MEKK1
Eilers et al., J Neurosci 1998 : Furthermore, expression of a constitutively active form of MEK kinase 1 (MEKK1) , which strongly activates the Jun kinase pathway, increased c-Jun protein levels and c-Jun phosphorylation and induced apoptosis in the presence of NGF
Pomérance et al., J Biol Chem 1998 : Grb2 interaction with MEK-kinase 1 is involved in regulation of Jun-kinase activities in response to epidermal growth factor