◀ 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