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JUN — MAP3K2
Text-mined interactions from Literome
Su et al., J Biol Chem 2001
:
AP-1 and interleukin-2 reporter gene induction in T-cells was also
inhibited by dominant negative
MEKK2 mutants
Huang et al., Biochem Biophys Res Commun 2003
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Select point mutations in subdomain X impair MEKK2 phosphorylation of the MAP2Ks, MKK7 and MEK5, abolish
MEKK2 induced
activation of the MAPKs, JNK1 and ERK5, and diminish MEKK2 dependent activation of an
AP-1 reporter gene
Wei et al., Eur J Immunol 2003
:
The MAPK kinase kinase
MEKK2 is
essential for activation of
c-Jun N-terminal kinase (JNK) and extracellular signal regulated kinase 5 ( ERK5 ) ... These results demonstrate the novel and important,
MEKK2 dependent role of MEF2C in induction of
c-Jun expression in mast cells activated through FcepsilonRI, a pathway distinct from that involving MEKK2-MEK5-ERK5 in the regulation of mast cell cytokine production
Kesavan et al., J Cell Physiol 2004
:
Thus,
MEKK2 regulates
AP-1 activity at two levels, by regulating both expression of AP-1 components and c-Jun N-terminal phosphorylation ... Thus,
MEKK2 regulates AP-1 activity at two levels, by regulating both expression of AP-1 components and
c-Jun N-terminal phosphorylation
Cheng et al., Mol Cell Biol 2005
:
In contrast, the knockdown of Mip1 expression by siRNA augmented the
MEKK2 mediated JNK and
AP-1 reporter activation
Jin et al., Dev Biol 2013
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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