◀ Back to MAPK9
ATF2 — MAPK9
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Bind_translation Interaction:
ATF2
—
MAPK9
(experimental interaction detection)
Fukunaga et al., EMBO J 1997
-
IRef Biogrid Interaction:
ATF2
—
MAPK9
(direct interaction, enzymatic study)
Ho et al., J Biol Chem 2006
-
IRef Biogrid Interaction:
ATF2
—
MAPK9
(direct interaction, enzymatic study)
Gupta et al., EMBO J 1996
-
IRef Biogrid Interaction:
ATF2
—
MAPK9
(direct interaction, pull down)
Gupta et al., EMBO J 1996
-
IRef Biogrid Interaction:
ATF2
—
MAPK9
(direct interaction, two hybrid)
Yao et al., Cancer Res 2007*
-
IRef Biogrid Interaction:
ATF2
—
MAPK9
(direct interaction, enzymatic study)
Ho et al., J Biol Chem 2003
-
IRef Hprd Interaction:
ATF2
—
MAPK9
(in vitro)
Ouwens et al., EMBO J 2002*, Ho et al., J Biol Chem 2003, Denys et al., Acta urologica Belgica 1977*, Livingstone et al., EMBO J 1995*
-
IRef Intact Interaction:
ATF2
—
MAPK9
(phosphorylation reaction, protein kinase assay)
Ho et al., J Biol Chem 2006
Text-mined interactions from Literome
Brinkman et al., J Biol Chem 1999
:
Engagement of tumor necrosis factor (TNF) receptor 1 leads to
ATF-2- and p38
mitogen activated protein kinase dependent TNF-alpha gene expression
Crowe et al., Anticancer Res 2000
(Carcinoma, Squamous Cell...) :
Of these, little is known about the
role of
ATF-2 in regulation of
MAPK signaling and cellular proliferation
Yosimichi et al., Eur J Biochem 2001
:
These inhibitors of MAPKK and
MAPK suppressed phosphorylation of ets-like gene-1 (Elk-1) and nuclear
activating transcription factor-2 ( Atf-2 ) induced by CTGF/Hcs24 in a dose dependent manner, respectively
Matsuoka et al., Am J Physiol Lung Cell Mol Physiol 2002
(Disease Models, Animal...) :
p38
MAPK and its substrate, activating transcription factor (ATF)-2, in bronchoalveolar lavage fluid cells were phosphorylated by intratracheal exposure of bleomycin, and the phosphorylation of
ATF-2 was
inhibited by subcutaneous administration of a specific inhibitor of p38 MAPK, FR-167653
Cao et al., Mol Cell Biol 2004
:
Activation of
ATF-2 by p38
MAPK additionally serves as the cAMP sensor that increases expression of the PGC-1alpha gene itself in brown adipose tissue
Ha et al., Proc Natl Acad Sci U S A 2004
:
Here, we demonstrate an additional mechanism whereby a significant reduction of proinflammatory gene expression such as IL-1beta, tumor necrosis factor alpha, and inducible nitricoxide synthase in PARP-1 ( -/- ) glial cells is linked to defective inflammatory stimuli induced
p38MAPK mediated phosphorylation of
ATF-2 and cAMP-response element binding protein and phosphorylation of NF-kappaB p65
Faour et al., J Biol Chem 2005
(Arthritis, Rheumatoid) :
Initial studies confirmed that PGE2 induces egr-1 mRNA expression and protein synthesis by restricted SAPK2/p38
MAPK dependent
activating transcription factor-2 ( ATF-2) dimer transactivation of the egr-1 promoter as judged by studies using wild-type ( WT ) and deletion mutant egr-1 promoter constructs, Northern and Western blotting, and standard and supershift electrophoretic mobility shift analyses
Si et al., J Virol 2005
:
JNK1/2 inhibitors reduced CVB3 induced phosphorylation of
activating transcription factor 2 , and the p38
MAPK inhibitor
reduced CVB3 induced phosphorylation of heat shock protein 27
Sooranna et al., J Cell Physiol 2007
(MAP Kinase Signaling System) :
All three stimuli increased PGHS-2 and IL-8 mRNA expression in a MAPK dependent manner, but while the
MAPK inhibitors
reduced the IL-1beta induced activation of activating transcription factor
(ATF)-2 , liver activating protein (LAP) and c-jun, the stretch induced increase in LAP was unaffected by MAPK-inhibition and only JNK inhibition appeared to reduce c-jun activation
Huang et al., Journal of molecular signaling 2008
:
It appears that this effect is mediated through p38 MAPK, because RA decreased p38 phosphorylation, and a selective inhibitor of p38
MAPK ( SB203580 ) also
inhibited the phosphorylation of
ATF-2
Hisatsune et al., J Immunol 2008
:
Molecular characterization of Helicobacter pylori VacA induction of IL-8 in U937 cells reveals a prominent
role for
p38MAPK in
activating transcription factor-2 , cAMP response element binding protein, and NF-kappaB activation
Cho et al., Mol Endocrinol 2009
:
The inhibition of
MAPK dependent
activating transcription factor 2/c-Jun phosphorylation by GR in COX-2 repression was a result of MAPK phosphatase-1 (MKP-1) induction
Zdanov et al., Biogerontology 2009
:
In this work, p38 (
MAPK )
activation and increased DNA binding activities of
ATF-2 and p53 are shown to mediate cyclooxygenase-2 overexpression in premature senescence
Truter et al., Cardiology 2009
(Aortic Valve Insufficiency...) :
JNK and
p38MAPK inhibition
reduced c-Jun and
ATF2 phosphorylation to NL ; ERK inhibition had no effect
Liss et al., Oncogene 2010
(Cell Transformation, Neoplastic...) :
Investigating the mode of ATF2 regulation revealed a positive feedback mechanism whereby
ATF2 induces p38
MAPK phosphorylation to further induce its own activity
Liu et al., Int J Biochem Cell Biol 2010
:
Taken together, our data indicate that Fas/FasL up-regulation in piceatannol treated U937 cells is elicited by Ca ( 2+ ) /p38alpha
MAPK mediated activation of c-Jun and
ATF-2 , and suggest that autocrine Fas mediated apoptotic mechanism is involved in piceatannol induced cell death
Wilkinson et al., Genes Dev 1996
:
ATF-2 is
regulated through phosphorylation in mammalian cells by the stress activated
mitogen activated protein ( MAP ) kinases SAPK/JNK and p38
Chen et al., J Biol Chem 1998
(Brain Neoplasms) :
The
involvement of p38 (
MAPK ) in the activation of
ATF-2 , which leads to the transactivation of rat grp78, is confirmed by electrophoretic mobility shift assay using a probe containing the CRE-like sequence as well as by transient transfection assays with a plasmid containing a 710-base pair stretch of the grp78 promoter
Cheong et al., J Biol Chem 1998
:
We demonstrate that p38beta
mitogen activated protein ( MAP ) kinase augments
ATF-2 transactivation activity on the PEPCK-C promoter, which is consistent with the interpretation that PEPCK-C promoter activity is maintained under stress through a p38 MAP kinase dependent pathway