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AHSA1 — FOS
Text-mined interactions from Literome
Arnould et al., Mol Cell Biol 1999
(Polycystic Kidney, Autosomal Dominant) :
The PKD2 mediated
AP-1 activity was
dependent upon activation of the mitogen activated protein kinases
p38 and JNK1 and protein kinase C (PKC) epsilon, a calcium independent PKC isozyme
Bhattacharyya et al., Biochem J 2002
:
While ERK1/2 activation could be linked to enhanced DNA binding of activator protein-1 (AP-1),
p38 MAPK signalling did not
affect AP-1 DNA binding
Chen et al., J Neurochem 2003
(MAP Kinase Signaling System) :
These results suggest a prominent role of JNK and
p38 , as well as their downstream
AP-1 binding
activation and p53 phosphorylation in mediating glutamate excitotoxicity
Silvers et al., Neoplasia (New York, N.Y.) 2003
(Skin Neoplasms) :
The role of JNK and
p38 MAPK activities in UVA induced signaling pathways
leading to
AP-1 activation and c-Fos expression
Zeliadt et al., Toxicol Appl Pharmacol 2003
:
Palytoxin does not
require JNK or
p38 to increase
c-Fos binding, however
Parameswaran et al., Cell Physiol Biochem 2003
:
Both an AM-induced increase in AP-1 mRNA expression and
AP-1 luciferase activities were
inhibited by H89 ( protein kinase-A inhibitor ) and SB203580 (
p38 MAPK inhibitor )
Kim et al., Eur J Immunol 2005
(Bacteroides Infections...) :
The
p38 inhibitor SB203580 and the ERK inhibitor U0126
reduced not only
AP-1 activity, but also decreased IL-8 and MCP-1 expression
Peng et al., Toxicology 2007
(Glioma) :
Inhibition of ERK,
p38 and JNK
block the activation of
AP-1 and NF-kappaB, suggesting these MAPKs are involved in ( Ac ) ( 5 ) GP-induced transcription regulation
Ding et al., FEMS Immunol Med Microbiol 2008
:
extracellular signal related kinase ( ERK ),
p38 , and c-Jun N-terminal kinase (JNK) each selectively
regulated AP-1 subcomponent expression and DNA binding activity
Shim et al., J Med Food 2009
:
Moreover, inhibition of phosphorylated ERK, JNK, and
p38 by K. pandurata extract
resulted in decreased
c-Fos expression and c-Jun phosphorylation induced by UV light
Yi et al., J Immunol 1998
(Lymphoma, B-Cell) :
Inhibition of
p38 led to the suppression of CpG DNA induced
AP-1 DNA binding activity and cytokine production, indicating that the p38 pathway is required for mediating these immune stimulatory effects of CpG DNA