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FOS — MAP2K1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Manna et al., Oncogene 1999
:
gamma-GCS also abolished the activation of
AP-1 induced by TNF and
inhibited TNF induced activation of JNK and
mitogen activated protein kinase kinase
Manna et al., J Immunol 2000
:
Vesnarinone also blocked NF-kappa B activation induced by several other inflammatory agents,
inhibited the TNF induced activation of transcription factor
AP-1 , and suppressed the TNF induced activation of c-Jun N-terminal kinase and
mitogen activated protein kinase kinase
Lotfi et al., Braz J Med Biol Res 2000
(Adrenal Cortex Neoplasms) :
In addition, ACTH is a poor activator of ERK-MAPK, but
c-Fos induction and DNA synthesis stimulation by ACTH are strongly
inhibited by the inhibitor of
MEK1 PD98059
Kolonics et al., Cell Signal 2001
(MAP Kinase Signaling System) :
The GM-CSF promoted cell survival and proliferation correlated with
MEK-1 dependent ERK1/2, Elk-1 and CREB phosphorylation and Egr-1, c-Fos expression as well as with increased STAT-5,
AP-1 , c-Myb and NF-kappaB DNA binding
Sun et al., J Biol Chem 2002
(Osteoarthritis) :
In addition, dominant negative Ras, Raf, and
MEK1/2 could block the induction of hMMP1, and a MEK1/2-specific inhibitor ( UO126 ) could
block the induction of hMMP1 and
c-Fos by BCP crystals
Hoffmann et al., J Biol Chem 2005
:
Additional experiments reveal that, in conjunction with p65 NF-kappaB, the
MEK1-ERK dependent synthesis of
c-Fos and Fra-1 serves to adjust the overall expression level of IL-8 in response to two of its physiological inducers, IL-1 and epidermal growth factor
Ryborg et al., Acta Derm Venereol 2004
:
The effects on transglutaminase-1 and
AP-1 were
dependent on protein kinase C and
mitogen activated protein kinase kinase
Wang et al., Planta Med 2007
(Leukemia...) :
Deerberry fruit extracts also blocked TPA- or UVB induced phosphorylation of ERKs and
MEK 1/2 , two upstream
regulators of
AP-1 and inhibited proliferation of human leukemia HL-60 cancer cells and human lung epithelial cancer A549 cells and induced apoptosis of HL-60 cells
Zhou et al., Cell Prolif 2007
(MAP Kinase Signaling System) :
The suppression of
MEK1/ERK1/2 activation
inhibited UV-induced expression of
c-Fos and JunD and increased caspase 3 activity and cell death
Hsieh et al., Biochim Biophys Acta 2008
:
Moreover, thrombin stimulated
activation of NF-kappaB,
AP-1 , and COX-2 promoter activity was blocked by the inhibitors of c-Src, PKC, EGFR,
MEK1/2 , AP-1 and NF-kappaB, suggesting that thrombin induces COX-2 promoter activity mediated through PKC ( delta ) /c-Src dependent EGFR transactivation, MEK-ERK1/2, AP-1, and NF-kappaB
Yang et al., J Cell Physiol 2010
(Arthritis, Rheumatoid) :
IL-1beta induced ICAM-1 expression, extracellular signal regulated kinase ( ERK ) and c-Jun-N-terminal kinase (JNK) phosphorylation,
AP-1 activation, and nuclear factor-kappaB (NF-kappaB) p65 translocation were
attenuated by the inhibitors of
MEK1/2 ( U0126 ), JNK ( SP600125 ), AP-1 ( tanshinone IIA ), and NF-kappaB ( helenalin ) or transfection with respective short hairpin RNA plasmids
Koumbadinga et al., Peptides 2010
:
The short-term PKC- and
MEK1 dependent increase of
c-Fos expression was best correlated to PMA induced ACE upregulation
Frost et al., Mol Cell Biol 1994
:
We found that coexpression of small t and either ERK1,
MEK1 , or BXB
resulted in an increase in
AP-1 activity, whereas expression of either small t or any of the kinases alone did not have any effect
Franklin et al., Oncogene 1995
(Leukemia) :
The induction of constitutively active
MEK1 protein expression
resulted in an increase in MEK1 activity, c-Jun and
AP-1 transcriptional activity and an inhibition of U937 cell growth