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FOS — HRAS
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 *
Text-mined interactions from Literome
Song et al., Cancer Res 2006
(Breast Neoplasms...) :
DNA binding and transcriptional activities of
AP-1 were
increased by MKK6 or
H-Ras as evidenced by electrophoretic mobility shift assay and luciferase assay using an AP-1-driven plasmid
Denko et al., Int J Oncol 1997
:
Gel shift analysis and reporter gene expression indicated that TPCK blocked Ha-ras induced NF-kappa B activity, while only having minimal effects on
Ha-ras induced
AP-1 activity
Frost et al., Proc Natl Acad Sci U S A 1994
:
A requirement for extracellular signal regulated kinase ( ERK ) function in the
activation of
AP-1 by
Ha-Ras , phorbol 12-myristate 13-acetate, and serum ... Overexpression of either kinase-deficient ERK-1 or kinase-deficient ERK-2 partially inhibited
AP-1 activation by wt
Ha-Ras but had no effect on PMA or serum induced activation ... Coexpression of both interfering mutants abolished
AP-1 induction by wt
Ha-Ras , PMA, or serum
Okimoto et al., Oncogene 1996
:
Both transient and permanent expression of H-ras enhanced AP-1 activity in mouse cells, but further co-introduction of dominant negative c-jun mutant encoding a transcriptionally inactive product inhibited the
H-ras dependent
AP-1 induction
Genot et al., EMBO J 1996
:
The
induction of
AP-1 by
p21ras also requires Rac-1 function
Swanson et al., J Biol Chem 1999
:
Fos kinase activation is
dependent on
p21(ras) and mitogen activated protein kinase/ERK kinase kinase ( MEK ) activity and is independent of phosphatidylinositol 3-kinase activity