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HRAS — JUN
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Okan et al., Oncogene 2001
:
Here we show that uPAR transcription is stimulated by V12
H-Ras , the effector loop mutant V12 H-Ras G37 and constitutively-active RalA 72L. RalA dependent transcription
required the presence of the ATF2-like
AP1-site at -70 bp and the c-Jun binding motif at -184 bp in the uPAR promoter
Blaine et al., J Biol Chem 2001
(Carcinoma, Non-Small-Cell Lung...) :
Expression of
Ha-Ras led to induction of
c-Jun protein, which showed functional cooperation with Sp1 in driving promoter activity
Schwarz et al., Neuroreport 2002
(MAP Kinase Signaling System) :
Bcl-2 up-regulates
ha-ras mRNA expression and
induces c-Jun phosphorylation at Ser73 via an ERK dependent pathway in PC 12 cells
Bulavin et al., Mol Cell Biol 2003
(MAP Kinase Signaling System) :
In this report we show that in Gadd45a ( -/- ) mouse embryo fibroblasts (MEF), overexpression of
H-ras activates extracellular signal regulated kinase ( ERK ) and
c-Jun N-terminal kinase (JNK) but not p38 kinase, and this correlates with the loss of H-ras induced cell cycle arrest ( premature senescence )
Youn et al., Cancer Res 2004
(Breast Neoplasms) :
From promoter analysis of ERCC1, an increase in the
Ap1 transcriptional activity as a
result of the expression of the oncogenic
H-Ras was found to be crucial for this induction
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
Yoo et al., Int J Oncol 2006
:
RASSF1A suppresses oncogenic
H-Ras induced
c-Jun N-terminal kinase activation
Oh et al., Cancer Res 2007
(Cell Transformation, Neoplastic...) :
Here, we reported that TOPK regulates UVB induced c-Jun-NH2-kinase 1 (JNK1) activity, and is essential for
H-Ras induced
activator protein-1 activity and cell transformation
Binétruy et al., Nature 1991
:
Ha-Ras augments
c-Jun activity and stimulates phosphorylation of its activation domain
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
Nilsson et al., J Biol Chem 1995
:
Activated
Ha-Ras but not TPA
induces transcription through binding sites for activating transcription factor
3/Jun and a novel nuclear factor
Natoli et al., Oncogene 1994
:
We show by use of Ha-Ras and Raf-1 dominant negative mutants that both
Ha-Ras and Raf-1 are
required for pX-induced activation of
c-Jun transcriptional 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