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JUN — RHO
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Li et al., J Clin Invest 1999
:
Although both Cdc42 and
Rho were
involved in the shear stress induced transcription factor
AP-1 acting on the 12-O-tetradecanoyl-13-phorbol-acetate-responsive element ( TRE ), only Cdc42 was sufficient to activate AP-1/TRE ... Dominant negative mutants of Cdc42 and Rho, as well as recombinant C3 exoenzyme, attenuated the shear stress activation of c-Jun NH2-terminal kinases (JNKs), suggesting that Cdc42 and
Rho regulate the shear stress induction of
AP-1/TRE activity through JNKs. Shear stress induced cell alignment and stress fiber formation were inhibited by the dominant negative mutants of Rho and p160ROCK, but not by the dominant negative mutant of Cdc42, indicating that the Rho-p160ROCK pathway regulates the cytoskeletal reorganization in response to shear stress
Ediger et al., Eur Respir J 2003
(Cell Transformation, Neoplastic...) :
Activation of
activator protein-1 is synergistic, and
Rho activation by lysophosphatidic acid is
required for synergism in both activator protein-1 activation and mitogenesis
Morigi et al., Am J Pathol 2005
(Chronic Disease...) :
These data suggest that reorganization of the actin cytoskeletal network in response to protein load is implicated in modulation of the ET-1 gene via
Rho kinase
dependent FAK activation of NF-kappaB and
Ap-1 in differentiated podocytes
Peng et al., Diabetes 2008
(Diabetes Mellitus, Experimental...) :
Activity of the transcription factor
AP-1 , increased in diabetic MCs and kidneys, is important in the profibrotic effects of glucose, and this was
dependent on
Rho-kinase signaling
Lee et al., Oncogene 2009
:
In summary, Galpha(12) and Galpha(13) regulate the expression of the TGFbeta1 gene through an increase in
Rho/Rac dependent
AP-1 activity, implying that the G-protein coupled receptor ( GPCR ) -Galpha(12) pathway is involved in the TGFbeta1 mediated transdifferentiation process
Juneja et al., PloS one 2011
(Breast Neoplasms...) :
Furthermore, expression of dominant negative
Rho or treatment of cells with an inhibitor of the Rho kinase, ROCK,
reduces G12 induced JNK and
c-Jun activation, and ROCK inhibitor treatment also inhibits G12 induced cellular invasion
Chang et al., Mol Cell Biol 1998
:
We demonstrate in this report that overexpression of an activated form of
Rho enhances
AP-1 activity in Jurkat T cells in the presence of phorbol myristate acetate ( PMA ), but activated Rho ( V14Rho ) has little or no effect on NFAT, Oct-1, and NF-kappaB enhancer element activities under similar conditions ... The effect of Rho on AP-1 is independent of the mitogen activated protein kinase pathway, as a dominant negative MEK and a MEK inhibitor ( PD98059 ) did not affect
Rho induced
AP-1 activity
Malliri et al., J Cell Biol 1998
:
Our data establish a novel link between
AP-1 activity and EGFR
activation of Rac and
Rho , which in turn mediate the actin cytoskeletal rearrangements required for cell motility and invasion