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CDC42 — EPHB2
Pathways - manually collected, often from reviews:
-
NCI Pathway Database EPHB forward signaling:
CDC42/GDP complex (CDC42)
→
Ephrin B/EPHB2/Intersectin/N-WASP complex (EFNB3_EFNB2_EFNB1-EPHB2-ITSN1-WASL)
(modification, collaborate)
Irie et al., Nat Neurosci 2002
Evidence: mutant phenotype, assay
-
Reactome Reaction:
EPHB2
→
CDC42
(reaction)
-
Reactome Reaction:
EPHB2
→
CDC42
(indirect_complex)
Text-mined interactions from Literome
Eblen et al., Mol Cell Biol 2002
(MAP Kinase Signaling System) :
Activated forms of Rac and
Cdc42 could
enhance the association of wild-type
ERK2 with MEK1 but not with MEK2 in serum starved adherent cells
Rul et al., Ann N Y Acad Sci 2002
(MAP Kinase Signaling System) :
Here, we describe that the inhibition of Rac1 or
Cdc42 signaling
leads to MAPK
ERK activation via a pathway involving PI(3)K, Akt, Raf, and MEK, but not Ras
Zhong et al., Blood 2003
(MAP Kinase Signaling System) :
Rac and
Cdc42 , but not Ras or Rho, were
responsible for this
MAPK/ERK activation ... We conclude from these data that
Rac/Cdc42 dependent activation of
MAPK/ERK is a critical event in the immediate phagocytic response of PMNs to microbial challenge
Hammarberg et al., Biochem Pharmacol 2004
:
In addition, inhibition of
Rac/Cdc42 , small GTPases of the Rho family, by clostridium toxin B, diminished p38 phosphorylation but did not
affect ERK1/2
Deroanne et al., J Cell Sci 2005
:
Silencing of
Cdc42 also
induced an increased phosphorylation of
ERK1/2 and p38 MAP kinase
Yano et al., Circ Res 2007
(Inflammation) :
However, DN-RhoA and
DN-Cdc42 activated p38 MAPK, but not
ERK1/2
Lim et al., Endocrinology 2009
:
Knockdown or inhibition of
Cdc42 and PAK1 activities also
prevented activation of MAPK/ERK
(MEK)-1/2-ERK1/2 by insulin, which was previously identified as a critical pathway for insulin regulated GLP-1 release
Bagrodia et al., J Biol Chem 1995
:
Activated
Cdc42 also stimulated the activity of the related p38 mitogen activated protein kinase but was a less effective
activator of
ERK2