Gene interactions and pathways from curated databases and text-mining

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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