Gene interactions and pathways from curated databases and text-mining

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PLXNB1 — RHOA

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

Aurandt et al., Proc Natl Acad Sci U S A 2002 : Semaphorin 4D is the ligand for the plexin-B1 receptor and stimulation of the plexin-B1 receptor activates the small GTPase RhoA
Oinuma et al., J Biol Chem 2003 : Recent studies have demonstrated that Plexin-B1 activates RhoA and induces growth cone collapse through Rho-specific guanine nucleotide exchange factor PDZ-RhoGEF ... We also found that Rnd1 promoted the interaction between Plexin-B1 and PDZ-RhoGEF and thereby dramatically potentiated the Plexin-B1 mediated RhoA activation
Swiercz et al., J Cell Biol 2004 : Plexin-B1/RhoGEF mediated RhoA activation involves the receptor tyrosine kinase ErbB-2 ... Our data indicate that ErbB-2 is an important component of the plexin-B receptor system and that ErbB-2 mediated phosphorylation of plexin-B1 is critically involved in Sema4D induced RhoA activation, which underlies cellular phenomena downstream of plexin-B1, including axonal growth cone collapse
Aurandt et al., Biochem J 2006 (MAP Kinase Signaling System) : We have found that the mechanism of activation requires the C-terminus of plexin-B1 and the activation of RhoA
Swiercz et al., Mol Cell Biol 2009 : The semaphorin 4D (Sema4D) receptor plexin-B1 constitutively interacts with particular Rho guanine nucleotide exchange factors ( RhoGEFs ) and thereby mediates Sema4D induced RhoA activation, a process which involves the tyrosine phosphorylation of plexin-B1 by ErbB-2
Negishi-Koga et al., Nat Med 2011 (Bone Resorption...) : The binding of Sema4D to its receptor Plexin-B1 on osteoblasts resulted in the activation of the small GTPase RhoA , which inhibits bone formation by suppressing insulin-like growth factor-1 (IGF-1) signaling and by modulating osteoblast motility