ArticleMolecular biology of the cell2010
The BNIP-2 and Cdc42GAP homology (BCH) domain of p50RhoGAP/Cdc42GAP sequesters RhoA from inactivation by the adjacent GTPase-activating protein domain.
Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- RKIP regulates bone marrow macrophage differentiation to mediate osteoclastogenesis and H-type vessel formation.Nature communications · 2025Article
- Structural basis for the distinct roles of non-conserved Pro116 and conserved Tyr124 of BCH domain of yeast p50RhoGAP.Cellular and molecular life sciences : CMLS · 2024Article
- BNIP-2 Activation of Cellular Contractility Inactivates YAP for H9c2 Cardiomyoblast Differentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- MLL regulates the actin cytoskeleton and cell migration by stabilising Rho GTPases via the expression of RhoGDI1.Journal of cell science · 2022Article
- Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022Review
- Analysis of ARHGAP4 Expression With Colorectal Cancer Clinical Characteristics and Prognosis.Frontiers in oncology · 2022Article
- Structural basis for p50RhoGAP BCH domain-mediated regulation of Rho inactivation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Rac1 and EGFR cooperate to activate Pak in response to nutrient stress.Biochemical and biophysical research communications · 2020Article
- Rab5a activates IRS1 to coordinate IGF-AKT-mTOR signaling and myoblast differentiation during muscle regeneration.Cell death and differentiation · 2020Article
- BNIP-2 retards breast cancer cell migration by coupling microtubule-mediated GEF-H1 and RhoA activation.Science advances · 2020Article
- Hsp70 Interacts with Mitogen-Activated Protein Kinase (MAPK)-Activated Protein Kinase 2 To Regulate p38MAPK Stability and Myoblast Differentiation during Skeletal Muscle Regeneration.Molecular and cellular biology · 2018Article
- KIF5B transports BNIP-2 to regulate p38 mitogen-activated protein kinase activation and myoblast differentiation.Molecular biology of the cell · 2015Article
- Functional cross-talk between ras and rho pathways: a Ras-specific GTPase-activating protein (p120RasGAP) competitively inhibits the RhoGAP activity of deleted in liver cancer (DLC) tumor suppressor by masking the catalytic arginine finger.The Journal of biological chemistry · 2014Article
- SmgGDS antagonizes BPGAP1-induced Ras/ERK activation and neuritogenesis in PC12 cell differentiation.Molecular biology of the cell · 2013Article
- Modified SH2 domain to phototrap and identify phosphotyrosine proteins from subcellular sites within cells.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- FIP3-endosome-dependent formation of the secondary ingression mediates ESCRT-III recruitment during cytokinesis.Nature cell biology · 2012Article
- Bmcc1s, a novel brain-isoform of Bmcc1, affects cell morphology by regulating MAP6/STOP functions.PloS one · 2012Article
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4 authors.
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Abstract
The BNIP-2 and Cdc42GAP homology (BCH) domain is a novel regulator for Rho GTPases, but its impact on p50-Rho GTPase-activating protein (p50RhoGAP or Cdc42GAP) in cells remains elusive. Here we show that deletion of the BCH domain from p50RhoGAP enhanced its GAP activity and caused drastic cell rounding. Introducing constitutively active RhoA or inactivating GAP domain blocked such effect, whereas replacing the BCH domain with endosome-targeting SNX3 excluded requirement of endosomal localization in regulating the GAP activity. Substitution with homologous BCH domain from Schizosaccharomyces pombe, which does not bind mammalian RhoA, also led to complete loss of suppression. Interestingly, the p50RhoGAP BCH domain only targeted RhoA, but not Cdc42 or Rac1, and it was unable to distinguish between GDP and the GTP-bound form of RhoA. Further mutagenesis revealed a RhoA-binding motif (residues 85-120), which when deleted, significantly reduced BCH inhibition on GAP-mediated cell rounding, whereas its full suppression also required an intramolecular interaction motif (residues 169-197). Therefore, BCH domain serves as a local modulator in cis to sequester RhoA from inactivation by the adjacent GAP domain, adding to a new paradigm for regulating p50RhoGAP signaling.
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