Literature DB >> 9548756

Regulation of RhoA GTP hydrolysis by the GTPase-activating proteins p190, p50RhoGAP, Bcr, and 3BP-1.

B Zhang1, Y Zheng.   

Abstract

The small GTP-binding protein RhoA becomes inactivated by hydrolyzing bound GTP to GDP through its intrinsic GTPase activity which is further stimulated by a family of Rho GTPase-activating proteins (GAPs). Here we have compared the kinetics of interaction between recombinant RhoA and the RhoGAP domains of p190, p50RhoGAP, Bcr, and 3BP-1. The intrinsic rate of GTP hydrolysis by RhoA is relatively slow when compared to other Rho-family GTPases such as Cdc42 or Rac1 with a rate constant of 0.022 min-1, which can be further stimulated at least 4000-fold by p190 or p50RhoGAP. The RhoGAP domains of Bcr and 3BP-1, which were thought to be inactive toward RhoA, are also found capable of stimulating the GTPase activity of RhoA in a dose-dependent manner. The supreme catalytic activities of p190 and p50RhoGAP toward RhoA reside mostly in their lower Km values (1.79 and 2.83 microM, respectively) which correlate well with their binding affinity for GMP-PNP-bound RhoA (2.18 and 2. 47 microM, respectively), in contrast with Bcr and 3BP-1 which interact with the activated RhoA with much higher Km (89 microM). However, the mechanisms of catalysis by p190 and p50RhoGAP are distinct in at least three aspects: (1) p50RhoGAP displays an effect of product inhibition by binding to the GDP-bound form of RhoA with a Kd of 6 microM in comparison with the Kd for p190 of 33 microM; (2) the Km of p190 increases drastically upon the increase of salt and Mg2+ concentrations, conditions under which only modest changes of Km for p50RhoGAP are observed; and (3) p50RhoGAP remains partially active toward the effector domain mutants of RhoA, Y34K, and T37A, whereas p190 is completely inactive toward Y34K and T37A. These results suggest that there exists a unique mechanism of functional interaction between RhoA and individual RhoGAP which involves distinct structural determinants of the small G-protein to cause the apparent differences in kinetic properties.

Entities:  

Mesh:

Substances:

Year:  1998        PMID: 9548756     DOI: 10.1021/bi9718447

Source DB:  PubMed          Journal:  Biochemistry        ISSN: 0006-2960            Impact factor:   3.162


  22 in total

1.  The hematopoiesis-specific GTP-binding protein RhoH is GTPase deficient and modulates activities of other Rho GTPases by an inhibitory function.

Authors:  Xiaoyu Li; Xia Bu; Binfeng Lu; Hava Avraham; Richard A Flavell; Bing Lim
Journal:  Mol Cell Biol       Date:  2002-02       Impact factor: 4.272

Review 2.  Dynamics of the Rho-family small GTPases in actin regulation and motility.

Authors:  Désirée Spiering; Louis Hodgson
Journal:  Cell Adh Migr       Date:  2011-03-01       Impact factor: 3.405

3.  Feedback regulation through myosin II confers robustness on RhoA signalling at E-cadherin junctions.

Authors:  Rashmi Priya; Guillermo A Gomez; Srikanth Budnar; Suzie Verma; Hayley L Cox; Nicholas A Hamilton; Alpha S Yap
Journal:  Nat Cell Biol       Date:  2015-09-14       Impact factor: 28.824

4.  Kinetic analysis of GTP hydrolysis catalysed by the Arf1-GTP-ASAP1 complex.

Authors:  Ruibai Luo; Bijan Ahvazi; Diana Amariei; Deborah Shroder; Beatriz Burrola; Wolfgang Losert; Paul A Randazzo
Journal:  Biochem J       Date:  2007-03-15       Impact factor: 3.857

5.  Integrin signaling through Arg activates p190RhoGAP by promoting its binding to p120RasGAP and recruitment to the membrane.

Authors:  William D Bradley; Samuel E Hernández; Jeffrey Settleman; Anthony J Koleske
Journal:  Mol Biol Cell       Date:  2006-09-13       Impact factor: 4.138

6.  Wave-pinning and cell polarity from a bistable reaction-diffusion system.

Authors:  Yoichiro Mori; Alexandra Jilkine; Leah Edelstein-Keshet
Journal:  Biophys J       Date:  2008-01-22       Impact factor: 4.033

7.  Rho activation is apically restricted by Arhgap1 in neural crest cells and drives epithelial-to-mesenchymal transition.

Authors:  Matthew R Clay; Mary C Halloran
Journal:  Development       Date:  2013-06-26       Impact factor: 6.868

8.  Real-time NMR study of three small GTPases reveals that fluorescent 2'(3')-O-(N-methylanthraniloyl)-tagged nucleotides alter hydrolysis and exchange kinetics.

Authors:  Mohammad T Mazhab-Jafari; Christopher B Marshall; Matthew Smith; Geneviève M C Gasmi-Seabrook; Vuk Stambolic; Robert Rottapel; Benjamin G Neel; Mitsuhiko Ikura
Journal:  J Biol Chem       Date:  2009-12-14       Impact factor: 5.157

9.  Different levels of Bfa1/Bub2 GAP activity are required to prevent mitotic exit of budding yeast depending on the type of perturbations.

Authors:  Junwon Kim; Selma Sun Jang; Kiwon Song
Journal:  Mol Biol Cell       Date:  2008-07-30       Impact factor: 4.138

10.  RHOA and PRKCZ control different aspects of cell motility in pancreatic cancer metastatic clones.

Authors:  Marco Della Peruta; Cinzia Giagulli; Carlo Laudanna; Aldo Scarpa; Claudio Sorio
Journal:  Mol Cancer       Date:  2010-03-17       Impact factor: 27.401

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.