The GAP1 family of GTPase-activating proteins: spatial and temporal regulators of small GTPase signalling.

S Yarwood, D Bouyoucef-Cherchalli, P J Cullen, S Kupzig
Author Information
  1. S Yarwood: The Henry Wellcome Integrated Signalling Laboratories, Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK.

Abstract

Ras proteins are binary switches that, by cycling between inactive GDP-bound and active GTP-bound conformations, regulate multiple cellular signalling pathways including those that control cell growth, differentiation and survival. Approximately 30% of all human tumours express Ras-containing oncogenic mutations that lock the protein into a constitutively active conformation. The activation status of Ras is regulated by two groups of proteins: GEFs (guanine nucleotide-exchange factors) bind to Ras and enhance the exchange of GDP for GTP, thereby activating it, whereas GAPs (GTPase-activating proteins) inactivate Ras by binding to the GTP-bound form and enhancing the hydrolysis of the bound nucleotide back to GDP. In this review, we focus on a group of key regulators of Ras inactivation, the GAP1 family of Ras-GAPs. The members of this family are GAP1m, GAP1IP4BP, CAPRI (Ca2+-promoted Ras inactivator) and RASAL (Ras-GTPase-activating-like protein) and, as we will discuss, they are emerging as important modulators of Ras and small GTPase signalling that are subject to regulation by a diverse array of events and second messenger signals.

Grants

  1. /Wellcome Trust

MeSH Term

GTP Phosphohydrolases
Humans
RNA Interference
RNA, Small Interfering
Signal Transduction
cdc42 GTP-Binding Protein
ras GTPase-Activating Proteins

Chemicals

RASA2 protein, human
RNA, Small Interfering
ras GTPase-Activating Proteins
GTP Phosphohydrolases
cdc42 GTP-Binding Protein

Word Cloud

Created with Highcharts 10.0.0RassignallingfamilyproteinsactiveGTP-boundproteinproteins:GDPGTPase-activatingregulatorsGAP1smallGTPasebinaryswitchescyclinginactiveGDP-boundconformationsregulatemultiplecellularpathwaysincludingcontrolcellgrowthdifferentiationsurvivalApproximately30%humantumoursexpressRas-containingoncogenicmutationslockconstitutivelyconformationactivationstatusregulatedtwogroupsGEFsguaninenucleotide-exchangefactorsbindenhanceexchangeGTPtherebyactivatingwhereasGAPsinactivatebindingformenhancinghydrolysisboundnucleotidebackreviewfocusgroupkeyinactivationRas-GAPsmembersGAP1mGAP1IP4BPCAPRICa2+-promotedinactivatorRASALRas-GTPase-activating-likewilldiscussemergingimportantmodulatorssubjectregulationdiversearrayeventssecondmessengersignalsspatialtemporal

Similar Articles

Cited By (28)