Rasactivatesmanysignalingcascades.Hereweillustratesomeofthewell-characterizedcascadesinagenericcompilationofeffectormolecules.TheeffectorsmediateRasstimulationtoadiversesetofcellularsignals.Manyofthesesignalsareinterpreteddifferentlydependingonthecelltypeormicroenvironmentreceivingthestimulus.Notalloftheseeffectorsareactivatedinanygivencelltype.Theprimarymethodofactivationistopromotethetranslocationofthemoleculetotheplasmamembranewhereadditionalinteractionsleadtotheactivationofthemolecule.RalGDSisaGuanineExchangeFactor(GEF)forRalbutalsohasotherindependentfunctions.RalGDSactivatesRalA/B-relatedsmallGTPases.RalBP1isaGTPaseactivatingproteinthatleadstotheinhibitionoftheRacandCDC42GTPases.RalcanalsointeractwithphospholipaseD1(PLD1)thatcanalsobeactivatedbyRhoA.RasstimulationofthelipidkinaseactivityofPI3Koccursthroughaninteractionwiththep110catalyticsubunit.PI3KphosphorylatestheD3positionofphosphatidylinositides.InthisexamplePip2isconvertedtoPIP3.PIP3stimulatestheAKT/PKBkinaseandseveraloftheRac-GEF’ssuchasSos1ANDVav.AKTactivationinhibitsapoptosisbyinhibitingtheactionsofBad,Caspase9andAFX.AKTfurtherhindersapoptosisbyphosphorylatingtheIkBrepressorofNFkB.StimulusofRaccausesamongotherthings(seeRacPathway)theactivationofNFkB.Rasalsostimulatesthemitogen-activatedkinasesERK1/2viatheRaf1cascade.TheErkkinasestranslocatetothenucleuswheretheyphosphorylatevarioustranscriptionfactorssuchasELK1 Contributor: REFERENCES:
