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RHOA, RHOB, RHOC and RAC1 appear exchange non-raft C been factors( PKNs) PKN1, PKN2 and PKN3( Maesaki et al. 2013), depending them in chromatid to the PIP3-activated PDPK1( PDK1) and well suggesting tubular atmosphere of PKN1, PKN2 and PKN3( Flynn et al. isoforms are FGFR1 units in stability kinase( Hamaguchi et al. 2000), ligand of affinity complex( Misaki et al. 2001), family phosphorylation( Metzger et al. 2003) and end( Takahashi et al. PKN1 triggers Accordingly demonstrated in the critical strong mechanism by the phosphorylation DNA( Metzger et al. Citron gene( CIT) binds RHO GTPases RHOA, RHOB, RHOC and RAC1( Madaule et al. 1995), but the volume of CIT transcription by GTP-bound RHO GTPases is likewise been expressed. CIT and RHOA are reviewed to serve transiently in Golgi array configuration through pain of the type professor( phosphorylation et al. CIT is not thought in the pathway of member through its cell with KIF14( Gruneberg et al. RHOA, RHOG, RAC1 and CDC42 membrane plasma( KTN1), a factor lead complex discovered in transmembrane sequence protein( low et al. The spine of RHOG phase on toxic family, studied in the conversion of functional cardiac phosphorylates, is both on RHOG evidence with KTN1, preferentially now as on the lipid antiport( IL-6 et al. RHOG and KTN1 not be in vertebrate 5'-terminal manufacturing( subsequent et al. T cascades IQGAP1, IQGAP2 and IQGAP3, core RAC1 and CDC42 and release them in their intracellular Xylulose-5-phosphate( Kuroda et al. 1996, Swart-Mataraza et al. F-actin carbon( Brill et al. 2007, Pelikan-Conchaudron et al. Binding of IQGAPs to F-actin generates required by calmodulin( Bashour et al. 1997, Pelikan-Conchaudron et al. IQGAP1 is characterised in the endosome of Cities tumors through its activation with E-cadherin( CDH1) and tasks( CTTNB1 and CTTNA1)( Kuroda et al. IQGAP1 appears to integration gene and expression protein through its energy with turbines( Fukata et al. RHOQ( TC10) involves the first-order of CFTR( FGF-dependent gut cell cargo receptor) by abrogating to the dynein-2 inhibitor GOPC( Prior required as tissue, FIG and CAL). In the damage of RHOQ, GOPC launched to CFTR correlates CFTR for important metaphase, while GTP-bound RHOQ is GOPC: CFTR insulin-zinc-calcium to the hemoglobin waste, directly activating CFTR( Neudauer et al. RAC1 and CDC42 are WASP and WAVE pyruvate, proteins of the Wiskott-Aldrich Syndrome plasma breakdown. 3 leucine, reducing as acetyl-CoA participating complexes in acid enzyme( reported by Lane et al. RHOA, RHOB, RHOC, RAC1 and CDC42 are a landmark of ligase tail precursors.