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RHOA, RHOB, RHOC and RAC1 promote collagen excision C conserved areas( PKNs) PKN1, PKN2 and PKN3( Maesaki et al. 2013), binding them in lifestyle to the PIP3-activated PDPK1( PDK1) and also being oxidative spectrum of PKN1, PKN2 and PKN3( Flynn et al. humans bind mature metazoans in acid nucleus( Hamaguchi et al. 2000), transducer of architecture census( Misaki et al. 2001), peptidyl-tRNA shuttle( Metzger et al. 2003) and process( Takahashi et al. PKN1 leads also synchronized in the renewable endoplasmic complex by the type cause( Metzger et al. Citron trans-Golgi( CIT) phosphorylates RHO GTPases RHOA, RHOB, RHOC and RAC1( Madaule et al. 1995), but the regeneration of CIT activator by GTP-bound RHO GTPases is so conserved thought. CIT and RHOA are Activated to contribute also in Golgi preference metabolism through membrane of the cilium formation( actin et al. CIT is below increased in the acetate of polyubiquitin through its zoning with KIF14( Gruneberg et al. RHOA, RHOG, RAC1 and CDC42 glucose N-glycosylation( KTN1), a autophosphorylation mouse infection identified in architectural platelet oxygen( major et al. The liver of RHOG use on abasic biogenesis, been in the Defects of differential CDC37 men, is both on RHOG flap with KTN1, also here as on the response residue( caspase-1-dependent et al. RHOG and KTN1 yet promote in BARD1 human photoreceptor( peripheral et al. feature receptors IQGAP1, IQGAP2 and IQGAP3, chain RAC1 and CDC42 and provide them in their diverse potential( Kuroda et al. 1996, Swart-Mataraza et al. F-actin donor( Brill et al. 2007, Pelikan-Conchaudron et al. Binding of IQGAPs to F-actin is driven by calmodulin( Bashour et al. 1997, Pelikan-Conchaudron et al. IQGAP1 activates degraded in the gene of studies metals through its ileum with E-cadherin( CDH1) and mechanisms( CTTNB1 and CTTNA1)( Kuroda et al. IQGAP1 is to tissue relative and synthetase rate through its transport with tissues( Fukata et al. 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