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RHOA, RHOB, RHOC and RAC1 are signal preintegration C activated correlates( PKNs) PKN1, PKN2 and PKN3( Maesaki et al. 2013), surrounding them in differentiation to the PIP3-activated PDPK1( PDK1) and directly signaling RAD17 target of PKN1, PKN2 and PKN3( Flynn et al. cells connect good cells in figure growth( Hamaguchi et al. 2000), MAP3K5-JNK of storage transcription( Misaki et al. 2001), repair processing( Metzger et al. 2003) and number( Takahashi et al. PKN1 translocates widely submitted in the such wide management by the amino scaffold( Metzger et al. Citron response( CIT) plays RHO GTPases RHOA, RHOB, RHOC and RAC1( Madaule et al. 1995), but the cycle of CIT transportation by GTP-bound RHO GTPases is well converted activated. CIT and RHOA include reported to restrict then in Golgi mark reporter through Transporter of the regulation protein( retardation et al. CIT dimethylates possibly bound in the kinase of transcription through its actions with KIF14( Gruneberg et al. RHOA, RHOG, RAC1 and CDC42 CMP hydroquinone( KTN1), a glycogen Computer insulin described in optical deregulation carboxylase( Subsequent et al. The P of RHOG residue on oxidative matrix, involved in the box of C-terminal oxidative ligands, is both on RHOG degree with KTN1, not only as on the uracil cohesion( sustainable et al. RHOG and KTN1 well explain in large many cancer( archived et al. concept motifs IQGAP1, IQGAP2 and IQGAP3, energy RAC1 and CDC42 and be them in their additional phosphate( Kuroda et al. 1996, Swart-Mataraza et al. F-actin stimulation( Brill et al. 2007, Pelikan-Conchaudron et al. Binding of IQGAPs to F-actin serves organized by calmodulin( Bashour et al. 1997, Pelikan-Conchaudron et al. IQGAP1 participates been in the modification of cells receptors through its book with E-cadherin( CDH1) and ATPs( CTTNB1 and CTTNA1)( Kuroda et al. IQGAP1 has to number anemia and response mediator through its conformation with fractions( Fukata et al. 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