Here , we show that a single Arginine ( R ) to Glycine ( G ) mutation at position 76 in the refp17 backbone ( p17R76G ) , as in the S75X variant , is per se sufficient to confer a B-cell clonogenic potential to the viral protein and modulate , through activation of the PTEN/PI3K/Akt signaling pathway , different molecules involved in apoptosis inhibition ( CASP-9 , CASP-7 , DFF-45 , NPM , YWHAZ , Src , PAX2 , MAPK8 ) , cell cycle promotion and cancer progression ( CDK1 , CDK2 , CDK8 , CHEK1 , CHEK2 , GSK-3 beta , NPM , PAK1 , PP2C-alpha ) .
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