Tyrosine kinase -activation of pdf receptor -end of receptor -cross phosphorylate -things in the cell have affinity for

the phosphorous -> signals to regulate growth

Cancer -autocrine: produce and receive own growth factor -overexpressed receptors: can bind without growth factors -truncated receptors -> constitutive signaling

Somatic mutation -> cancer -accidental mutations in the body (not in gonads)

RSV -ssRNA -> reverse transciptase -> integrate with host genome -viral transforming gene/cancer causing gene = src i.e. oncogene -src gene originate in eukaryotic genome and picked up by RSV -src in chicken = proto-oncogene -> potential to become oncogene -when viruses not present: mutations can change protooncogene into oncogene

RAS -binding of GF -> causes RAS to get GTP and become active state -active state -> signals growth -automatic shut down by hydrolyzing GTFP to GDP -> stop growth signaling -Mutation loses GTPase and RAS always active