Activating mutations for transformation by p53 produce a gene product that forms an hsc70-p53 complex with an altered half-life.

摘要: The 11-4 p53 cDNA clone failed to transform primary rat fibroblasts when cotransfected with the ras oncogene. Two linker insertion mutations at amino acid 158 or 215 (of 390 acids) activated this for transformation ras. These mutant cDNAs produced a protein that lacked an epitope, recognized by monoclonal antibody PAb246 (localized acids 88 110 in protein) and preferentially bound heat shock protein, hsc70. In cells transformed genomic plus ras, two populations of proteins were detected, PAb246/sup +/ -/, which did not bind antibody, respectively. -/ associated hsc70, has half-life 4- 20-fold longer than free (PAb246/sup +/). data suggest possible functional role hsc70 process. derived from methylcholanthrene-transformed cooperation oncogene produce proteins. Recombinant clones between Meth A tested ability cells. single substitution residue 132 was sufficientmore » activate transformation. studies have identified region which, mutated, can cDNA. results also call into question what correct wild-type sequence is whether gene culture.« less