title: Wiring the oncogenic circuitry: Pin1 unleashes mutant p53.
abstract: Unlike several tumor suppressor genes, whose inactivation is due to deletions or truncating mutations, TP53 is most frequently hit by missense mutations in its DNA binding domain.
authors.affiliation: Laboratorio Nazionale CIB (LNCIB), Area Science Park, Trieste, Italy.
authors.forename: Marco
authors.initials: M
authors.lastname: Napoli
authors.forename: Javier E
authors.initials: JE
authors.lastname: Girardini
authors.forename: Silvano
authors.initials: S
authors.lastname: Piazza
authors.forename: Giannino
authors.initials: G
authors.lastname: Del Sal
mesh_terms: D000818:Animals; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism; D002471:Cell Transformation, Neoplastic / Q000235:genetics* / Q000378:metabolism; D005260:Female; D006801:Humans; D051379:Mice; D000072340:NIMA-Interacting Peptidylprolyl Isomerase; D019696:Peptidylprolyl Isomerase / Q000235:genetics* / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000378:metabolism
chemical_list: D000072340:NIMA-Interacting Peptidylprolyl Isomerase; D016159:Tumor Suppressor Protein p53; C000606846:PIN1 protein, human; D019696:Peptidylprolyl Isomerase; C000606850:Pin1 protein, mouse