Wiring the oncogenic circuitry: Pin1 unleashes mutant p53

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.

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Published in:Oncotarget 2011-09, Vol.2 (9), p.654-656
Main Authors: Napoli, Marco, Girardini, Javier E, Piazza, Silvano, Del Sal, Giannino
Format: Article
Language:English
Subjects:
Animals
Breast Neoplasms - genetics
Breast Neoplasms - metabolism
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Female
Humans
Mice
NIMA-Interacting Peptidylprolyl Isomerase
Peptidylprolyl Isomerase - genetics
Peptidylprolyl Isomerase - metabolism
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
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cited_by cdi_FETCH-LOGICAL-c392t-710019ce7fbde3227668806a1f5f72f6ecd5d6566c76b7ffd01056f38a9bf3543
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creator Napoli, Marco
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description 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.
doi_str_mv 10.18632/oncotarget.329
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subjects Animals
Breast Neoplasms - genetics
Breast Neoplasms - metabolism
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Female
Humans
Mice
NIMA-Interacting Peptidylprolyl Isomerase
Peptidylprolyl Isomerase - genetics
Peptidylprolyl Isomerase - metabolism
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
title Wiring the oncogenic circuitry: Pin1 unleashes mutant p53
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