Carol Prives
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Carol Prives has a total of 332 co-authors. Here are the top co-authors by number of shared publications:
- Chen Katz
Department of Biological Sciences, Columbia University, New York, New York, USA
51 shared publications - Ana Maria Low-Calle
Department of Biological Sciences, Columbia University, New York, New York, USA
50 shared publications - Bita Alaghebandan
Department of Biological Sciences, Columbia University, New York, New York
50 shared publications - Joshua H. Choe
Division of Medical Sciences, Harvard Medical School, Boston, Massachusetts
50 shared publications - Ruiying Zhao
Department of Integrative Biology and Pharmacology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, USA
50 shared publications - Tatsuya Kawase
Astellas Pharma Inc
50 shared publications
Latest Publications
- Open Access
- 15 December 2025
- Published by Cold Spring Harbor Laboratory in Genes & Development
- Vol. 40 (1-2) , 4-25
Mutant p53: evolving perspectives
The discovery of the p53 tumor suppressor protein raised fundamental questions about cell cycle regulation that have spanned several decades. TP53 mutations are found in most human cancers, most frequently as missense alterations in the DNA-binding domain (DBD). As a master regulator of both cell-intrinsic and cell-extrinsic functions, mutant p53 contributes to pro-oncogenic activities through gain-of-function (GOF) properties in addition to loss-of-function (LOF) and dominant-negative effects (DNEs). New technologies and improved fidelity of model systems are uncovering the functional consequences caused by p53 mutations at the molecular, cellular, and tissue levels. In a new era of precision medicine, with the context of recent success in targeting genetic mutations, ongoing and future understanding of fundamental mutant p53 biology is of paramount importance.
- 15 December 2025
- Published by Cold Spring Harbor Laboratory in Genes & Development
- Vol. 40 (1-2) , 4-25
Open AccessMutant p53: evolving perspectives
The discovery of the p53 tumor suppressor protein raised fundamental questions about cell cycle regulation that have spanned several decades. TP53 mutations are found in most human cancers, most frequently as missense alterations in the DNA-binding domain (DBD). As a master regulator of both cell-intrinsic and cell-extrinsic functions, mutant p53 contributes to pro-oncogenic activities through gain-of-function (GOF) properties in addition to loss-of-function (LOF) and dominant-negative effects (DNEs). New technologies and improved fidelity of model systems are uncovering the functional consequences caused by p53 mutations at the molecular, cellular, and tissue levels. In a new era of precision medicine, with the context of recent success in targeting genetic mutations, ongoing and future understanding of fundamental mutant p53 biology is of paramount importance.
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Data 3 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Differentially expressed genes in osteoblasts derived from normal and LFS individuals
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data 3 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Differentially expressed genes in osteoblasts derived from normal and LFS individuals
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Data 1 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Differentially expressed genes in U2OS cells varying in p53 allelic status
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data 1 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Differentially expressed genes in U2OS cells varying in p53 allelic status
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Data 2 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Differentially expressed genes in U2OS cells varying in p53 allelic status combined from two independent RNA library preparations
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data 2 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Differentially expressed genes in U2OS cells varying in p53 allelic status combined from two independent RNA library preparations
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table 2 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Characteristics of LFS patients' fibroblasts and derivatives
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 2 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Characteristics of LFS patients' fibroblasts and derivatives
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Data 6 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
P53 ChIPseq peaks from osteoblasts derived from normal and LFS individuals
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data 6 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
P53 ChIPseq peaks from osteoblasts derived from normal and LFS individuals
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table 1 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Summary of GOF vs. LOF activities of p53(A347D) in U2OS cells
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 1 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Summary of GOF vs. LOF activities of p53(A347D) in U2OS cells
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Data 5 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
P53 ChIPseq peaks from U2OS cells varying in p53 allelic status
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data 5 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
P53 ChIPseq peaks from U2OS cells varying in p53 allelic status
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figures from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Supplementary Figures 1-9 demonstrating the GOF and LOF activities of p53(A347D)
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figures from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Supplementary Figures 1-9 demonstrating the GOF and LOF activities of p53(A347D)
- Open Access
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Data 4 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
P53 ChIPseq peaks from U2OS cells varying in p53 allelic status
- 11 December 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data 4 from Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
P53 ChIPseq peaks from U2OS cells varying in p53 allelic status