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Gain of function of mutant p53 by coaggregation with multiple tumor suppressors

Nature chemical biology, 2011-05, Vol.7 (5), p.285-295

2011

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Human pluripotent stem cells recurrently acquire and expand dominant negative P53 mutations

Nature (London), 2017-05, Vol.545 (7653), p.229-233

2017

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EGCG binds intrinsically disordered N-terminal domain of p53 and disrupts p53-MDM2 interaction

Nature communications, 2021-02, Vol.12 (1), p.986-11, Article 986

2021

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Why are there hotspot mutations in the TP53 gene in human cancers?

Cell death and differentiation, 2018-01, Vol.25 (1), p.154-160

2018

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DAXX represents a new type of protein-folding enabler

Nature (London), 2021-09, Vol.597 (7874), p.132-137

2021

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Long-range regulation of p53 DNA binding by its intrinsically disordered N-terminal transactivation domain

Proceedings of the National Academy of Sciences - PNAS, 2018-11, Vol.115 (48), p.E11302-E11310

2018

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Protein mimetic amyloid inhibitor potently abrogates cancer-associated mutant p53 aggregation and restores tumor suppressor function

Nature communications, 2021-06, Vol.12 (1), p.3962-24, Article 3962

2021

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Tumor suppressive role for kinases phosphorylating p53 in DNA damage‐induced apoptosis

Cancer science, 2018-11, Vol.109 (11), p.3376-3382

2018

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p53 β-hydroxybutyrylation attenuates p53 activity

Cell death & disease, 2019-03, Vol.10 (3), p.243, Article 243

2019

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Mesoscopic protein-rich clusters host the nucleation of mutant p53 amyloid fibrils

Proceedings of the National Academy of Sciences - PNAS, 2021-03, Vol.118 (10), p.1-10

2021

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Liquid-like droplet formation by tumor suppressor p53 induced by multivalent electrostatic interactions between two disordered domains

Scientific reports, 2020-01, Vol.10 (1), p.580-580, Article 580

2020

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Allele-Specific p53 Mutant Reactivation

Cancer cell, 2012-05, Vol.21 (5), p.614-625

2012

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The Emerging Landscape of p53 Isoforms in Physiology, Cancer and Degenerative Diseases

International journal of molecular sciences, 2019-12, Vol.20 (24), p.6257

2019

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Mechanistic basis for impaired ferroptosis in cells expressing the African-centric S47 variant of p53

Proceedings of the National Academy of Sciences - PNAS, 2019-04, Vol.116 (17), p.8390-8396

2019

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iSEE: Interface structure, evolution, and energy‐based machine learning predictor of binding affinity changes upon mutations

Proteins, structure, function, and bioinformatics, 2019-02, Vol.87 (2), p.110-119

2019

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Interaction between p53 N terminus and core domain regulates specific and nonspecific DNA binding

Proceedings of the National Academy of Sciences - PNAS, 2019-04, Vol.116 (18), p.8859-8868

2019

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Bridging Microscopic and Macroscopic Mechanisms of p53-MDM2 Binding with Kinetic Network Models

Biophysical journal, 2017-08, Vol.113 (4), p.785-793

2017

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EZH2 cooperates with gain‐of‐function p53 mutants to promote cancer growth and metastasis

The EMBO journal, 2019-03, Vol.38 (5), p.n/a

2019

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p53 pathway dysfunction is highly prevalent in acute myeloid leukemia independent of TP53 mutational status

Leukemia, 2017-06, Vol.31 (6), p.1296-1305

2017

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Prediction of mutation-induced protein stability changes based on the geometric representations learned by a self-supervised method

BMC bioinformatics, 2024-08, Vol.25 (1), p.282-19, Article 282

2024

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Hydrophobic Interactions Are a Key to MDM2 Inhibition by Polyphenols as Revealed by Molecular Dynamics Simulations and MM/PBSA Free Energy Calculations

PloS one, 2016-02, Vol.11 (2), p.e0149014-e0149014

2016

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A phosphorylation-dependent switch in the disordered p53 transactivation domain regulates DNA binding

Proceedings of the National Academy of Sciences - PNAS, 2021-01, Vol.118 (1), p.1-10

2021

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CHIP promotes autophagy‐mediated degradation of aggregating mutant p53 in hypoxic conditions

The FEBS journal, 2018-09, Vol.285 (17), p.3197-3214

2018

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Structural dynamics of the E6AP/UBE3A-E6-p53 enzyme-substrate complex

Nature communications, 2018-10, Vol.9 (1), p.4441-12, Article 4441

2018

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The influence of a modified p53 C-terminal peptide by using a tumor-targeting sequence on cellular apoptosis and tumor treatment

Apoptosis (London), 2024-06, Vol.29 (5-6), p.865-881

2024

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Gain of function of mutant p53 by coaggregation with multiple tumor suppressors

Human pluripotent stem cells recurrently acquire and expand dominant negative P53 mutations

EGCG binds intrinsically disordered N-terminal domain of p53 and disrupts p53-MDM2 interaction

Why are there hotspot mutations in the TP53 gene in human cancers?

DAXX represents a new type of protein-folding enabler

Long-range regulation of p53 DNA binding by its intrinsically disordered N-terminal transactivation domain

Protein mimetic amyloid inhibitor potently abrogates cancer-associated mutant p53 aggregation and restores tumor suppressor function

Tumor suppressive role for kinases phosphorylating p53 in DNA damage‐induced apoptosis

p53 β-hydroxybutyrylation attenuates p53 activity

Mesoscopic protein-rich clusters host the nucleation of mutant p53 amyloid fibrils

Liquid-like droplet formation by tumor suppressor p53 induced by multivalent electrostatic interactions between two disordered domains

Allele-Specific p53 Mutant Reactivation

The Emerging Landscape of p53 Isoforms in Physiology, Cancer and Degenerative Diseases

Mechanistic basis for impaired ferroptosis in cells expressing the African-centric S47 variant of p53

iSEE: Interface structure, evolution, and energy‐based machine learning predictor of binding affinity changes upon mutations

Interaction between p53 N terminus and core domain regulates specific and nonspecific DNA binding

Bridging Microscopic and Macroscopic Mechanisms of p53-MDM2 Binding with Kinetic Network Models

EZH2 cooperates with gain‐of‐function p53 mutants to promote cancer growth and metastasis

p53 pathway dysfunction is highly prevalent in acute myeloid leukemia independent of TP53 mutational status

Prediction of mutation-induced protein stability changes based on the geometric representations learned by a self-supervised method

Hydrophobic Interactions Are a Key to MDM2 Inhibition by Polyphenols as Revealed by Molecular Dynamics Simulations and MM/PBSA Free Energy Calculations

A phosphorylation-dependent switch in the disordered p53 transactivation domain regulates DNA binding

CHIP promotes autophagy‐mediated degradation of aggregating mutant p53 in hypoxic conditions

Structural dynamics of the E6AP/UBE3A-E6-p53 enzyme-substrate complex

The influence of a modified p53 C-terminal peptide by using a tumor-targeting sequence on cellular apoptosis and tumor treatment

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