Evidence map›Paper›PMID 24258024›Full record

ArticleMolecular biology of the cell2014

XPC promotes MDM2-mediated degradation of the p53 tumor suppressor.

Jing Yan Krzeszinski, Vitnary Choe, Jia Shao, Xin Bao, Haili Cheng, Shiwen Luo, Keke Huo, Hai Rao

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. A molecular mechanism for the "digital" response of p53 to stress.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Review
  4. Comparative study of cytotoxic effects induced by environmental genotoxins using XPC- and CSB-deficient human lymphoblastoid TK6 cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2019
    Article
  5. Article
  6. Article
  7. Negative auto-regulators trap p53 in their web.Journal of molecular cell biology · 2017
    Review
  8. Article
  9. Architecture of the human XPC DNA repair and stem cell coactivator complex.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  10. Review
  11. Genetic Evidence for XPC-KRAS Interactions During Lung Cancer Development.Journal of genetics and genomics = Yi chuan xue bao · 2015
    Article
  12. Article
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Jing Yan KrzeszinskiState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai 200433, People's Republic of China Department of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229 First Affiliated Hospital, Nanchang University, Jiangxi 330006, People's Republic of China.
Vitnary Choe
Jia Shao
Xin Bao
Haili Cheng
Shiwen Luo
Keke Huo
Hai Rao
The University of Texas Health Science Center at San Antonio · USNanchang University · CNFudan University · CN

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lei Zheng · 1991 to 2026
$59.1M
Targeting ubiquitylated proteins to the proteasomeR01GM078085 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI RAO, HAI · 2007 to 2011
$1.3M
NCI NIH HHS P30 CA054174NIGMS NIH HHS GM 078085NIGMS NIH HHS R01 GM078085
6 · The paper itself

Abstract

Although ubiquitin receptor Rad23 has been implicated in bringing ubiquitylated p53 to the proteasome, how Rad23 recognizes p53 remains unclear. We demonstrate that XPC, a Rad23-binding protein, regulates p53 turnover. p53 protein in XPC-deficient cells remains ubiquitylated, but its association with the proteasome is drastically reduced, indicating that XPC regulates a postubiquitylation event. Furthermore, we found that XPC participates in the MDM2-mediated p53 degradation pathway via direct interaction with MDM2. XPC W690S pathogenic mutant is specifically defective for MDM2 binding and p53 degradation. p53 is known to become stabilized following UV irradiation but can be rendered unstable by XPC overexpression, underscoring a critical role of XPC in p53 regulation. Elucidation of the proteolytic role of XPC in cancer cells will help to unravel the detailed mechanisms underlying the coordination of DNA repair and proteolysis.

Indexed as

ProteolysisDNA-Binding ProteinsDNA Repair EnzymesHumansMutationProteasome Endopeptidase ComplexProtein BindingProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53UbiquitinDNA-Binding ProteinsDNA Repair EnzymesMDM2 protein, humanProteasome Endopeptidase ComplexProto-Oncogene Proteins c-mdm2RAD23A protein, humanTP53 protein, humanTumor Suppressor Protein p53UbiquitinXPC protein, human

Identifiers

PMID24258024
PMCPMC3890342
OpenAlexW2137561800

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.