Evidence map›Paper›PMID 24786831›Full record

ArticleCell death and differentiation2014

Proline, glutamic acid and leucine-rich protein-1 is essential for optimal p53-mediated DNA damage response.

B C Nair, S R Krishnan, G R Sareddy, M Mann, B Xu, M Natarajan, P Hasty, D Brann, R R Tekmal, R K Vadlamudi

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 33 citations in OpenAlex.

  1. PELP1 expression is associated with disease progression in inflammation-driven oral cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

10 authors at 2 institutions in 1 country.

B C NairUniversity of Texas Health Science Center, and Cancer Therapy and Research Center, San Antonio, TX, USA.
S R KrishnanUniversity of Texas Health Science Center, and Cancer Therapy and Research Center, San Antonio, TX, USA.
G R SareddyUniversity of Texas Health Science Center, and Cancer Therapy and Research Center, San Antonio, TX, USA.
M MannUniversity of Texas Health Science Center, and Cancer Therapy and Research Center, San Antonio, TX, USA.
B XuMolecular Radiation Biology Laboratory, Research Institute, South Birmingham, AL, USA.
M NatarajanUniversity of Texas Health Science Center, and Cancer Therapy and Research Center, San Antonio, TX, USA.
P HastyUniversity of Texas Health Science Center, and Cancer Therapy and Research Center, San Antonio, TX, USA.
D BrannInstitute of Molecular Medicine and Genetics, Georgia Reagents University, Augusta, GA, USA.
R R TekmalUniversity of Texas Health Science Center, and Cancer Therapy and Research Center, San Antonio, TX, USA.
R K VadlamudiUniversity of Texas Health Science Center, and Cancer Therapy and Research Center, San Antonio, TX, USA.
The University of Texas Health Science Center at San Antonio · USAugusta University Health · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lei Zheng · 1991 to 2026
$59.1M
Neuroprotective and Neurogenic Actions of E2 and SERMsR01NS050730 · NINDS · MEDICAL COLLEGE OF GEORGIA (MCG) · PI BRANN, DARRELL W, VADLAMUDI, RATNA K · 2005 to 2014
$3.2M
PELP1, a Novel Regulator of Estrogen ReceptorR01CA095681 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI VADLAMUDI, RATNA K · 2003 to 2013
$2.5M
Mechanisms of Mitotic Activation of the ATM kinaseR01CA133093 · NCI · SOUTHERN RESEARCH INSTITUTE · PI MITRA, SANKAR · 2009 to 2013
$1.4M
A Novel Pathway Involving ATM, PP1 and I-2R01ES016354 · NIEHS · SOUTHERN RESEARCH INSTITUTE · PI MITRA, SANKAR · 2009 to 2012
$1.1M
NCI NIH HHS CA095681NCI NIH HHS P30 CA054174NCI NIH HHS P30CA054174-17NCI NIH HHS R01 CA095681NCI NIH HHS R01 CA133093NCI NIH HHS R01CA133093NIEHS NIH HHS R01 ES016354NIEHS NIH HHS R01ES016354NINDS NIH HHS NS050730NINDS NIH HHS R01 NS050730
6 · The paper itself

Abstract

Proline-, glutamic acid- and leucine-rich protein-1 (PELP1) is a scaffolding oncogenic protein that functions as a coregulator for a number of nuclear receptors. p53 is an important transcription factor and tumor suppressor that has a critical role in DNA damage response (DDR) including cell cycle arrest, repair or apoptosis. In this study, we found an unexpected role for PELP1 in modulating p53-mediated DDR. PELP1 is phosphorylated at Serine1033 by various DDR kinases like ataxia-telangiectasia mutated, ataxia telangiectasia and Rad3-related or DNAPKc and this phosphorylation of PELP1 is important for p53 coactivation functions. PELP1-depleted p53 (wild-type) breast cancer cells were less sensitive to various genotoxic agents including etoposide, camptothecin or γ-radiation. PELP1 interacts with p53, functions as p53-coactivator and is required for optimal activation of p53 target genes under genomic stress. Overall, these studies established a new role of PELP1 in DDRs and these findings will have future implications in our understanding of PELP1's role in cancer progression.

Indexed as

DNA DamageCell Line, TumorCo-Repressor ProteinsHumansMCF-7 CellsPhosphorylationTranscription FactorsTumor Suppressor Protein p53Co-Repressor ProteinsPELP1 protein, humanTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID24786831
PMCPMC4131173
OpenAlexW2079873134

What OpenQuestion holds

Textmetadata
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.