Evidence map›Paper›PMID 17403783›Full record

ArticleGenes & development2007

HLA-B-associated transcript 3 (Bat3)/Scythe is essential for p300-mediated acetylation of p53.

Toru Sasaki, Eugene C Gan, Andrew Wakeham, Sally Kornbluth, Tak W Mak, Hitoshi Okada

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 5 pooled it
–field-weighted citation impact
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

83 citing papers in PubMed, 5 syntheses or guidelines pooled it, 127 citations in OpenAlex.

  1. Effect of HLA-B-associated transcript 3 polymorphisms on lung cancer risk: a meta-analysis.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Pooled it
  2. BAT3 rs1052486 and rs3117582 polymorphisms are associated with lung cancer risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
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  11. TEP RNA: a new frontier for early diagnosis of NSCLC.Journal of cancer research and clinical oncology · 2024
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23 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Toru SasakiThe Campbell Family Institute for Breast Cancer Research (CFIBCR), Ontario Cancer Institute (OCI), University Health Network, Toronto, Ontario M5G 2C1, Canada.
Eugene C Gan
Andrew Wakeham
Sally Kornbluth
Tak W Mak
Hitoshi Okada
University Health Network · CADuke University Hospital · USOntario Institute for Cancer Research · CA

Funding

APOPTOTIC SIGNALING PATHWAYSR01GM061919 · NIGMS · DUKE UNIVERSITY · PI KORNBLUTH, SALLY A · 2000 to 2008
$2.4M
NIGMS NIH HHS R01 GM061919NIGMS NIH HHS R01 GM61919
6 · The paper itself

Abstract

In response to DNA damage, p53 undergoes post-translational modifications (including acetylation) that are critical for its transcriptional activity. However, the mechanism by which p53 acetylation is regulated is still unclear. Here, we describe an essential role for HLA-B-associated transcript 3 (Bat3)/Scythe in controlling the acetylation of p53 required for DNA damage responses. Depletion of Bat3 from human and mouse cells markedly impairs p53-mediated transactivation of its target genes Puma and p21. Although DNA damage-induced phosphorylation, stabilization, and nuclear accumulation of p53 are not significantly affected by Bat3 depletion, p53 acetylation is almost completely abolished. Bat3 forms a complex with p300, and an increased amount of Bat3 enhances the recruitment of p53 to p300 and facilitates subsequent p53 acetylation. In contrast, Bat3-depleted cells show reduced p53-p300 complex formation and decreased p53 acetylation. Furthermore, consistent with our in vitro findings, thymocytes from Bat3-deficient mice exhibit reduced induction of puma and p21, and are resistant to DNA damage-induced apoptosis in vivo. Our data indicate that Bat3 is a novel and essential regulator of p53-mediated responses to genotoxic stress, and that Bat3 controls DNA damage-induced acetylation of p53.

Indexed as

AcetylationAmino Acid SequenceAnimalsApoptosisCell Cycle ProteinsCells, CulturedDNA DamageHCT116 CellsHistone AcetyltransferasesHumansMiceMolecular ChaperonesMolecular Sequence Datap300-CBP-Associated Factorp300-CBP Transcription FactorsProteinsBAG6 protein, humanCell Cycle ProteinsHistone AcetyltransferasesMolecular Chaperonesp300-CBP-Associated Factorp300-CBP Transcription FactorsProteinsTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID17403783
PMCPMC1838535
OpenAlexW2130076355

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.