Evidence map›Paper›PMID 23798621›Full record

ArticleOncotarget2013

Acetylation of the cell-fate factor dachshund determines p53 binding and signaling modules in breast cancer.

Ke Chen, Kongming Wu, Michael Gormley, Adam Ertel, Jing Wang, Wei Zhang, Jie Zhou, Gabriele Disante, Zhiping Li, Hallgeir Rui and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  8. The insights of Let-7 miRNAs in oncogenesis and stem cell potency.Journal of cellular and molecular medicine · 2016
    Review
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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

16 authors at 3 institutions in 1 country.

Ke ChenDepartment of Cancer Biology, Thomas Jefferson University, Philadelphia, PA, USA.
Kongming Wu
Michael Gormley
Adam Ertel
Jing Wang
Wei Zhang
Jie Zhou
Gabriele Disante
Zhiping Li
Hallgeir Rui
Andrew A Quong
Steven B McMahon
Haiteng Deng
Michael P Lisanti
Chenguang Wang
Richard G Pestell
Thomas Jefferson University · USSidney Kimmel Cancer Center · USRockefeller University · US

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI DANIEL P SILVER · 1995 to 2026
$94.8M
Initiation and Maintenance In Mammary TumorigenesisR01CA075503 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 1998 to 2011
$4.6M
CYCLIN D1 FUNCTION IN PROSTATE CANCERR01CA086072 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 2001 to 2013
$3.3M
REGULATION OF CYCLIN D1 EXPRESSIONR01CA070896 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 2000 to 2010
$3.2M
Functional analysis of transcriptional program regulated by the c-MYC oncoproteinR01CA090465 · NCI · WISTAR INSTITUTE · PI MCMAHON, STEVEN B. · 2002 to 2012
$2.9M
Impact of Cyclin D1 Isoforms in Breast CancerR01CA137494 · NCI · THOMAS JEFFERSON UNIVERSITY · PI KNUDSEN, ERIK, PESTELL, RICHARD G · 2010 to 2014
$1.5M
NCI NIH HHS P30 CA056036NCI NIH HHS P30CA56036NCI NIH HHS R01 CA070896NCI NIH HHS R01CA070896NCI NIH HHS R01 CA075503NCI NIH HHS R01CA075503NCI NIH HHS R01 CA086072NCI NIH HHS R01CA086072NCI NIH HHS R01 CA090465NCI NIH HHS R01CA090465NCI NIH HHS R01 CA137494NCI NIH HHS R01CA137494NCI NIH HHS R21CA152784
6 · The paper itself

Abstract

Breast cancer is a leading form of cancer in the world. The Drosophila Dac gene was cloned as an inhibitor of the hyperactive epidermal growth factor (EGFR), ellipse. Herein, endogenous DACH1 co-localized with p53 in a nuclear, extranucleolar compartment and bound to p53 in human breast cancer cell lines, p53 and DACH1 bound common genes in Chip-Seq. Full inhibition of breast cancer contact-independent growth by DACH1 required p53. The p53 breast cancer mutants R248Q and R273H, evaded DACH1 binding. DACH1 phosphorylation at serine residue (S439) inhibited p53 binding and phosphorylation at p53 amino-terminal sites (S15, S20) enhanced DACH1 binding. DACH1 binding to p53 was inhibited by NAD-dependent deacetylation via DACH1 K628. DACH1 repressed p21CIP1 and induced RAD51, an association found in basal breast cancer. DACH1 inhibits breast cancer cellular growth in an NAD and p53-dependent manner through direct protein-protein association.

Indexed as

AcetylationAmino Acid SequenceApoptosisBinding SitesBreast NeoplasmsCell Cycle CheckpointsCell DifferentiationCell Line, TumorChromatinDNA DamageEye ProteinsFemaleGene ExpressionHEK293 CellsHumansMutationChromatinDACH1 protein, humanEye ProteinsTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID23798621
PMCPMC3757249
OpenAlexW2148207479

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.