Evidence map›Paper›PMID 25755280›Full record

ArticleMolecular and cellular biology2015

PATZ1 Is a DNA Damage-Responsive Transcription Factor That Inhibits p53 Function.

Nazli Keskin, Emre Deniz, Jitka Eryilmaz, Manolya Un, Tugce Batur, Tulin Ersahin, Rengul Cetin Atalay, Shinya Sakaguchi, Wilfried Ellmeier, Batu Erman

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

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  17. Structural analysis of the PATZ1 BTB domain homodimer.Acta crystallographica. Section D, Structural biology · 2020
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  18. POZ/BTB and AT-Hook-Containing Zinc Finger Protein 1 (PATZ1) Suppresses Progression of Ovarian Cancer and Serves as an Independent Prognosis Factor.Medical science monitor : international medical journal of experimental and clinical research · 2018
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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 3 institutions in 2 countries.

Nazli KeskinBiological Sciences and Bioengineering Program, Faculty of Engineering and Natural Sciences, Sabanci University, Istanbul, Turkey Sabanci University Nanotechnology Research and Application Center-SUNUM, Istanbul, Turkey.
Emre DenizBiological Sciences and Bioengineering Program, Faculty of Engineering and Natural Sciences, Sabanci University, Istanbul, Turkey Sabanci University Nanotechnology Research and Application Center-SUNUM, Istanbul, Turkey.
Jitka EryilmazBiological Sciences and Bioengineering Program, Faculty of Engineering and Natural Sciences, Sabanci University, Istanbul, Turkey.
Manolya UnBiological Sciences and Bioengineering Program, Faculty of Engineering and Natural Sciences, Sabanci University, Istanbul, Turkey.
Tugce BaturBiological Sciences and Bioengineering Program, Faculty of Engineering and Natural Sciences, Sabanci University, Istanbul, Turkey.
Tulin ErsahinDepartment of Molecular Biology and Genetics, Bilkent University, Ankara, Turkey Informatics Institute, Middle East Technical University, Ankara, Turkey.
Rengul Cetin AtalayDepartment of Molecular Biology and Genetics, Bilkent University, Ankara, Turkey Informatics Institute, Middle East Technical University, Ankara, Turkey.
Shinya SakaguchiDivision of Immunobiology, Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Wilfried EllmeierDivision of Immunobiology, Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Batu ErmanBiological Sciences and Bioengineering Program, Faculty of Engineering and Natural Sciences, Sabanci University, Istanbul, Turkey Sabanci University Nanotechnology Research and Application Center-SUNUM, Istanbul, Turkey batu@sabanciuniv.edu.
Sabancı Üniversitesi · TRMedical University of Vienna · ATMiddle East Technical University · TR

Funding

Austrian Science Fund FWF P 23641
6 · The paper itself

Abstract

Insults to cellular health cause p53 protein accumulation, and loss of p53 function leads to tumorigenesis. Thus, p53 has to be tightly controlled. Here we report that the BTB/POZ domain transcription factor PATZ1 (MAZR), previously known for its transcriptional suppressor functions in T lymphocytes, is a crucial regulator of p53. The novel role of PATZ1 as an inhibitor of the p53 protein marks its gene as a proto-oncogene. PATZ1-deficient cells have reduced proliferative capacity, which we assessed by transcriptome sequencing (RNA-Seq) and real-time cell growth rate analysis. PATZ1 modifies the expression of p53 target genes associated with cell proliferation gene ontology terms. Moreover, PATZ1 regulates several genes involved in cellular adhesion and morphogenesis. Significantly, treatment with the DNA damage-inducing drug doxorubicin results in the loss of the PATZ1 transcription factor as p53 accumulates. We find that PATZ1 binds to p53 and inhibits p53-dependent transcription activation. We examine the mechanism of this functional inhibitory interaction and demonstrate that PATZ1 excludes p53 from DNA binding. This study documents PATZ1 as a novel player in the p53 pathway.

Indexed as

AnimalsCell AdhesionCell LineCell ProliferationDNA RepairDoxorubicinGene Expression ProfilingHCT116 CellsHEK293 CellsHeLa CellsHumansKruppel-Like Transcription FactorsMiceMolecular Sequence DataNeoplasm ProteinsNIH 3T3 CellsDoxorubicinKruppel-Like Transcription FactorsMAS1 protein, humanNeoplasm ProteinsPATZ1 protein, humanProto-Oncogene MasRepressor ProteinsTP53 protein, humanTumor Suppressor Protein p53Zfp278 protein, mouse

Identifiers

PMID25755280
PMCPMC4405645
OpenAlexW2147879403

What OpenQuestion holds

Textmetadata
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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.