Evidence map›Paper›PMID 19889979›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Functional genomic screens identify CINP as a genome maintenance protein.

Courtney A Lovejoy, Xin Xu, Carol E Bansbach, Gloria G Glick, Runxiang Zhao, Fei Ye, Bianca M Sirbu, Laura C Titus, Yu Shyr, David Cortez

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.6field-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

45 citing papers in PubMed, 68 citations in OpenAlex.

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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 1 institution in 1 country.

Courtney A LovejoyDepartment of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Xin Xu
Carol E Bansbach
Gloria G Glick
Runxiang Zhao
Fei Ye
Bianca M Sirbu
Laura C Titus
Yu Shyr
David Cortez
Vanderbilt University · US

Funding

TISSUE CoreP50CA098131 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PARK, BEN HO, PIETENPOL, JENNIFER A · 2003 to 2024
$48.7M
Structural Biology Facility CoreP30ES000267 · NIEHS · VANDERBILT UNIVERSITY · PI GUENGERICH, F PETER · 1985 to 2014
$20.3M
Function of the ATR-ATRIP ComplexR01CA102729 · NCI · VANDERBILT UNIVERSITY · PI CORTEZ, DAVID K · 2003 to 2018
$4.2M
Functional Analysis of Replication Stress Response ProteinsR01CA136933 · NCI · VANDERBILT UNIVERSITY · PI CORTEZ, DAVID K · 2009 to 2013
$1.6M
Regulation of Genome Stability by ATMR21CA132010 · NCI · VANDERBILT UNIVERSITY · PI CORTEZ, DAVID K · 2008 to 2009
$380k
NCI NIH HHS P50 CA098131NCI NIH HHS R01 CA102729NCI NIH HHS R01 CA136933NCI NIH HHS R21 CA132010NCI NIH HHS R21CA132010NIEHS NIH HHS P30 ES000267
6 · The paper itself

Abstract

The DNA damage response (DDR) has a critical role in maintaining genome integrity and serves as a barrier to tumorigenesis by promoting cell-cycle arrest, DNA repair, and apoptosis. The DDR is activated not only by genotoxic agents that induce DNA damage, but also during aberrant cell-division cycles caused by activated oncogenes and inactivated tumor suppressors. Here we use RNAi and cDNA overexpression screens in human cells to identify genes that, when deregulated, lead to activation of the DDR. The RNAi screen identified 73 genes that, when silenced in at least two cell types, cause DDR activation. Silencing several of these genes also caused an increased frequency of micronuclei, a marker of genetically unstable cells. The cDNA screen identified 97 genes that when overexpressed induce DDR activation in the absence of any exogenous genotoxic agent, with an overrepresentation of genes linked to cancer. Secondary RNAi screens identified CDK2-interacting protein (CINP) as a cell-cycle checkpoint protein. CINP interacts with ATR-interacting protein and regulates ATR-dependent signaling, resistance to replication stress, and G2 checkpoint integrity.

Indexed as

Genome, HumanAdaptor Proteins, Signal TransducingAtaxia Telangiectasia Mutated ProteinsCarrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA DamageGenomicsHeLa CellsHumansProtein Serine-Threonine KinasesTwo-Hybrid System TechniquesAdaptor Proteins, Signal TransducingAtaxia Telangiectasia Mutated ProteinsATRIP protein, humanATR protein, humanCarrier ProteinsCell Cycle ProteinsCINP protein, humanDNA-Binding ProteinsProtein Serine-Threonine Kinases

Identifiers

PMID19889979
PMCPMC2780779
OpenAlexW1972890601

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.