Evidence map›Paper›PMID 18211700›Full record

ArticleVirology journal2008

Evidence that the Nijmegen breakage syndrome protein, an early sensor of double-strand DNA breaks (DSB), is involved in HIV-1 post-integration repair by recruiting the ataxia telangiectasia-mutated kinase in a process similar to, but distinct from, cellular DSB repair.

Johanna A Smith, Feng-Xiang Wang, Hui Zhang, Kou-Juey Wu, Kevin Jon Williams, René Daniel

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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  11. Identification of SNF2h, a chromatin-remodeling factor, as a novel binding protein of Vpr of human immunodeficiency virus type 1.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011
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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

6 authors at 3 institutions in 2 countries.

Johanna A SmithDivision of Infectious Diseases - Center for Human Virology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA. Johanna.Smith@jefferson.edu
Feng-Xiang Wang
Hui Zhang
Kou-Juey Wu
Kevin Jon Williams
René Daniel
Abramson Center for Jewish Life · USSidney Kimmel Cancer Center · USThomas Jefferson University · US

Funding

Cellular co-factors in stable retroviral transductionR01CA125272 · NCI · THOMAS JEFFERSON UNIVERSITY · PI DANIEL, RENE · 2007 to 2011
$1.2M
Cellular Response to Retroviral DNA IntegrationK01CA098090 · NCI · THOMAS JEFFERSON UNIVERSITY · PI DANIEL, RENE · 2003 to 2007
$730k
Transmigration of HIV-1-infected cells in NeuroAIDSR21MH070279 · NIMH · THOMAS JEFFERSON UNIVERSITY · PI WILLIAMS, KEVIN JON · 2005 to 2006
$463k
NCI NIH HHS CA125272NCI NIH HHS CA98090NCI NIH HHS K01 CA098090NCI NIH HHS R01 CA125272NIMH NIH HHS MH70279NIMH NIH HHS R21 MH070279
6 · The paper itself

Abstract

Retroviral transduction involves integrase-dependent linkage of viral and host DNA that leaves an intermediate that requires post-integration repair (PIR). We and others proposed that PIR hijacks the host cell double-strand DNA break (DSB) repair pathways. Nevertheless, the geometry of retroviral DNA integration differs considerably from that of DSB repair and so the precise role of host-cell mechanisms in PIR remains unclear. In the current study, we found that the Nijmegen breakage syndrome 1 protein (NBS1), an early sensor of DSBs, associates with HIV-1 DNA, recruits the ataxia telangiectasia-mutated (ATM) kinase, promotes stable retroviral transduction, mediates efficient integration of viral DNA and blocks integrase-dependent apoptosis that can arise from unrepaired viral-host DNA linkages. Moreover, we demonstrate that the ATM kinase, recruited by NBS1, is itself required for efficient retroviral transduction. Surprisingly, recruitment of the ATR kinase, which in the context of DSB requires both NBS1 and ATM, proceeds independently of these two proteins. A model is proposed emphasizing similarities and differences between PIR and DSB repair. Differences between the pathways may eventually allow strategies to block PIR while still allowing DSB repair.

Indexed as

Ataxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell Line, TransformedCell NucleusDNA-Activated Protein KinaseDNA-Binding ProteinsDNA DamageDNA RepairHIV-1HumansNijmegen Breakage SyndromeNuclear ProteinsProtein Serine-Threonine KinasesRetroviridaeTumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA-Activated Protein KinaseDNA-Binding ProteinsNuclear ProteinsProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID18211700
PMCPMC2262065
OpenAlexW2022879942

What OpenQuestion holds

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Registered trials

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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.