Evidence map›Paper›PMID 22940690›Full record

ArticleThe EMBO journal2012

The hSSB1 orthologue Obfc2b is essential for skeletogenesis but dispensable for the DNA damage response in vivo.

Niklas Feldhahn, Elisabetta Ferretti, Davide F Robbiani, Elsa Callen, Stephanie Deroubaix, Licia Selleri, Andre Nussenzweig, Michel C Nussenzweig

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 35 citations in OpenAlex.

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  11. Molecular basis of cleft palates in mice.World journal of biological chemistry · 2015
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Niklas FeldhahnLaboratory of Molecular Immunology, Rockefeller University, New York, NY 10065, USA. nfeldhahn@rockefeller.edu
Elisabetta Ferretti
Davide F Robbiani
Elsa Callen
Stephanie Deroubaix
Licia Selleri
Andre Nussenzweig
Michel C Nussenzweig
Rockefeller University · USCornell University · USHoward Hughes Medical Institute · USNational Cancer Institute · USNational Human Genome Research Institute · US

Funding

DNA RepairZIABC010283 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 2009 to 2025
$27.0M
Relationship between DNA damage detection and signalingZIABC010959 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 2009 to 2025
$27.0M
SIGNALLING PATHWAYS IN AUTOIMMUNITYR01AI037526 · NIAID · ROCKEFELLER UNIVERSITY · PI NUSSENZWEIG, MICHEL C · 1994 to 2012
$5.0M
Mechanisms of Pbx-directed Genetic &Transcriptional Control of Limb DevelopmentR01HD043997 · NICHD · WEILL MEDICAL COLL OF CORNELL UNIV · PI SELLERI, LICIA · 2004 to 2016
$3.7M
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI037526NIAID NIH HHS R01 AI037526-18NICHD NIH HHS R01 HD043997
6 · The paper itself

Abstract

Human single-stranded DNA-binding protein 1 (hSSB1), encoded by OBFC2B, was recently characterized as an essential factor for the initiation of DNA damage checkpoints and the maintenance of genomic stability. Here, we report that loss of Obfc2b in mice results in perinatal lethality characterized by growth delay and skeletal abnormalities. These abnormalities are associated with accumulation of γH2ax, apoptosis and defective pre-cartilage condensation, which is essential for normal bone formation. However, deficiency of Obfc2b does not affect the initiation of DNA damage checkpoints, Atm activation, or the maintenance of genomic stability in B lymphocytes and primary fibroblasts. Loss of Obfc2b results in increased expression of its homologue Obfc2a (hSSB2). In contrast to Obfc2b deficiency, depletion of Obfc2a in fibroblasts results in impaired proliferation, accumulation of γH2ax and increased genomic instability. Thus, the hSSB1 orthologue Obfc2b has a unique function during embryogenesis limited to cell types that contribute to bone formation. While being dispensable in most other cell lineages, its absence leads to a compensatory increase in Obfc2a protein, a homologue required for the maintenance of genomic integrity.

Indexed as

DNA DamageAnimalsApoptosisB-LymphocytesBone and BonesCell DivisionChondrocytesDNA-Binding ProteinsDNA RepairDNA ReplicationFibroblastsGene Expression Regulation, DevelopmentalGenes, LethalGenes, p53HistonesHumansDNA-Binding Proteinsgamma-H2AX protein, mouseHistonesMitochondrial ProteinsSSBP1 protein, mouseSsbp2 protein, mouse

Identifiers

PMID22940690
PMCPMC3474923
OpenAlexW1908423914

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.