Evidence map›Paper›PMID 23678004›Full record

ArticleBlood2013

Parp-2 is required to maintain hematopoiesis following sublethal γ-irradiation in mice.

Jordi Farrés, Juan Martín-Caballero, Carlos Martínez, Juan J Lozano, Laura Llacuna, Coral Ampurdanés, Cristina Ruiz-Herguido, Françoise Dantzer, Valérie Schreiber, Andreas Villunger and 2 more

Abstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 3 pooled it
2.5field-weighted citation impact, top 10% 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

69 citing papers in PubMed, 3 syntheses or guidelines pooled it, 139 citations in OpenAlex.

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  13. Neutropenic events associated with new anticancer treatments, from pathophysiology to practice: a scoping review-NEW Group (Neutropenic Events Working Group).Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2025
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9 more citing papers are in PubMed but not listed here.

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

12 authors at 7 institutions in 3 countries.

Jordi FarrésCancer Research Program, Hospital del Mar Medical Research Institute, Barcelona, Spain.
Juan Martín-Caballero
Carlos Martínez
Juan J Lozano
Laura Llacuna
Coral Ampurdanés
Cristina Ruiz-Herguido
Françoise Dantzer
Valérie Schreiber
Andreas Villunger
Anna Bigas
José Yélamos
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESHospital Del Mar · ESHospital del Mar Research Institute · ESBarcelona Biomedical Research Park · ESBiotechnologie et Signalisation Cellulaire · FRÉcole Supérieure de Biotechnologie de Strasbourg · FRInnsbruck Medical University · AT

Funding

Austrian Science Fund FWF F 2110
6 · The paper itself

Abstract

Hematopoietic stem cells self-renew for life to guarantee the continuous supply of all blood cell lineages. Here we show that Poly(ADP-ribose) polymerase-2 (Parp-2) plays an essential role in hematopoietic stem/progenitor cells (HSPC) survival under steady-state conditions and in response to stress. Increased levels of cell death were observed in HSPC from untreated Parp-2-/- mice, but this deficit was compensated by increased rates of self-renewal, associated with impaired reconstitution of hematopoiesis upon serial bone marrow transplantation. Cell death after γ-irradiation correlated with an impaired capacity to repair DNA damage in the absence of Parp-2. Upon exposure to sublethal doses of γ-irradiation, Parp-2-/- mice exhibited bone marrow failure that correlated with reduced long-term repopulation potential of irradiated Parp-2-/- HSPC under competitive conditions. In line with a protective role of Parp-2 against irradiation-induced apoptosis, loss of p53 or the pro-apoptotic BH3-only protein Puma restored survival of irradiated Parp-2-/- mice, whereas loss of Noxa had no such effect. Our results show that Parp-2 plays essential roles in the surveillance of genome integrity of HSPC by orchestrating DNA repair and restraining p53-induced and Puma-mediated apoptosis. The data may affect the design of drugs targeting Parp proteins and the improvement of radiotherapy-based therapeutic strategies.

Indexed as

Anemia, AplasticAnimalsApoptosisApoptosis Regulatory ProteinsBone Marrow DiseasesBone Marrow Failure DisordersCell SurvivalDNA DamageDNA RepairFemaleGamma RaysHematopoiesisHemoglobinuria, ParoxysmalHomeostasisMaleMiceApoptosis Regulatory ProteinsParp1 protein, mouseParp2 protein, mousePmaip1 protein, mousePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2PUMA protein, mouseTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID23678004
PMCPMC4918799
OpenAlexW2021250240

What OpenQuestion holds

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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.