Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Differential requirement for H2AX and 53BP1 in organismal development and genome maintenance in the absence of poly(ADP)ribosyl polymerase 1.

Molecular and cellular biology - 1 May 2010

Orsburn Benjamin, Escudero Beatriz, Prakash Mansi, Gesheva Silvia, Liu Guosheng, Huso David L, Franco Sonia

Abstract excerpt

Combined deficiencies of poly(ADP)ribosyl polymerase 1 (PARP1) and ataxia telangiectasia mutated (ATM) result in synthetic lethality and, in the mouse, early embryonic death. Here, we investigated the genetic requirements for this lethality via analysis of mice deficient for PARP1 and either of two ATM-regulated DNA damage response (DDR) factors: histone H2AX and 53BP1. We found that, like ATM, H2AX is essential...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to DNA-Activated Protein Kinase
Share to Mitomycin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Nucleic Acid Synthesis Inhibitors

Share to Poly (ADP-Ribose) Polymerase-1

Share to Poly(ADP-ribose) Polymerases

Share to Radiation, Ionizing

Share to Sister Chromatid Exchange

Share to Tumor Suppressor p53-Binding Protein 1

Source

Open in PubMed Open full text

Identifiers

PMID: 20231360
DOI: 10.1128/MCB.00091-10
PMCID: PMC2863712

Genes

ATM
PARP1
RAD51

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Differential requirement for H2AX and 53BP1 in organismal development and genome maintenance in the absence of poly(ADP)ribosyl polymerase 1.PMID 20231360Read ↗

DNA strand break-sensing molecule poly(ADP-Ribose) polymerase cooperates with p53 in telomere function, chromosome stability, and tumor suppression.Semantic proximity Read ↗

Early embryonic lethality in PARP-1 Atm double-mutant mice suggests a functional synergy in cell proliferation during development.Semantic proximity Read ↗

Inactive PARP1 causes embryonic lethality and genome instability in a dominant-negative manner.Semantic proximity Read ↗

53BP1 cooperates with p53 and functions as a haploinsufficient tumor suppressor in mice.Semantic proximity Read ↗

PARP inhibitor synthetic lethality reveals homologous recombination sub-pathway architectureSemantic proximity Read ↗

The impact of heterochromatin on DSB repair.Semantic proximity Read ↗

Phenotypic characterization of Parp-1 and Parp-2 deficient mice and cells.Semantic proximity Read ↗

Pleiotropic Cellular Functions of PARP1 in Longevity and Aging: Genome Maintenance Meets InflammationSemantic proximity Read ↗

Requirement of poly(ADP-ribose) polymerase in recovery from DNA damage in mice and in cells.Semantic proximity Read ↗

p53 Binding protein 53BP1 is required for DNA damage responses and tumor suppression in mice.Semantic proximity Read ↗

53BP1 and p53 synergize to suppress genomic instability and lymphomagenesis.Semantic proximity Read ↗

PARP1 and DNA-PKcs synergize to suppress p53 mutation and telomere fusions during T-lineage lymphomagenesis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.