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

Absence of p53-dependent apoptosis combined with nonhomologous end-joining deficiency leads to a severe diabetic phenotype in mice.

Diabetes - 1 Jan 2010

Tavana Omid, Puebla-Osorio Nahum, Sang Mei, Zhu Chengming

Abstract excerpt

OBJECTIVE: Regulation of pancreatic beta-cell mass is essential to preserve sufficient insulin levels for the maintenance of glucose homeostasis. Previously, we reported that DNA double-strand breaks (DSBs) resulting from nonhomologous end-joining (NHEJ) deficiency induce apoptosis and, when combined with p53 deficiency, progressed rapidly into lymphomagenesis in mice. Combination of NHEJ deficiency with a...

Read the complete abstract on PubMed

Topics

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

Share to Cellular Senescence
Share to Diabetes Mellitus, Experimental

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA Ligase ATP

Share to DNA Ligases

Share to Glucose Intolerance

Share to Insulin Secretion

Share to Islets of Langerhans

Share to Pancreas

Source

Open in PubMed Open full text

Identifiers

PMID: 19833883
DOI: 10.2337/db09-0792
PMCID: PMC2797914

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

Absence of p53-dependent apoptosis combined with nonhomologous end-joining deficiency leads to a severe diabetic phenotype in mice.PMID 19833883Read ↗

DNA damage models phenotypes of β cell senescence in Type 1 DiabetesSemantic proximity Read ↗

DNA damage to β cells in culture recapitulates features of senescent β cells that accumulate in type 1 diabetesSemantic proximity Read ↗

Failure to Repair Endogenous DNA Damage in β-Cells Causes Adult-Onset Diabetes in MiceSemantic proximity Read ↗

Loss of Deubiquitinase USP1 Blocks Pancreatic β-Cell Apoptosis by Inhibiting DNA Damage ResponseSemantic proximity Read ↗

Pancreatic β-cell senescence in diabetes: mechanisms, markers and therapiesSemantic proximity Read ↗

Too many breaks (brakes): Pancreatic β-cell senescence leads to diabetesSemantic proximity Read ↗

DNA damage-induced cellular senescence is sufficient to suppress tumorigenesis: a mouse model.Semantic proximity Read ↗

Increased double strand breaks in diabetic β-cells with a p21 response that limits apoptosisSemantic proximity Read ↗

Absence of p53-dependent apoptosis leads to UV radiation hypersensitivity, enhanced immunosuppression and cellular senescence.Semantic proximity Read ↗

Developmental control of DNA damage responses in α- and β-cells shapes the selective beta-cell susceptibility in diabetesSemantic proximity Read ↗

Pancreatic cancer triggers diabetes through TGF-β–mediated selective depletion of islet β-cellsSemantic proximity Read ↗

Pancreatic beta-cell failure and diabetes in mice with a deletion mutation of the endoplasmic reticulum molecular chaperone gene P58IPK.Semantic proximity Read ↗

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