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

TBX-3, the gene mutated in Ulnar-Mammary Syndrome, is a negative regulator of p19ARF and inhibits senescence.

The Journal of biological chemistry - 22 Feb 2002

Brummelkamp Thijn R, Kortlever Roderik M, Lingbeek Merel, Trettel Flavia, MacDonald Marcy E, van Lohuizen Maarten, Bernards René

Abstract excerpt

Prolonged culturing of rodent cells in vitro activates p19(ARF) (named p14(ARF) in man), resulting in a p53-dependent proliferation arrest known as senescence. The p19(ARF)-Mdm2-p53 pathway also serves to protect primary cells against oncogenic transformation. We have used a genetic screen in mouse neuronal cells, conditionally immortalized by a temperature-sensitive mutant of SV40 large T antigen, to identify...

Read the complete abstract on PubMed

Topics

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

Share to Aging
Share to Cell Line

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Cells, Cultured

Share to COS Cells

Share to Gene Expression Regulation

Share to Gene Library

Share to Genes, p53

Source

Identifiers

PMID: 11748239
DOI: 10.1074/jbc.M110492200

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

TBX-3, the gene mutated in Ulnar-Mammary Syndrome, is a negative regulator of p19ARF and inhibits senescence.PMID 11748239Read ↗

TBX3, the gene mutated in ulnar-mammary syndrome, promotes growth of mammary epithelial cells via repression of p19ARF, independently of p53.Semantic proximity Read ↗

Tbx3 impinges on the p53 pathway to suppress apoptosis, facilitate cell transformation and block myogenic differentiation.Semantic proximity Read ↗

A dominant repression domain in Tbx3 mediates transcriptional repression and cell immortalization: relevance to mutations in Tbx3 that cause ulnar-mammary syndrome.Semantic proximity Read ↗

Tbx3, the ulnar-mammary syndrome gene, and Tbx2 interact in mammary gland development through a p19Arf/p53-independent pathway.Semantic proximity Read ↗

Tbx3 controls the fate of hepatic progenitor cells in liver development by suppressing <i>p19ARF</i> expressionSemantic proximity Read ↗

An RNA interference screen for identifying downstream effectors of the p53 and pRB tumour suppressor pathways involved in senescenceSemantic proximity Read ↗

TBX3 and its splice variant TBX3 + exon 2a are functionally similarSemantic proximity Read ↗

Tbx2 Is Overexpressed and Plays an Important Role in Maintaining Proliferation and Suppression of Senescence in MelanomasSemantic proximity Read ↗

The T-box repressors TBX2 and TBX3 specifically regulate the tumor suppressor gene p14ARF via a variant T-site in the initiator.Semantic proximity Read ↗

Therapeutic Response to Non-genotoxic Activation of p53 by Nutlin3a Is Driven by PUMA-Mediated Apoptosis in Lymphoma CellsSemantic proximity Read ↗

Zeb1 links epithelial-mesenchymal transition and cellular senescence.Semantic proximity Read ↗

Mouse TBX3 mutants suggest novel molecular mechanisms for Ulnar-mammary syndrome.Semantic proximity Read ↗

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