Cited by 413Cancer-related Molecular PathwaysTelomeres, Telomerase, and SenescenceRetinal Development and Disorders

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Ablation of the Retinoblastoma gene family deregulates G1 control causing immortalization and increased cell turnover under growth-restricting conditions

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Dannenberg, Jan-Hermen, van Rossum, Agnes, Schuijff, Leontine, te Riele, Hein·2000·Genes & Development

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Abstract

The retinoblastoma suppressor pRB belongs to the family of so-called pocket proteins, which also includes p107 and p130. These proteins may functionally overlap in cell cycle control and tumor suppression. We have generated an isogenic set of embryonic stem (ES) cell lines carrying single or compound loss-of-function mutations in the Rb gene family, including a cell line completely devoid of all three pocket proteins. None of the knockout combinations affected the growth characteristics of ES cells; however, concomitant ablation of all three pocket proteins strongly impaired their differentiation capacity. For the generated genotypes, primary mouse embryonic fibroblasts (MEFs) also were obtained. While inactivation of Rb alone did not alleviate the senescence response of MEFs, pRB/p107-deficient MEFs, after having adapted to in vitro culturing, continued to proliferate at modest rate. Additional ablation of p130 rendered MEFs completely insensitive to senescence-inducing signals and strongly increased their proliferation rate. Although triple-knockout MEFs retained anchorage dependence, they lacked proper G 1 control and showed increased cell turnover under growth-inhibiting conditions.

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Authors: Dannenberg, J.-H., van Rossum, A., Schuijff, L., & te Riele, H.
Affiliations: The Netherlands Cancer Institute (NL)
Venue: Genes & Development
Publisher: Cold Spring Harbor Laboratory
Published: 2000-12-01
Volume: 14
Issue: 23
Pages: 3051-3064
ISSN: 0890-9369 (ISSN-L)
1549-5477
DOI: 10.1101/gad.847700
PMC: PMC317114
OpenAlex: W2001004678
Cited by: 413
References: 96
Citations by year: 2026: 1 · 2025: 1 · 2024: 5 · 2023: 8 · 2022: 6 · 2021: 8 · 2020: 12 · 2019: 3 · 2018: 12 · 2017: 8 · 2016: 9 · 2015: 10 · 2014: 11 · 2013: 21 · 2012: 17
Type: posted content
Language: en
Open access: bronze
doi.org
Locations: Genes & Development (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
Health Sciences › Medicine › Ophthalmology › Retinal Development and Disorders
Keywords: retinoblastoma protein, p107, p130, pocket proteins, cellular senescence, cell immortalization, cell turnover, embryonic stem cells, mouse embryonic fibroblasts, differentiation capacity, loss-of-function mutations, tumor suppression
MeSH terms: Animals, Cell Adhesion, Cell Differentiation, Cell Division, Cell Line, Mice, Inbred C57BL, Mice, Nude, Nuclear Proteins, Phosphoproteins, Proteins, Stem Cells, Tumor Suppressor Protein p53, Retinoblastoma Protein, G1 Phase, Teratocarcinoma, Mice, Knockout, Tumor Suppressor Protein p14ARF, Retinoblastoma-Like Protein p130, Retinoblastoma-Like Protein p107, Mice

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Ablation of the Retinoblastoma gene family deregulates G1 control causing immortalization and increased cell turnover under growth-restricting conditions

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