Cited by 431Cancer-related Molecular PathwaysGenomics and Chromatin DynamicsSignaling Pathways in Disease

pRB and p107/p130 are required for the regulated expression of different sets of E2F responsive genes

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Hurford, R K, Cobrinik, D, Lee, M H, Dyson, N·1997·Genes & Development

Abstract

The activity of the E2F transcription factor is controlled by physical association with the retinoblastoma protein (pRB) and two related proteins, p107 and p130. The pRB family members are thought to control different aspects of E2F activity, but it has been unclear what the respective functions of these proteins might be. To dissect the specific functions of pRB, p107, and p130 we have investigated how the expression of E2F-regulated genes is changed in cultures of primary cells lacking each of these family members. Whereas no changes were found in the expression of E2F-target genes in cells lacking either p107 or p130, deregulated expression of E2F targets was seen in cells lacking pRB and in cells lacking both p107 and p130. Surprisingly, the genes that were disregulated in these two settings were completely different. These findings show that pRB and p107/p130 indeed provide different functions in E2F regulation and identify target genes that are dependent on pRB family proteins for their normal expression.

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Crossref · 10.1101/gad.11.11.1447

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  • Previous studies suggested that RB family proteins regulate different E2F targets (Hurford et al., 1997) and that RB loss increases replication complex loading on chromatin (Srinivasan et al., 2007).

    “Although previous studies hinted that RB family proteins can regulate different E2F targets (Hurford et al., 1997) and that loss of RB can ultimately lead to increased loading of replications complexes on chromatin (Srinivasan et al., 2007), the selectivity of RB towards repressing replication genes was not appreciated.”

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  1. Tabor, S. and K. Struhl. 1994. DNA-dependent DNA polymer- ases. In Current protocols in molecular biology (ed. F.M. Ausubel, R. Brent, R.E. Kingston, D.D. Moore, J.G. Seidman, J.A. Smith, and K. Struhl), pp. 3.5.1-3.5.15. Wiley/Greene, New York, NY.

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Authors
Hurford, R. K., Cobrinik, D., Lee, M. H., & Dyson, N.
Affiliations
Massachusetts General Hospital (US)
Venue
Genes & Development
Published
1997-06-01
Volume
11
Issue
11
Pages
1447-1463
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
OpenAlex
W2151812144
Cited by
431
References
85
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 7 · 2021: 4 · 2020: 3 · 2019: 5 · 2018: 2 · 2017: 4 · 2016: 6 · 2015: 7 · 2014: 5 · 2013: 11 · 2012: 7
Type
posted content
Language
en
Open access
Locations
  • Genes & Development (publishedVersion)
  • PubMed (publishedVersion)
  • HighWire Press Open Archive (submittedVersion)
Funders
  • National Institutes of Health
  • National Cancer Institute (CA64402, R01CA064402)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
retinoblastoma protein, p107, p130, E2F transcription factors, E2F target genes, gene expression regulation, cell cycle regulation, cell cycle-dependent transcription
MeSH terms
Animals, Carrier Proteins, Cell Cycle, Cells, Cultured, DNA-Binding Proteins, Embryo, Mammalian, Fibroblasts, Gene Expression Regulation, Nuclear Proteins, Phosphoproteins, Promoter Regions, Genetic, Protein Binding, Proteins, Transcription Factors, Transfection, Trans-Activators, Retinoblastoma Protein, Culture Media, Serum-Free, Genes, Reporter, Mice, Knockout, Cell Cycle Proteins, Transcription Factor DP1, E2F Transcription Factors, Retinoblastoma-Like Protein p130, Retinoblastoma-Like Protein p107, Mice, Retinoblastoma-Binding Protein 1

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