The regulation of E2F by pRB-family proteins.

Dyson, Nicholas

doi:10.1101/gad.12.15.2245

Cited by 2,317Cancer-related Molecular PathwaysGenomics and Chromatin DynamicsSignaling Pathways in Disease

The regulation of E2F by pRB-family proteins.

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Dyson, Nicholas·1998·Genes & Development

DOI 10.1101/gad.12.15.2245

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These proteins share a common bipartite pocket region comprising a LXCXE motif, which allows them to interact directly with other proteins.
“These proteins share a common bipartite pocket region comprising a LXCXE motif, which allows them to interact directly with other proteins (Dyson, 1998).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Dyson, 1998
Senescence signaling typically acts by decreasing cyclin-CDK activity or increasing CDK inhibitor levels.
“Due to the critical regulatory role of these cell cycle factors, senescence signaling typically acts by decreasing cyclin–CDK activity or increasing CDK inhibitor levels.”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [33]
Rb pathway mutations promote tumour development by deregulating E2F transcription factors and causing uncontrolled cell cycle progression.
“These mutations promote tumour development by deregulating the E2F family of transcription factors leading to uncontrolled cell cycle progression 3 .”
From Rb inactivation promotes genomic instability by uncoupling cell cycle progression from mitotic control (2004) · cites this paper as [3]
CDK4/6 phosphorylates RB to prime it for inactivation by other CDKs later in G1, releasing E2F transcription factors to induce S-phase genes.
“Together, these results implied that the role of CDK4/6 was to phosphorylate RB, priming it for inactivation by other CDKs later in G1, and releasing E2F transcription factors from RB constraint to allow their coordinate induction of a suite of genes whose activities are jointly required for initiation of S phase [reviewed in detail in (16) (29-31)].”
From Targeting CDK4 and CDK6: From Discovery to Therapy (2016) · cites this paper as [29]

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“The activated E2F mediates quiescent cells for S phase entry and cell cycle progression (Dyson, 1998; Nevins, 1998; Trimarchi and Lees, 2002; Dimova and Dyson, 2005; Song et al., 2007).”
Background
E2F regulates DDB2: consequences for DNA repair in Rb-deficient cells
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Self-citation

Authors: Dyson, N.
Affiliations: Massachusetts General Hospital (US)
Corresponding author: Dyson, Nicholas
ORCID: Dyson, Nicholas
Venue: Genes & Development
Publisher: Cold Spring Harbor Laboratory
Published: 1998-08-01
Volume: 12
Issue: 15
Pages: 2245-2262
ISSN: 0890-9369 (ISSN-L)
1549-5477
DOI: 10.1101/gad.12.15.2245
OpenAlex: W2034277114
Cited by: 2,317
References: 205
Citations by year: 2026: 14 · 2025: 27 · 2024: 27 · 2023: 35 · 2022: 41 · 2021: 63 · 2020: 49 · 2019: 36 · 2018: 39 · 2017: 48 · 2016: 43 · 2015: 49 · 2014: 54 · 2013: 66 · 2012: 78
Type: posted content
Language: en
Open access: bronze
doi.org
Locations: Genes & Development (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Cancer Institute (CA64402, R01CA064402)
National Institute of General Medical Sciences (GM-53203, R01GM053203)
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: E2F transcription factors, retinoblastoma protein, cell cycle regulation, transcriptional repression, cell cycle checkpoints
MeSH terms: Animals, Binding Sites, Carrier Proteins, DNA-Binding Proteins, Humans, Oncogenes, Phosphorylation, Repressor Proteins, Transcription Factors, Transcriptional Activation, Genes, Tumor Suppressor, Retinoblastoma Protein, S Phase, Apoptosis, Cell Cycle Proteins, Transcription Factor DP1, E2F Transcription Factors, Retinoblastoma-Binding Protein 1

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