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Tytuł pozycji:

The broken cycle: E2F dysfunction in cancer.

Tytuł:
The broken cycle: E2F dysfunction in cancer.
Autorzy:
Kent LN; Department of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
Leone G; Department of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA. .
Źródło:
Nature reviews. Cancer [Nat Rev Cancer] 2019 Jun; Vol. 19 (6), pp. 326-338.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
Język:
English
Imprint Name(s):
Original Publication: London, UK : Nature Pub. Group, [c2001-
MeSH Terms:
E2F Transcription Factors/*metabolism
Neoplasms/*drug therapy
Neoplasms/*pathology
Animals ; Apoptosis/physiology ; Cell Proliferation ; Chromosomal Instability ; DNA Damage/physiology ; E2F Transcription Factors/genetics ; Humans ; Molecular Targeted Therapy/methods ; Multigene Family ; Neoplasms/genetics ; Protein Processing, Post-Translational ; Protein Stability
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Grant Information:
R01 CA121275 United States CA NCI NIH HHS
Substance Nomenclature:
0 (E2F Transcription Factors)
Entry Date(s):
Date Created: 20190505 Date Completed: 20190704 Latest Revision: 20220416
Update Code:
20240105
DOI:
10.1038/s41568-019-0143-7
PMID:
31053804
Czasopismo naukowe
The cyclin-dependent kinase (CDK)-RB-E2F axis forms the core transcriptional machinery driving cell cycle progression, dictating the timing and fidelity of genome replication and ensuring genetic material is accurately passed through each cell division cycle. The ultimate effectors of this axis are members of a family of eight distinct E2F genes encoding transcriptional activators and repressors. E2F transcriptional activity is tightly regulated throughout the cell cycle via transcriptional and translational regulation, post-translational modifications, protein degradation, binding to cofactors and subcellular localization. Alterations in one or more key components of this axis (CDKs, cyclins, CDK inhibitors and the RB family of proteins) occur in virtually all cancers and result in heightened oncogenic E2F activity, leading to uncontrolled proliferation. In this Review, we discuss the activities of E2F proteins with an emphasis on the newest atypical E2F family members, the specific and redundant functions of E2F proteins, how misexpression of E2F transcriptional targets promotes cancer and both current and developing therapeutic strategies being used to target this oncogenic pathway.

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