The E2F transcription factor 2: What do we know?
Animals
Apoptosis
/ genetics
Cell Cycle
/ genetics
Cell Division
/ genetics
Cell Movement
/ genetics
Cell Proliferation
/ genetics
Disease Models, Animal
E2F2 Transcription Factor
/ metabolism
Gene Expression Regulation, Neoplastic
Humans
Inflammation
/ genetics
Neoplasm Invasiveness
/ genetics
Neoplasms
/ genetics
E2F2
biological effect
diseases
Journal
Bioscience trends
ISSN: 1881-7823
Titre abrégé: Biosci Trends
Pays: Japan
ID NLM: 101502754
Informations de publication
Date de publication:
11 May 2021
11 May 2021
Historique:
pubmed:
7
5
2021
medline:
30
11
2021
entrez:
6
5
2021
Statut:
ppublish
Résumé
E2F transcription factor 2 (E2F2) is a member of the E2F family of transcription factors. The classical view is that some E2Fs act as "activators" and others "inhibitors" of cell cycle gene expression. However, the so-called "activator" E2F2 is particularly enigmatic, with seemingly contradictory roles in the cell cycle, proliferation, apoptosis, inflammation, and cell migration and invasion. How can we rationalize the apparently opposing functions of E2F2 in different situations? This is difficult because different methods of studying E2F2 have yielded conflicting results, so extrapolating mechanisms from an observed endpoint is challenging. This review will attempt to summarize and clarify these issues. This review focuses on genetic studies that have helped elucidate the biological functions of E2F2 and that have enhanced our understanding of how E2F2 is integrated into pathways controlling the cell cycle, proliferation, apoptosis, inflammation, and cell migration and invasion. This review will also discuss the function of E2F2 in cancer and other diseases. This review provides a strong basis for further research on the biological function and clinical potential of E2F2.
Identifiants
pubmed: 33952804
doi: 10.5582/bst.2021.01072
doi:
Substances chimiques
E2F2 Transcription Factor
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM