期刊
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
卷 1872, 期 1, 页码 11-23出版社
ELSEVIER
DOI: 10.1016/j.bbcan.2019.04.003
关键词
AP-1; Fos; Jun; Transcription; Enhancer; Promoter
资金
- French Ligue Nationale contre le Cancer
- INCa PLBio program
- Montpellier EpiGenMed Labex
- GSO Canceropole Emergence program
- Lebanese Association de Specialisation et d'Orientation Scientifique
The ubiquitous family of AP-1 dimeric transcription complexes is involved in virtually all cellular and physiological functions. It is paramount for cells to reprogram gene expression in response to cues of many sorts and is involved in many tumorigenic processes. How AP-1 controls gene transcription has largely remained elusive till recently. The advent of the omics technologies permitting genome-wide studies of transcription factors has however changed and improved our view of AP-1 mechanistical actions. If these studies confirm that AP-1 can sometimes act as a local transcriptional switch operating in the vicinity of transcription start sites (TSS), they strikingly indicate that AP-1 principally operates as a remote command binding to distal enhancers, placing chromatin architecture dynamics at the heart of its transcriptional actions. They also unveil novel constraints operating on AP-1, as well as novel mechanisms used to regulate gene expression via transcription-pioneering-, chromatin-remodeling- and chromatin accessibility maintenance effects.
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