NF-Y is a Transcription Factor that regulates transcription through binding to the CCAAT-box. To understand its strategy, we analyzed 16 ChIP-seq datasets from human and mouse cells. Shared loci, mostly located in promoters of expressed genes of cell cycle, metabolism and gene expression pathways, are associated with histone marks of active chromatin and specific modules of TFs. Other peaks are in enhancers and Transposable Elements -TE- of retroviral origin in human and mouse. We evaluated the relationship with USF1, a common synergistic partner in promoters and MLT1 TEs, upon NF-YB inactivation: USF1 binding decreases in promoters, modestly in MLT1, suggesting a pioneering role of NF-Y in formers, not in the latters. These data define a common set of NF-Y functional targets across different mammalian cell types, suggesting a pioneering role in promoters with respect to TEs.
Keyphrases
- signaling pathway
- transcription factor
- lps induced
- gene expression
- cell cycle
- pi k akt
- genome wide
- nuclear factor
- induced apoptosis
- endothelial cells
- oxidative stress
- dna methylation
- dna binding
- single cell
- inflammatory response
- cell cycle arrest
- rna seq
- binding protein
- copy number
- stem cells
- pluripotent stem cells
- bone marrow
- mesenchymal stem cells
- artificial intelligence
- deep learning
- antiretroviral therapy
- men who have sex with men
- energy transfer
- hiv infected