ArticleMolecular cell2018
Architectural Proteins and Pluripotency Factors Cooperate to Orchestrate the Transcriptional Response of hESCs to Temperature Stress.
Article in Molecular cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed.
- Establishing Polycomb regulatory landscapes in human early development.Nature genetics · 2026Article
- Pioneer transcription factors direct tissue-specific cohesin chromatin entry and three-dimensional genome organization.Nature genetics · 2026Article
- RepliSage: a stochastic graph-based framework for 3D chromatin modeling across the cell cycle.Nucleic acids research · 2026Article
- LlR3MYB-mediated flavonoid biosynthesis confers cold stress tolerance inHorticulture research · 2026Article
- Impaired cohesin loading disrupts pancreatic differentiation by Polycomb-driven chromatin rewiring and loop collapse.Communications biology · 2026Article
- Epromoters bind key stress-related transcription factors to regulate clusters of stress response genes.The EMBO journal · 2026Article
- Dissecting the contribution of transposable elements to interphase chromosome structure.Genome biology · 2026Article
- Pre-established ATF4 occupancy and chromatin organization instruct selective transcription activation during integrated stress response.Nature communications · 2025Article
- RobusTAD: reference panel based annotation of nested topologically associating domains.Genome biology · 2025Article
- Improved cohesin HiChIP protocol and bioinformatic analysis for robust detection of chromatin loops and stripes.Communications biology · 2025Article
- The nuclear matrix stabilizes primed-specific genes in human pluripotent stem cells.Nature cell biology · 2025Article
- MONITTR allows real-time imaging of transcription and endogenous proteins in C. elegans.The Journal of cell biology · 2025Article
- The Functions and Mechanisms of the Cohesin Complex in Regulating the Fate Determinations of Stem Cells.Research (Washington, D.C.) · 2025Review
- The zinc-finger protein Z4 cooperates with condensin II to regulate somatic chromosome pairing and 3D chromatin organization.Nucleic acids research · 2024Article
- 3C methods in cancer research: recent advances and future prospects.Experimental & molecular medicine · 2024Review
- A distant global control region is essential for normal expression of anterior HOXA genes during mouse and human craniofacial development.Nature communications · 2024Article
- MICA: a multi-omics method to predict gene regulatory networks in early human embryos.Life science alliance · 2024Article
- Transcriptional responses of cancer cells to heat shock-inducing stimuli involve amplification of robust HSF1 binding.Nature communications · 2023Article
- Statistical learning quantifies transposable element-mediated cis-regulation.Genome biology · 2023Article
- Inflammatory stress-mediated chromatin changes underlie dysfunction in endothelial cells.bioRxiv : the preprint server for biology · 2023Article
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3 authors.
Funding
Abstract
Cells respond to temperature stress via up- and downregulation of hundreds of genes. This process is thought to be regulated by the heat shock factor HSF1, which controls the release of RNAPII from promoter-proximal pausing. Here, we analyze the events taking place in hESCs upstream of RNAPII release. We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4 accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac. Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins. These alterations tether and untether enhancers to their cognate promoters or refashion insulated neighborhoods, thus transforming the landscape of enhancer-promoter interactions. Details of the 3D interactome remodeling process support loop extrusion initiating at random sites as a mechanism for the establishment of CTCF/cohesin loops.
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