ArticleNucleic acids research2016
Differential cytokine sensitivities of STAT5-dependent enhancers rely on Stat5 autoregulation.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Progress in Research on Key Factors Regulating Lactation Initiation in the Mammary Glands of Dairy Cows.Genes · 2023Review
- The NFIB/CARM1 partnership is a driver in preclinical models of small cell lung cancer.Nature communications · 2023Article
- Redundant and non-redundant cytokine-activated enhancers control Csn1s2b expression in the lactating mouse mammary gland.Nature communications · 2021Article
- Temporal dynamics of a CSF1R signaling gene regulatory network involved in epilepsy.PLoS computational biology · 2021Article
- Activation of the SARS-CoV-2 Receptor Ace2 through JAK/STAT-Dependent Enhancers during Pregnancy.Cell reports · 2020Article
- The interdependence of mammary-specific super-enhancers and their native promoters facilitates gene activation during pregnancy.Experimental & molecular medicine · 2020Article
- STAT3-dependent analysis reveals PDK4 as independent predictor of recurrence in prostate cancer.Molecular systems biology · 2020Article
- STAT5-Driven Enhancers Tightly Control Temporal Expression of Mammary-Specific Genes.Journal of mammary gland biology and neoplasia · 2019Review
- Dissecting Tissue-Specific Super-Enhancers by Integrating Genome-Wide Analyses and CRISPR/Cas9 Genome Editing.Journal of mammary gland biology and neoplasia · 2019Review
- Extensive epigenomic integration of the glucocorticoid response in primary human monocytes and in vitro derived macrophages.Scientific reports · 2019Article
- Genome-Wide Maps of Transcription Regulatory Elements and Transcription Enhancers in Development and Disease.Comprehensive Physiology · 2018Review
- Progressing super-enhancer landscape during mammary differentiation controls tissue-specific gene regulation.Nucleic acids research · 2018Article
- CRISPR/Cas9 targeting events cause complex deletions and insertions at 17 sites in the mouse genome.Nature communications · 2017Article
- Functional assessment of CTCF sites at cytokine-sensing mammary enhancers using CRISPR/Cas9 gene editing in mice.Nucleic acids research · 2017Article
- Activation of Male Liver Chromatin Accessibility and STAT5-Dependent Gene Transcription by Plasma Growth Hormone Pulses.Endocrinology · 2017Article
- Mechanisms and consequences of Jak-STAT signaling in the immune system.Nature immunology · 2017Review
- Functional Enhancers As Master Regulators of Tissue-Specific Gene Regulation and Cancer Development.Molecules and cells · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Cytokines utilize the transcription factor STAT5 to control cell-specific genes at a larger scale than universal genes, with a mechanistic explanation yet to be supplied. Genome-wide studies have identified putative STAT5-based mammary-specific and universal enhancers, an opportunity to investigate mechanisms underlying their differential response to cytokines. We have now interrogated the integrity and function of both categories of regulatory elements using biological and genetic approaches. During lactation, STAT5 occupies mammary-specific and universal cytokine-responsive elements. Following lactation, prolactin levels decline and mammary-specific STAT5-dependent enhancers are decommissioned within 24 h, while universal regulatory complexes remain intact. These differential sensitivities are linked to STAT5 concentrations and the mammary-specific Stat5 autoregulatory enhancer. In its absence, mammary-specific enhancers, but not universal elements, fail to be fully established. Upon termination of lactation STAT5 binding to a subset of mammary enhancers is substituted by STAT3. No STAT3 binding was observed at the most sensitive STAT5 enhancers suggesting that upon hormone withdrawal their chromatin becomes inaccessible. Lastly, we demonstrate that the mammary-enriched transcription factors GR, ELF5 and NFIB associate with STAT5 at sites lacking bona fide binding motifs. This study provides, for the first time, molecular insight into the differential sensitivities of mammary-specific and universal cytokine-sensing enhancers.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.