ArticleMolecular endocrinology (Baltimore, Md.)2014
Coregulation of genetic programs by the transcription factors NFIB and STAT5.
Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- A novel mRNA-based multi-cytokine strategy to reprogram the peritoneal tumor microenvironment in ovarian cancer.Journal of nanobiotechnology · 2026Article
- Disease-Associated Mutations of the STAT5B SH2 Domain Regulate Cytokine-Driven Enhancer Function and Mammary Development.Journal of mammary gland biology and neoplasia · 2025Article
- Roles of the NFI/CTF gene family in transcription and development: update 2025.Academia biology · 2025Article
- Fused in sarcoma (FUS) inhibits milk production efficiency in mammals.Nature communications · 2024Article
- STAT5B SH2 variants disrupt mammary enhancers and the stability of genetic programs during pregnancy.bioRxiv : the preprint server for biology · 2024Article
- Cell-specific and shared regulatory elements control a multigene locus active in mammary and salivary glands.Nature communications · 2023Article
- Mammary-Enriched Transcription Factors Synergize to Activate theInternational journal of molecular sciences · 2022Article
- Contribution of the STAT Family of Transcription Factors to the Expression of the Serotonin 2B (HTR2B) Receptor in Human Uveal Melanoma.International journal of molecular sciences · 2022Article
- Redundant and non-redundant cytokine-activated enhancers control Csn1s2b expression in the lactating mouse mammary gland.Nature communications · 2021Article
- 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
- CRISPR/Cas9 targeting events cause complex deletions and insertions at 17 sites in the mouse genome.Nature communications · 2017Article
- Activation of Male Liver Chromatin Accessibility and STAT5-Dependent Gene Transcription by Plasma Growth Hormone Pulses.Endocrinology · 2017Article
- Differential cytokine sensitivities of STAT5-dependent enhancers rely on Stat5 autoregulation.Nucleic acids research · 2016Article
- Hierarchy within the mammary STAT5-driven Wap super-enhancer.Nature genetics · 2016Article
- An autoregulatory enhancer controls mammary-specific STAT5 functions.Nucleic acids research · 2016Article
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10 authors.
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Abstract
Mammary-specific genetic programs are activated during pregnancy by the common transcription factor signal transducer and activator of transcription (STAT) 5. More than one third of these genes carry nuclear factor I/B (NFIB) binding motifs that coincide with STAT5 in vivo binding, suggesting functional synergy between these two transcription factors. The role of NFIB in this governance was investigated in mice from which Nfib had been inactivated in mammary stem cells or in differentiating alveolar epithelium. Although NFIB was not required for alveolar expansion, the combined absence of NFIB and STAT5 prevented the formation of functional alveoli. NFIB controlled the expression of mammary-specific and STAT5-regulated genes and chromatin immunoprecipitation-sequencing established STAT5 and NFIB binding at composite regulatory elements containing histone H3 lysine dimethylation enhancer marks and progesterone receptor binding. By integrating previously published chromatin immunoprecipitation-sequencing data sets, the presence of NFIB-STAT5 modules in other cell types was investigated. Notably, genomic sites bound by NFIB in hair follicle stem cells were also occupied by STAT5 in mammary epithelium and coincided with enhancer marks. Many of these genes were under NFIB control in both hair follicle stem cells and mammary alveolar epithelium. We propose that NFIB-STAT5 modules, possibly in conjunction with other transcription factors, control cell-specific genetic programs.
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