ArticleProceedings of the National Academy of Sciences of the United States of America1997
Requirement of STAT5b for sexual dimorphism of body growth rates and liver gene expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 322 papers, 1 of them a synthesis that pooled it.
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Who cites it
322 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,000 citations in OpenAlex.
- The Prognostic Role of STAT5B Across Cancer Types and Comparative Analysis with STAT5A: A Systematic Review.Biomolecules · 2025Pooled it
- Ablation of CDK6 and STAT5B rewires T cell developmental dynamics and prevents ALKNature communications · 2026Article
- Stafib-2-CR: an Improved Nanomolar and Selective Inhibitor of the Transcription Factor STAT5b Developed by Conformational Restriction of Stafib-2.Chemistry (Weinheim an der Bergstrasse, Germany) · 2026Article
- Reproductive experience promotes permanent body growth independently of growth hormone.bioRxiv : the preprint server for biology · 2026Article
- Genetic deletion of miR-200a/200b increases growth and feed conversion efficiency in yellow catfish.Science China. Life sciences · 2026Article
- Advances in Sources, Content Determination, and Bioactivity of 20α-Hydroxyprogesterone.Endocrine, metabolic & immune disorders drug targets · 2026Review
- Cytokine inducible SH2-containing protein: a versatile negative regulator of cytokine receptor signaling.Frontiers in immunology · 2026Review
- Inborn errors of regulatory T-cell differentiation and function.The Journal of allergy and clinical immunology · 2025Review
- Cross-tissue molecular responses in the liver and blood after toxicant exposures.Research square · 2025Article
- Low Liver-Derived IGF-1 Drives the Alterations in Growth Hormone Secretion in Food-Restricted Male Mice.Endocrinology · 2025Article
- Transcriptome alterations underlying metabolic dysfunction and liver disease in myotonic dystrophy type 1.Human molecular genetics · 2025Article
- Y665F variant of mouse Stat5b protects against acute kidney injury through transcriptomic shifts in renal gene expression.Scientific reports · 2025Article
- STAT5B leukemic mutations, altering SH2 tyrosine 665, have opposing impacts on immune gene programs.Life science alliance · 2025Article
- Article
- Disease-Associated Mutations of the STAT5B SH2 Domain Regulate Cytokine-Driven Enhancer Function and Mammary Development.Journal of mammary gland biology and neoplasia · 2025Article
- GH-Releasing Hormone Neurons Regulate the Hypothalamic-Pituitary-Somatotropic Axis via Short-Loop Negative Feedback.Endocrinology · 2025Article
- Maintenance of hematopoietic stem cells by tyrosine-unphosphorylated STAT5 and JAK inhibition.Blood advances · 2025Article
- Tyrosine phosphorylation of both STAT5A and STAT5B is necessary for maximal IL-2 signaling and T cell proliferation.Nature communications · 2024Article
- STAT5B SH2 variants disrupt mammary enhancers and the stability of genetic programs during pregnancy.bioRxiv : the preprint server for biology · 2024Article
- Sexual dimorphism of circadian liver transcriptome.iScience · 2024Article
262 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The signal transducer and activator of transcription, STAT5b, has been implicated in signal transduction pathways for a number of cytokines and growth factors, including growth hormone (GH). Pulsatile but not continuous GH exposure activates liver STAT5b by tyrosine phosphorylation, leading to dimerization, nuclear translocation, and transcriptional activation of the STAT, which is proposed to play a key role in regulating the sexual dimorphism of liver gene expression induced by pulsatile plasma GH. We have evaluated the importance of STAT5b for the physiological effects of GH pulses using a mouse gene knockout model. STAT5b gene disruption led to a major loss of multiple, sexually differentiated responses associated with the sexually dimorphic pattern of pituitary GH secretion. Male-characteristic body growth rates and male-specific liver gene expression were decreased to wild-type female levels in STAT5b-/- males, while female-predominant liver gene products were increased to a level intermediate between wild-type male and female levels. Although these responses are similar to those observed in GH-deficient Little mice, STAT5b-/- mice are not GH-deficient, suggesting that they may be GH pulse-resistant. Indeed, the dwarfism, elevated plasma GH, low plasma insulin-like growth factor I, and development of obesity seen in STAT5b-/- mice are all characteristics of Laron-type dwarfism, a human GH-resistance disease generally associated with a defective GH receptor. The requirement of STAT5b to maintain sexual dimorphism of body growth rates and liver gene expression suggests that STAT5b may be the major, if not the sole, STAT protein that mediates the sexually dimorphic effects of GH pulses in liver and perhaps other target tissues. STAT5b thus has unique physiological functions for which, surprisingly, the highly homologous STAT5a is unable to substitute.
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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.