ArticlePloS one2012
The Jak/STAT signaling pathway is downregulated at febrile temperatures.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Impact of heat stress on prolactin-mediated ovarian JAK-STAT signaling in postpubertal gilts.Journal of animal science · 2022Article
- Growth Hormone Receptor Regulation in Cancer and Chronic Diseases.Frontiers in endocrinology · 2020Review
- Identification of the acclimation genes in transcriptomic responses to heat stress of White Pekin duck.Cell stress & chaperones · 2017Article
- Acute heat stress activated inflammatory signaling in porcine oxidative skeletal muscle.Physiological reports · 2017Article
- JAK2-centered interactome hotspot identified by an integrative network algorithm in acute Stanford type A aortic dissection.PloS one · 2014Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe Janus family of kinases (JAKs), Jak1, Jak2, Jak3, and Tyk2, constitute a subgroup of non-receptor protein tyrosine kinases. Upon cytokine binding, the receptor-associated kinases are activated and phosphorylate tyrosine residues in their cognate cytokine receptors. Their activities are controlled at several levels and include cellular concentration, auto-activation, and degradation. PRINCIPAL
findingsOur findings show that elevated temperatures in the fever range irreversibly aggregate Jak2 and considerably reduce functional Jak2 protein levels. Jak2 synthesis remains unaltered. We observed that also the protein level of the signal transducer and activator of transcription, STAT5b, is transiently decreased at temperatures above 37°C. Consequently, the signaling response, e.g. via the growth hormone receptor, is reduced. CONCLUSIONS/SIGNIFICANCE: These findings predict that elevated body temperatures lower the responsiveness of cytokine receptors.
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Registered trials
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