ArticleEndocrinology2017
Kinase Inactive Tyrosine Kinase (Tyk2) Supports Differentiation of Brown Fat Cells.
Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
The trial behind it
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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Cell-type-specific requirement for TYK2 in murine immune cells under steady state and challenged conditions.Cellular and molecular life sciences : CMLS · 2025Article
- Directly targeting PRDM16 in thermogenic adipose tissue to treat obesity and its related metabolic diseases.Frontiers in endocrinology · 2024Review
- TYK2 licenses non-canonical inflammasome activation during endotoxemia.Cell death and differentiation · 2021Article
- TYK2 in Tumor Immunosurveillance.Cancers · 2020Review
- TYK2: An Upstream Kinase of STATs in Cancer.Cancers · 2019Review
- STAT3 suppresses Wnt/β-catenin signaling during the induction phase of primary Myf5+ brown adipogenesis.Cytokine · 2018Article
- Brown and Beige Adipose Tissues in Health and Disease.Comprehensive Physiology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
It has been known for decades that brown adipose tissue (BAT) plays a central role in maintaining body temperature in hibernating animals and human infants. Recently, it has become evident that there are also depots of brown fat in adult humans, and the mass of brown fat is inversely correlated with body weight. There are a variety of transcription factors implicated in the differentiation of classical Myf5+ brown preadipocytes, one of the most important of which is PRDM16. We have recently identified that in addition to PRDM16, the tyrosine kinase Tyk2 and the STAT3 transcription factor are required for the differentiation of Myf5 positive brown preadipocytes both in cell culture and in mice. Tyk2 is a member of the Jak family of tyrosine kinases, which are activated by exposure of cells to different cytokines and growth factors. In this study we report the surprising observation that a mutated form of Tyk2, which lacks tyrosine kinase activity (Tyk2KD) restores differentiation of brown preadipocytes in vitro as well as in Tyk2-/- mice. Furthermore, expression of the Tyk2KD transgene in brown fat reverses the obese phenotype of Tyk2-/- animals. Treatment of cells with Jak-selective inhibitors suggests that the mechanism by which Tyk2KD functions to restore BAT differentiation is by dimerizing with kinase active Jak1 or Jak2. These results indicate that there are redundant mechanisms by which members of the Jak family can contribute to differentiation of BAT.
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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.