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  • QKI regulates adipose tissue metabolism by acting as a brake on thermogenesis and promoting obesity.

QKI regulates adipose tissue metabolism by acting as a brake on thermogenesis and promoting obesity.

EMBO reports (2019-12-24)
Huanyu Lu, Zichen Ye, Yue Zhai, Li Wang, Ying Liu, Jiye Wang, Wenbin Zhang, Wenjing Luo, Zifan Lu, Jingyuan Chen
ABSTRACT

Adipose tissue controls numerous physiological processes, and its dysfunction has a causative role in the development of systemic metabolic disorders. The role of posttranscriptional regulation in adipose metabolism has yet to be fully understood. Here, we show that the RNA-binding protein quaking (QKI) plays an important role in controlling metabolic homeostasis of the adipose tissue. QKI-deficient mice are resistant to high-fat-diet (HFD)-induced obesity. Additionally, QKI depletion increased brown fat energy dissipation and browning of subcutaneous white fat. Adipose tissue-specific depletion of QKI in mice enhances cold-induced thermogenesis, thereby preventing hypothermia in response to cold stimulus. Further mechanistic analysis reveals that QKI is transcriptionally induced by the cAMP-cAMP response element-binding protein (CREB) axis and restricts adipose tissue energy consumption by decreasing stability, nuclear export, and translation of mRNAs encoding UCP1 and PGC1α. These findings extend our knowledge of the significance of posttranscriptional regulation in adipose metabolic homeostasis and provide a potential therapeutic target to defend against obesity and its related metabolic diseases.

MATERIALS
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Product Description

Sigma-Aldrich
Anti-QKI antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
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