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Assaying Protein Kinase Activity with Radiolabeled ATP
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PAS kinase is required for normal cellular energy balance.

Huai-Xiang Hao1, Caleb M Cardon, Wojtek Swiatek

  • 1Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.

Proceedings of the National Academy of Sciences of the United States of America
|September 20, 2007
PubMed
Summary

PAS kinase (PASK) deletion protects against metabolic syndrome by improving cellular energy homeostasis. PASK deficiency in mice prevented high-fat diet-induced obesity and insulin resistance, highlighting PASK as a therapeutic target.

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Area of Science:

  • Metabolic disease research
  • Cellular metabolism
  • Endocrinology

Background:

  • Metabolic syndrome, characterized by obesity and diabetes, poses a significant global health challenge.
  • It stems from impaired cellular sensing and response to metabolic signals.
  • PAS kinase (PASK) is a key cellular metabolic sensor.

Purpose of the Study:

  • To investigate the role of PAS kinase (PASK) in metabolic disease pathogenesis.
  • To elucidate the function of PASK as a cellular metabolic sensor.
  • To evaluate PASK deficiency as a potential therapeutic strategy for metabolic disorders.

Main Methods:

  • Utilized PASK knockout (PASK(-/-)) mice to study metabolic phenotypes.
  • Analyzed tissue-specific metabolic changes in PASK(-/-) mice.
  • Examined cellular metabolic rates and ATP production in cultured cells.

Main Results:

  • PASK(-/-) mice displayed impaired glucose-stimulated insulin secretion, altered liver triglyceride storage, and increased skeletal muscle metabolic rate.
  • PASK deletion conferred significant protection against high-fat diet-induced obesity and insulin resistance.
  • Cultured cells lacking PASK showed increased oxidative metabolism and ATP production.

Conclusions:

  • PASK plays a crucial role in maintaining cellular energy homeostasis.
  • PASK acts in a cell-autonomous manner to regulate metabolic responses.
  • Targeting PASK presents a promising therapeutic avenue for metabolic diseases like obesity and insulin resistance.