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DEC1 negatively regulates AMPK activity via LKB1
Fuyuki Sato1, Yasuteru Muragaki2, Yanping Zhang3
1Department of Radiation Oncology and Lineberger Comprehensive Cancer Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA; Department of Pathology, Wakayama Medical University School of Medicine, Wakayama 641-8509, Japan.
Biochemical and Biophysical Research Communications
|October 27, 2015
Summary
Basic helix-loop-helix transcription factor DEC1 negatively regulates AMP-activated protein kinase (AMPK) activity. DEC1 impacts liver circadian rhythms by controlling LKB1, influencing metabolic processes and cell death.
Area of Science:
- Chronobiology
- Molecular Biology
- Metabolic Regulation
Background:
- Circadian rhythms govern physiological processes, including clock genes like DEC1.
- AMP-activated protein kinase (AMPK) is crucial for metabolism and cell death, exhibiting its own circadian rhythm.
- Mechanisms linking DEC1 and AMPK circadian rhythms remain largely unknown.
Purpose of the Study:
- To investigate the direct correlation between DEC1 expression and AMPK activity.
- To elucidate the regulatory role of DEC1 in the circadian rhythm of AMPK activity.
Main Methods:
- Analyzing circadian rhythms of DEC1 and AMPK in mouse liver.
- Manipulating DEC1 expression (knockdown and overexpression) and assessing its impact on AMPK activity.
- Investigating DEC1 binding to the LKB1 promoter and its effect on LKB1 activity and levels.
Main Results:
- DEC1 protein and AMPK activity exhibit distinct circadian rhythms in mouse liver.
- DEC1 knockdown enhances AMPK activity; DEC1 overexpression reduces it.
- DEC1 binds to the LKB1 promoter, decreasing LKB1 activity and protein levels, indicating an inverse relationship with AMPK activity.
Conclusions:
- DEC1 negatively regulates AMPK activity through modulation of LKB1.
- DEC1 plays a role in the circadian control of metabolic pathways via the LKB1-AMPK axis.
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