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New Collaborative Publication from the Kazak Lab

Prof. Lawrence Kazak's lab, Department of Biochemistry, just published an article entitled "ADRA1A-G鈲簈 signalling potentiates adipocyte thermogenesis through CKB and TNAP" in the journal Nature Metabolism, on a project led by postdoctoral fellow Janane Rahbani.

What would you highlight as the most important finding of this paper?

The conventional view of adipocyte thermogenesis activation is through adrenergic receptor (encoded by ADRB3) stimulation, signaling through cyclic AMP, and thermogenesis by uncoupling protein 1 (UCP1). We find that activation of the alpha-adrenergic receptor (encoded by ADRA1A) potentiates thermogenesis by the cyclic AMP-UCP1 axis by triggering a parallel pathway of thermogenesis called the Futile Creatine Cycle.

How is this finding helping to advance the science of cancer?

Since thermogenesis requires the combustion of metabolic fuels, activating brown fat thermogenesis may compete for nutrients that cancer cells use to promote their proliferation.

What other institutions did you collaborate with on this study?

We had many collaborators for this project: the University of Birmingham, the University of Pennsylvania, the University of Copenhagen, the Maine Medical Center Research Institute, the Joslin Diabetes Center at Harvard Medical School, the Beth Israel Deaconess Medical Center at Harvard Medical School, the University of California, Davis, the Washington University School of Medicine, Rutgers University, the Johns Hopkins University School of Medicine, the National Institute of Diabetes and Digestive and Kidney Diseases at the National Institute of Health, and Aarhus University.

Read the full article:听

Disclaimer: This article was originally published on the website of the听Rosalind and Morris Goodman Cancer Institute.

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