SEP 27, 2017 10:30 AM PDT
Combining Seahorse XF analysis with stable isotope tracing to reveal novel drug targets for metabolic and neurodegenerative disease
Presented at the Cell Biology 2017 Virtual Event
SPONSORED BY: Agilent Technologies
CONTINUING EDUCATION (CME/CE/CEU) CREDITS: P.A.C.E. CE | Florida CE
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Speakers:
  • Assistant Professor, Molecular and Medical Pharmacology, University of California Los Angeles (UCLA)
    Biography
      Dr. Ajit Divakaruni joined the faculty of the University of California, Los Angeles in January 2017 as an Assistant Professor of Molecular and Medical Pharmacology. He earned his B.S. (summa cum laude) from the University of Arizona in 2006 with a triple-major (Honors) in Biochemistry, Molecular Biology, and Applied Mathematics. He subsequently attended graduate school at University of Cambridge on a Marshall Scholarship and NSF Graduate Research Fellowship. He conducted his doctoral research under the supervision of Dr. Martin Brand at the MRC Mitochondrial Biology Unit, studying the efficiency of oxidative phosphorylation and its regulation by mitochondrial uncoupling proteins (UCPs). In late 2011, he moved to the University of California, San Diego as a Seahorse Postdoctoral Fellow under Dr. Anne Murphy in the Department of Pharmacology, with a focus on developing mitochondrial proteins as therapeutic drug targets. He has a longstanding interest in assay development using the Agilent Seahorse XF Analyzer, and has authored over 20 peer-reviewed manuscripts using the technology.

    Abstract:

    To study cell metabolism, our laboratory has found it exceedingly informative to integrate Agilent Seahorse XF Analyzers with mass spectrometry-based measurements of metabolomics and stable isotope tracing to fully reveal metabolic changes in response to drug candidates.  This seminar will discuss how merging quantitative, rate-based measurements of oxygen consumption with detailed pathway analysis using mass spectrometry have revealed the mitochondrial pyruvate carrier (MPC) as a central regulator of metabolic flexibility. Metabolic flexibility is the ability of cells to fuel energy metabolism and biosynthesis with multiple nutrients, and its loss is associated with disease pathogenesis in contexts as varied as type 2 diabetes, cardiac dysfunction, neurodegeneration, and certain cancers. 

    For Research Use Only. Not for use in diagnostic procedures. 


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