Brandon Desousa

Brandon Desousa, Kampmann lab

[email protected]
Graduate student, BMS
Joint with the Jain Lab



  • PhD Student, UCSF Biomedical Sciences Graduate Program
  • B.S. in Biochemistry and Molecular Biology, Neuroscience, University of Miami


Research Experience

  • Divakaruni Lab, Dept. of Molecular and Medical Pharmacology, UCLA (2017-2019)
    • Development of extracellular flux-based assays for quantifying cellular ATP production rates
    • Application of respirometry and stable isotope tracing towards understanding changes in immune and cancer cell substrate utilization
  • Bullock Lab, The Miami Project Project to Cure Paralysis (2014-2017)
    • Development of stem cell-based therapies for treating penetrating traumatic brain injuries
    • Understanding a role for astrocyte transdifferentiation in recovery from brain injury



  • Kerr N., García-Contreras M., Abbassi S., Mejias N.H., Desousa B.R., Ricordi C., Dietrich W.D., Keane R.W. and de Rivero Vaccari J.P. (2018) Inflammasome Proteins in Serum and Serum-Derived Extracellular Vesicles as Biomarkers of Stroke. Front. Mol. Neurosci. 11:309. doi: 10.3389/fnmol.2018.00309
  • Divakaruni, A. S., Hsieh, W. Y., Minarrieta, L., Duong, T. N., Kim, K. K. O., Desousa, B. R., … Murphy, A. N. (2018). Etomoxir Inhibits Macrophage Polarization by Disrupting CoA Homeostasis. Cell Metabolism.
  • Veliova, M., Ferreira, C.M., Benador, I.Y., Jones, A.E., Desousa, B.R., Mahdaviani, K., Acín-Pérez, R., Petcherski, A., Divakaruni, A.S., Corkey, B.E., Liesa, M., Oliveira, M.F., Shirihai, O.S. (2019) Inhibition of the mitochondrial pyruvate carrier increases energy expenditure in brown adipocytes by activating lipid cycling. BioRxiv


Research Interests

Mitochondrial dysfunction is a common hallmark across a myriad of neurodegenerative conditions, including but not limited to Parkinson’s Disease and Leigh’s Syndrome. While mitochondrial dysfunction has been implicated as a key driver of disease etiology, it is still unclear as to which mitochondrial processes are primarily affected. Interestingly, a select subset of mitochondrial disease genes (both mitochondrial and nuclear encoded) appear to be responsive to hypoxia therapy. I hope to leverage the power of functional genomics to pinpoint mitochondrial disease states that are receptive to hypoxia therapy, as well as uncover the mechanism for hypoxia rescue. Additionally, I hope to understand how the intersection of mitochondrial biology and oxygen metabolism influences neuronal and glial cell biology.


Other Interests

Coffee, tacos, B-movies, video games