Postdoctoral Fellow, 2016 – 2019
Graduate Degree: University of Connecticut (Storrs, CT)
Gaurav’s Publications from the Sarosiek Laboratory:
Age-dependent regulation of SARS-CoV-2 cell entry genes and cell death programs correlates with COVID-19 severity.
Zintis Inde, Ben A. Croker (co-first author), Clarence Yapp, Gaurav Joshi, Johan Spetz, Cameron Fraser, Xingping Qin, Le Xu, Brian Deskin, Elisa Ghelfi, Gabrielle Webb, Aaron F. Carlin, Yangfei Peipei Zhu, Sandra Leibel, Aaron F. Garretson, Alex E. Clark, Jason M. Duran, Victor Pretorius, Laura E. Crotty-Alexander, Chendi Li, Jamie Casey Lee, Chhinder Sodhi, David J. Hackam, Xin Sun, Aaron Hata, Lester Kobzik, Jeffrey Miller, Jin-Ah Park, Douglas Brownfield, Hongpeng Jia, Kristopher A. Sarosiek.
Science Advances, August 18, 2021. PDF. PubMed.
Zintis Inde, Clarence Yapp, Gaurav Joshi, Johan Spetz, Cameron Fraser, Brian Deskin, Elisa Ghelfi, Chhinder Sodhi, David J. Hackam, Lester Kobzik, Ben A. Croker, Douglas Brownfield, Hongpeng Jia, Kristopher A. Sarosiek. Age-dependent regulation of SARS-CoV-2 cell entry genes and cell death programs correlates with COVID-19 disease severity (Preprint).
BioRxiv, September 13, 2020. PDF. BioRxiv.
HSF1 phase transition mediates stress adaptation and cell fate decisions.
Nature Cell Biology, 2020 Feb 03. Pubmed.
Safer-by-design Flame-Sprayed Silicon Dioxide Nanoparticles: The Role of Silanol Content on ROS Generation, Surface Activity and Cytotoxicity.
Particle and Fibre Toxicology, 2019 Oct 29. Pubmed.
My scientific interests include any thing and every thing cell death, oxidative stress, lysosomes, nanoparticles and microscopy. I joined the Sarosiek lab to further understand cell death processes and apply this knowledge to either induce cell death (in case of cancer) or inhibit cell death to prevent some of the disease pathologies. My particular interest is to characterize the intrinsic cell death pathway following lysosomal leakage.
I did my grad school at the University of Connecticut (not far from here) where I studied silica induced oxidative stress and cell death in alveolar macrophages. Silica is responsible for the fibrotic lung disease silicosis in workers exposed to silica dust over a long period of time in certain occupational settings. Using live cell imaging, I have tracked the fate of macrophages from silica particle uptake to death. We found that silica can generate reactive oxygen species independent of NADPH oxidases and cause phagolysosomal leakage to induce cell death. Further, there is heterogeneity in cell death, where in, most cells die by apoptosis whereas some by necrosis. Please check out some of the movies from my work:
During summers I like to bike (wouldn’t call myself a cyclist) and kayak. During winters, I enjoy exploring Boston.
Click here for my pubmed