Shivangi Srivastava
Bristol-Myers Squibb, Memorial Sloan-Kettering Cancer Center, University of Houston
0000-0002-7971-5804
About
Highly motivated and driven drug discovery scientist interested in driving drug discovery in oncology, cardiovascular and immunology disease areas by performing high throughput screenings and designing in vitro assays.
• Extensive technical expertise in in-vitro cell viability and cell death assays, CRISPR screen, flow cytometry, protein-ligand interaction assays, xenograft mouse models, orthotopic survival surgery, and metabolomics pathway analysis tools.
• Organize panel discussions and career events on transitioning from academia to industry.
• Independent thinker with the ability to formulate scientific hypotheses.
• Excellent communication skills with teaching and mentorship experience.
Employment
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Bristol-Myers Squibb Scientist2022 - Present
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Memorial Sloan-Kettering Cancer Center Postdoctoral Fellow2021 - 2022
Education
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University of Houston PhD2015 - 2020
Projects & Funding
Projects & funding information is unavailable.
Publications (7)
- Discovery of Triazine-Based Toll-Like Receptor 9 Antagonists with Oral Activity. Save
- Discovery of Potent and Selective Reversible Ubiquitin-Like Modifier Activating Enzyme 5 Inhibitors Targeting the UFMylation Pathway. Save
- A Novel Liver X Receptor Inverse Agonist Impairs Cholesterol and Phospholipid Metabolism and Induces Apoptosis and Necroptosis in Pancreatic Ductal Adenocarcinoma Cells Save
- Novel Liver X Receptor Ligand GAC0001E5 Disrupts Glutamine Metabolism and Induces Oxidative Stress in Pancreatic Cancer Cells Save
- Screening of Focused Compound Library Targeting Liver X Receptors in Pancreatic Cancer Identified Ligands with Inverse Agonist and Degrader Activity Save
- Kinase-Inactivated EGFR Is Required for the Survival of Wild-Type EGFR-Expressing Cancer Cells Treated with Tyrosine Kinase Inhibitors Save
- Targeted reduction of the EGFR protein, but not inhibition of its kinase activity, induces mitophagy and death of cancer cells through activation of mTORC2 and Akt Save