Sudharshan  Ravi

Sudharshan Ravi, Dr.

Post-Doctoral Research Associate

Social Genomics

Tel.: 044 634 06 68

Raumbezeichnung: AND 4.14

sudharshan.ravi@jacobscenter.uzh.ch

Sudharshan Ravi received his doctoral degree in Chemical and Bioengineering from the Swiss Federal Institute of Technology (ETH) Zurich where his research focused on the investigation of metabolic networks and its application in understanding the biology of human aging. Through the development of algorithms designed to predict metabolic perturbations with the incorporation of differential transcriptomic data, his work shed light on the transcriptional roadmap of events in the aging and neurodegenerative processes. His research interests include integrative omics analysis, systems biology, and bioinformatics particularly in human diseases. As a post-doctoral research associate at the Jacobs Center, he studies the impact of socio-economic gradients on gene expression in humans and macaques, and its implications in phenotypical modulations.

Prior to his doctoral work, he had attained his bachelor’s degree in industrial biotechnology in 2012. He had researched on breast cancer chemotherapy tolerance during his time at the Harvard – MIT HST (Health Science and Technology) collaborative program before moving to Switzerland to complete his master’s degree in Chemical and Bioengineering from ETH, Zurich in 2015. 

Research Interests

  • Integrative omics
  • Systems Biology
  • Metabolic network analysis
  • Bioinformatics

Publications

  • Ravi S, Gunawan R. ΔFBA—Predicting metabolic flux alterations using genome-scale metabolic models and differential transcriptomic data. PLoS Comput Biol 17(11): e1009589 (2021). https://doi.org/10.1371/journal.pcbi.1009589
  • Teo E, Ravi S, Barardo D, et al. Metabolic stress is a primary pathogenic event in transgenic Caenorhabditis elegans expressing pan-neuronal human amyloid beta. Elife 8:e50069 (2019). https://doi.org/10.7554/eLife.50069
  • Goldman A, Majumder B, Dhawan A, Ravi S, et al. Temporally sequenced anticancer drugs overcome adaptive resistance by targeting a vulnerable chemotherapy-induced phenotypic transition. Nat Commun 6, 6139 (2015). https://doi.org/10.1038/ncomms7139