Ping Zhang

The maps of human genetic variants that associate with disease susceptibility allow us to generate and test biological hypotheses. Emerging evidence suggests that causal variants underlying disease susceptibility often function through regulatory effects on the transcription of target genes. However, there are challenges in harnessing of susceptibility loci for drug target identification and therapeutic application, including limitations in (i) exposition of causal variants within susceptibility loci, (ii) understanding of the specific affected genes and pathways that are therapeutically targetable, and (iii) mechanistic insights into their influence on cellular behaviours and clinical outcomes.

My current research is centered on identifying and characterizing regulatory variants modulating extreme innate immune response phenotypes in order to gain insights into the causal alleles driving heterogeneity of pathogenesis in sepsis and other diseases caused by immune dysfunction. The research combines bioinformatics, high-throughput CRISPR screening and multi-omics approaches to study variants in disease relevant cells and iPSC-derived models.

I am a molecular biologist by training with postdoctoral experience in bioinformatics and statistical analysis. I did my doctoral thesis at the Karlsruhe Institute of Technology and obtained my PhD in molecular biology from Ruprecht-Karls-Universität Heidelberg studying evolutionarily conserved regulators of the tumor suppressor p53/Mdm2 circuit. During my time in Oxford, I worked in genetics and genomics at the Ludwig Institute for Cancer Research investigating how germline and somatic genetic variants in the p53 pathway genes interact to affect cancer risk, progression and drug response.