I am strongly interested in genetic basis of type 2 diabetes (T2D) and related metabolic traits. Specifically, I aim to elucidate biological processes implicated by large-scale genetic studies in light of the fact that most disease-associated genetic markers (i.e. SNPs) map to non-coding regions of the genome.
Currently, I am working as a joint member of the Gloyn and McCarthy labs to integrate epigentic maps of chromatin accessibility, regulatory state, and physical interactions with eQTL maps in order to elucidate genes and pathways mediating the effects of disease-promoting alleles in primary human islets and glucose-responsive beta cell lines. By leveraging high-performance computing in combination with advanced statistical methods, I aim to spotlight candidate genes and regulatory mechanisms that can be targeted in experimental validation studies and guide the discovery of novel therapies.
Loss of RREB1 in pancreatic beta cells reduces cellular insulin content and affects endocrine cell gene expression.
Mattis KK. et al, (2023), Diabetologia
Human genetics uncovers MAP3K15 as an obesity-independent therapeutic target for diabetes.
Nag A. et al, (2022), Sci Adv, 8
Multiancestry exome sequencing reveals INHBE mutations associated with favorable fat distribution and protection from diabetes.
Akbari P. et al, (2022), Nat Commun, 13
Genotyping, sequencing and analysis of 140,000 adults from the Mexico City Prospective Study
Ziyatdinov A. et al, (2022)
Multi-ancestry genetic study of type 2 diabetes highlights the power of diverse populations for discovery and translation.
Mahajan A. et al, (2022), Nat Genet, 54, 560 - 572