Shaonil Binti

This study uses middle-down phosphoproteomics to analyze how protein partitioning into biomolecular condensates changes under proteostatic stress, revealing phosphorylation-dependent and independent mechanisms.

The paper investigates the differential stability of cardiac protein isoforms using proteogenomics and heavy water-based turnover analysis in mouse hearts, revealing widespread stability differences.

The paper identifies widespread isoform usage shifts in fetal and postnatal mouse hearts using proteome-wide ratio quantification, revealing novel isoform switches and evolutionary patterns.

The paper identifies catp-1 as a suppressor of molting defects in nekl-2; nekl-3 mutants in C. elegans, suggesting it modulates membrane trafficking by altering electrochemical gradients.

This study identifies novel functions of the conserved phosphatase PTPN-22 in C. elegans, showing its role in molting, cell adhesion, and cytoskeletal regulation through genetic and proteomic analyses.

This paper identifies ADM-2 as a negative regulator of molting in C. elegans, showing it inhibits molting by regulating LRP-1 and endocytic trafficking.

The paper shows that transitioning through the L2d stage can rescue molting defects in C. elegans with reduced NEKL function by restoring transcriptional defects associated with molting.