Ling Hao

The paper develops a platform to measure protein turnover in human iPSC-derived neurons, revealing conserved and subtype-specific proteome dynamics.

This paper optimizes a secretome proteomics platform for iPSCs and applies it to study progranulin deficiency's effects on extracellular and intracellular proteomes.

The paper identifies TMEM106B fibril accumulation as a shared mechanism in neurodegeneration linked to genetic variants in TMEM106B and GRN.

This study identifies the CC2D1A interactome in human neurodevelopmental disorders, revealing synaptic roles and novel interactions in the brain.

The paper identifies BORC as a modifier of TDP-43 protein levels in neurons, showing lysosome transport is required for TDP-43 turnover.

The paper identifies CHIP-mediated microautophagy as a protective mechanism against lysosomal damage caused by CLN4 mutations, showing its therapeutic potential in neurodegenerative diseases.

The paper introduces ContamSPOT, a method to detect and remove trace contaminants in mass spectrometry samples using TLC plates, improving data quality and instrument longevity.

This study uses proteomic techniques to show that PGRN deficiency impairs lysosomal function and proteostasis in neurons by altering pH, enzyme levels, and protein turnover.

This study develops universal protein contaminant libraries for DDA and DIA proteomics to reduce false discoveries and improve protein identification without affecting quantification accuracy.

This study integrates proteomic and metabolomic analyses of patient-derived fibroblasts to identify dysregulated pathways in MELAS, revealing OXPHOS defects and arginine biosynthesis downregulation.

The paper develops and evaluates a proximity labeling method to study the endolysosomal proteome in human neurons, showing improved data normalization and complementary coverage compared to overexpression approaches.