Yansheng Liu

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

The paper introduces aaRSID, an engineered pyrrolysyl-tRNA synthetase for proximity labeling, improving upon existing tools by reducing background and enabling multiplexed proteomics.

The paper shows that METTL3 phosphorylation by CDK1 promotes transcriptional elongation and cell cycle progression through the m6A/7SK/P-TEFb axis.

The paper introduces a multi-omics framework to analyze protein activity in context-specific networks, demonstrating its utility in linking molecular profiles to phenotypic outcomes using HeLa and Kyoto cell lines.

This study identifies Fibulin-2 as a matrix cue that transduces fibrotic ECM remodeling into mitochondrial metabolic reprogramming in kidney fibrosis.

The paper examines the molecular effects of seven KRAS mutant variants in pancreatic cancer cells and finds that baseline cellular state, not allele identity, primarily drives molecular variation.

This study shows that acute Pum1/2 degradation in mouse ESCs reveals a biphasic post-transcriptional regulatory network affecting pluripotency and lineage decisions.

This study identifies Mfap2 as a key ECM component that regulates kidney repair by linking mechanical cues to metabolic reprogramming through Esr2-mediated transcriptional control.

This study identifies a shared trans-acting mechanism in splicing factor mutant cancers that drives retained intron (RI) splicing defects through DDR-induced AMPK-AKT imbalance and SRSF1 hypophosphorylation.

The paper identifies phenotype-specific signaling networks in glioblastoma cells, showing that invasive spread is linked to DNA damage response and AKT-mTOR activation, with 14-3-3 proteins mediating phosphorylation and predictive phospho-site signatures for patient survival.

This study shows PI3K promotes resistance to KRAS inhibition in PDAC by activating wild-type RAS signaling through GAB1 recruitment and MAPK activation.

This study identifies NAT10 as a master regulator of brain metastasis through an in vivo shRNA screen and shows its role in promoting tumor growth and metastasis via downstream effectors.

Alzheimer's mouse model proteomes capture 30% (amyloid-only models) to 42% (adding tau and splicing models) of consensus human AD protein changes; in 5xFAD, plaques slow degradation of plaque-associated proteins.

This study identifies Chk2 as a regulator of PLK1 activity during mitosis, showing its role in preventing chromosome segregation errors and genome instability.

This paper introduces a platform for high-throughput extraction of membrane proteins into native nanodiscs while preserving their local membrane context and provides a database for optimized extraction conditions.

The paper identifies Master Protein abundance Regulators (MaPRs) across ten cancer types using a computational pipeline, finding they mediate up to 79% of post-transcriptional regulatory networks and predict tumor proteomic subtypes more accurately.

This study introduces a robust multiplex DIA-MS workflow with machine learning and statistical filtering to profile protein turnover in cisplatin-resistant cancer cells, revealing correlations between transcript regulation and protein degradation.

The paper presents Turnover-PPT, a resource mapping protein and phosphoprotein turnover across mouse tissues and brain regions, revealing tissue-specific protein lifetimes and phosphorylation's impact on stability.

This study shows that atrial AMPK deletion shifts metabolism from fatty acid oxidation to pyruvate oxidation and disrupts metabolic pathways, contributing to atrial remodeling and arrhythmia.

This study introduces PulsPhos, a method to quantify site-specific phosphorylation lifetimes in living cells and applies it to pharmacological perturbations.

The paper uses phosphoproteomic time-series data and the VESPA algorithm to analyze drug resistance mechanisms in colon cancer cells, revealing adaptive signaling rewiring confirmed by CRISPRko assays.

The paper shows that m6A methylation of 7SK RNA promotes transcriptional activity in response to growth factor stimulation by releasing the HEXIM1/P-TEFb complex.

This study investigates how 7q11.23 CNVs affect protein synthesis and neuronal excitability in neurodevelopmental disorders using patient-derived neurons and multi-omics approaches.

The paper quantifies proteomic and phosphoproteomic layers in mammalian fibroblasts to show transcriptome-proteome co-evolution and variability control across species.

This study uses DIA-MS to profile proteomes and phosphoproteomes of melanoma cell lines, revealing proteotype determinants and validating DIA-MS as a competitive method.

BoxCarmax improves DIA-MS analysis of protein turnover and complex samples by enhancing quantitative accuracy in SILAC and pSILAC experiments.

SECAT quantifies differential protein-protein interaction states across cellular states by analyzing PPI networks, showing improved scalability and effectiveness over previous methods.

The paper introduces DeltaSILAC, a proteomic method to quantify how phosphorylation affects protein endurance in cancer cells, revealing its global impact on protein turnover and identifying sequence features associated with endurance changes.

The paper quantifies proteome assembly state changes during mitosis using SEC-SWATH-MS and identifies new mitotic complex disassembly events.

This study uses DIA-MS to rapidly assess proteomic changes after CRISPR-mediated HMGN1 knockout in cancer cells, identifying 147 significantly altered proteins and their functional impacts.