Ke Ding

The paper identifies a dynamic stem cell state marked by Panx3 that responds to environmental cues and enables regeneration in aged and osteoarthritic joints.

This study modifies a molecule to create two variants with different target selectivity, showing how small structural changes can control degradation activity.

This study identifies a stress-lipid kinase axis in NEPC driven by PIKfyve, revealing a synthetic vulnerability between PIKfyve and FASN that can be exploited for therapeutic targeting.

This study identifies TRIB2 as a therapeutic target in AML by demonstrating that its degradation via PROTACs and small molecules can reverse chemoresistance and enhance chemotherapy efficacy.

The paper benchmarks large language models for cell-type and gene set annotation using AnnDictionary, finding high accuracy in cell-type annotation and strong functional gene set recovery.

This study identifies PIKfyve as a targetable vulnerability in pancreatic cancer by showing its role in lipid metabolism and synthetic lethality with KRAS-MAPK inhibitors.

This study shows CDK12 loss drives prostate cancer development and identifies CDK13 as a therapeutic target through paralog-based synthetic lethality in CDK12-mutant tumors.

This study identifies NSD2 as a critical component of the AR neo-enhanceosome in prostate cancer, showing its role in AR enhancer circuitry and tumor progression.

The paper introduces Translatomer, a transformer model that predicts cell-type-specific translation from mRNA and sequence data, identifies disease variants affecting translation, and reveals non-eQTL regulatory mechanisms.