Junwei Shi

This study uses CRISPR-Cas9 to identify EZH2 mutations that reactivate fetal hemoglobin without compromising cell fitness, showing potential for treating sickle cell disease and beta-thalassemia.

The paper develops a CRISPRi platform to annotate functional enhancers in human T cells, identifying novel CREs and their regulatory roles in immune responses.

This study shows SS18-SSX sustains oncogenic transcription without needing SWI/SNF activity, identifies P300 as a critical co-factor, and demonstrates targeting P300 or SWI/SNF as therapeutic strategies.

This study identifies how histone modifications regulate gene expression in memory and exhausted CD8 T cells, revealing distinct epigenetic programs between these cell types.

This study identifies inflammatory memory as a mechanism for cancer resistance to immunotherapy and shows that combining JAK and TBK1 inhibitors can prevent it.

The paper introduces multiAsCas12a, an engineered CRISPR-Cas12a variant enabling higher-order combinatorial chromatin perturbations, and demonstrates its use in discovering new enhancer elements and dissecting cis-regulatory element functions.

This study shows that DIMT1's non-catalytic function is essential for AML proliferation and identifies a target region for therapeutic intervention.

The paper identifies ZNF410 as a highly specific transcriptional activator in erythroid cells that regulates CHD4 and fetal hemoglobin expression.