Mitchell J. Weiss

This study identifies conventionally and unconventionally secreted proteins from HUVECs under inflammatory stress, revealing novel UCPS cargo and their functional roles.

This study identifies a BACH2-NRF2 axis regulating fetal hemoglobin activation through genetic and functional analyses in a large multi-ancestry cohort.

The paper compares transcriptomes and chromatin accessibility in MEP, ERY, and MEG cells to reveal divergence in gene regulation during differentiation.

This study develops a genome-edited autologous CD34+ cell therapy to induce fetal hemoglobin for sickle cell disease, showing efficient editing, therapeutic HbF levels, and no off-target effects.

This study identifies conserved and species-specific cis-regulatory elements in human and mouse blood cells using integrative epigenomic analysis and clustering.

This paper shows that CRISPR-Cas9-induced DNA breaks can lead to chromothripsis, a catastrophic chromosomal rearrangement, which is an on-target toxicity in genome editing.

This study uses proteomics to analyze dynamic phospho-signaling networks in human erythropoiesis, identifying key regulatory mechanisms and markers across differentiation stages.

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

The paper integrates epigenomic and transcriptomic data from mouse hematopoiesis to identify regulatory elements and their dynamics across cell types.

The paper integrates GATA transcription factors and epigenomes in mouse hematopoietic cells using IDEAS to map regulatory landscapes and identify candidate cis-regulatory elements.

Rapamycin alleviates β-thalassemia by stimulating ULK1-dependent autophagy of toxic free α-globin.