Jesse M. Engreitz

1 month ago | cell.com | Gabriella E Martyn |Michael Montgomery |Hank Jones |Katherine Guo |Benjamin Doughty |Johannes Linder | +14 more

1Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA 2Basic Science and Engineering Initiative, Stanford Children’s Health, Betty Irene Moore Children’s Heart Center, Stanford, CA 94305, USA 3Calico Life Sciences LLC, South San Francisco, CA 94080, USA 4Department of Genitourinary Medical Oncology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA 5Department of Genomic Medicine, The University of Texas...

Mar 19, 2024 | nature.com | David Yao |Josh Tycko |Lexi R. Bounds |Benjamin Doughty |Alexander White |Xingjie Ren | +16 more

AbstractThe ENCODE Consortium’s efforts to annotate noncoding cis-regulatory elements (CREs) have advanced our understanding of gene regulatory landscapes. Pooled, noncoding CRISPR screens offer a systematic approach to investigate cis-regulatory mechanisms. The ENCODE4 Functional Characterization Centers conducted 108 screens in human cell lines, comprising >540,000 perturbations across 24.85 megabases of the genome.

Feb 7, 2024 | nature.com | Jesse M. Engreitz

Nov 20, 2023 | nature.com | Sarasa Isobe |Rebecca Harper |Jakob Körbelin |Jesse M. Engreitz |Michael Snyder |Shoichiro Otsuki | +2 more

AbstractPulmonary arterial hypertension (PAH) is a progressive disease in which pulmonary arterial (PA) endothelial cell (EC) dysfunction is associated with unrepaired DNA damage. BMPR2 is the most common genetic cause of PAH. We report that human PAEC with reduced BMPR2 have persistent DNA damage in room air after hypoxia (reoxygenation), as do mice with EC-specific deletion of Bmpr2 (EC-Bmpr2-/-) and persistent pulmonary hypertension.

Jul 13, 2023 | nature.com | Jacob C. Ulirsch |Masahiro Kanai |Francois Aguet |Taibo Li |Aviv Regev |Jesse M. Engreitz

AbstractGenome-wide association studies (GWASs) are a valuable tool for understanding the biology of complex human traits and diseases, but associated variants rarely point directly to causal genes. In the present study, we introduce a new method, polygenic priority score (PoPS), that learns trait-relevant gene features, such as cell-type-specific expression, to prioritize genes at GWAS loci.