Charles A. Gersbach

The paper uses CRISPR-based functional genomics to identify noncoding regulatory elements and variants affecting schizophrenia-associated gene expression.

This study quantifies intrinsic dCas9-DNA recognition using TANGO, identifying key factors affecting gRNA performance and revealing new aspects of dCas9 specificity.

The paper identifies multi-enhancer regulatory hubs critical for Th17 cell identity by analyzing chromatin accessibility and enhancer function in mouse CD4+ T cell subsets.

FRACTEL improves power and replication in CRISPR screens by analyzing region-level effects and informing experimental design.

The paper identifies transcription factor collaborations that shape CD8+ T cell states and demonstrates how engineering these interactions can influence cell fate for therapeutic applications.

This paper shows that astrocytes reprogram neuronal gene expression and chromatin accessibility, affecting thousands of genes and regulatory elements, including those linked to schizophrenia and Alzheimer's disease.

The paper identifies a CRISPRa gRNA with broad off-target activity that enables genome-wide transcriptional reprogramming, showing that mismatch tolerance and PAM-proximal bases determine binding specificity.

This study identifies hundreds of new cis-regulatory element-gene connections in the MHC locus using CRISPR screens and single-cell transcriptomics, revealing cell type-specific regulatory mechanisms.

DeltaNMF improves differential gene program discovery in case-control studies by separating baseline and case-specific programs using a two-stage neural NMF framework.

The paper identifies SMARCA2 as a critical cofactor for a subset of glucocorticoid response genes in A549 cells through a CRISPR screen and functional analysis.

The paper introduces CRISPR-rabies virus (CRV) to enable precise circuit-level gene modulation in neurons, demonstrating its ability to regulate synaptic transmission in the hippocampus.

This study identifies RELB as a key regulator that enhances TIL expansion and function, improving adoptive cell therapy for solid tumors.

The paper identifies transcription factors for reprogramming human astrocytes to neurons using CRISPRa screens and scRNA-seq, showing INSM1's broad neurogenic activity and cofactor interactions.

The paper identifies mechanoenhancers that regulate transcription in response to matrix stiffness and shows their potential for reprogramming cellular responses to mechanical cues.

The paper identifies a gene regulatory element that modulates MYH6 expression and influences cardiomyocyte response to stress.

The paper develops CLEANSER, a model to filter ambient gRNAs in single-cell CRISPR screens, improving gRNA-cell assignment accuracy and differential gene expression analysis.

The paper uses CRISPR-based epigenome editing to activate the silenced maternal SNRPN gene in PWS iPSCs, showing that DNA demethylation can lead to stable expression.

This paper introduces a CRISPRi system using dHyperLbCas12a for highly multiplexed epigenome editing and demonstrates its application in proliferation and CRE analysis screens.

This paper introduces launch-dCas9, a machine learning framework to predict guide RNA effects in CRISPR epigenome editing, showing high accuracy and improved gRNA selection.

The paper uses CRISPR screens to identify transcriptional and epigenetic regulators of human CD8 T cell function, finding BATF3 as a key gene that enhances memory T cell features and improves CAR T cell therapy outcomes.

The paper reports 109 non-coding CRISPR screens analyzing 13.3Mb of the genome, identifies CRE-gene links, and provides guidelines and tools for screening non-coding regulatory elements.

The paper develops a proximity proteomics method in mice to identify protein interactions relevant to autism, revealing new genetic risk factors and functional interactions.

The paper screens non-coding regulatory elements in human cells to identify those affecting cell fitness and establishes connections between regulatory elements and target genes.

This paper describes the generation of two transgenic mouse lines for in vivo epigenome editing using CRISPR-based systems to activate or repress gene expression.

The paper identifies enhancer-gene regulatory links using eRNAs and shows their functional importance in neuronal systems.

The paper quantifies incomplete gene expression and chromatin accessibility changes during MyoD-induced transdifferentiation of human fibroblasts into myoblasts, linking chromatin remodeling deficiencies to incomplete reprogramming.