CRISPR screen

SPARCS enables genome-wide CRISPR screening for spatial cellular phenotypes by combining laser microdissection with deep learning, identifying key genes involved in autophagosome formation.

CRISPR-Analytics provides a tool and pipeline for accurate gene editing analysis and simulation, improving precision in experimental design and results interpretation.

This study achieves near-perfect on-target gene editing in human hematopoietic stem and progenitor cells with high efficiency and minimal off-target effects.

This paper develops a synthetic niche to expand nephron progenitor cells, enabling organoid generation and CRISPR screening for kidney development and disease.

The paper introduces POMBOX, a toolkit for constructing genetic circuits in fission yeast, enabling modular assembly of multi-gene pathways and testing synthetic elements in metabolic engineering.

This paper develops a landing pad system for efficient multicopy gene integration in Issatchenkia orientalis using CRISPR-Cas9, enabling the construction of complex metabolic pathways with high integration efficiency.

The paper introduces MuRCiS, a CRISPRi-Seq method to identify gene combinations critical for virulence in L. pneumophila, finding that lpg2888 and lpg3000 have redundant roles in macrophages, while lpg3000 is essential in amoebae.

AMLdb is a multi-omics platform for AML research that identifies potential therapeutic targets, including five genes, with ENO1 as a novel candidate.

The paper compares four promoters in the CRISPR-Cas12a system in human cells, finding CAG provides the highest editing efficiency while CMV and EF1a offer higher specificity.

piCRISPR uses physically informed deep learning to predict CRISPR/Cas9 off-target cleavage, showing improved performance over existing methods by incorporating sequence context and chromatin accessibility.

CRISPRδ uses dCas13 to specifically block translation without affecting mRNA stability, achieving high gene knockdown specificity in mammalian cells.

The paper develops a CRISPRi-based single-cell screening approach to map non-coding regulatory elements to genes in primary human CD4+ T cells and demonstrates its utility for GWAS effector gene identification.

TransCRISPR designs sgRNAs targeting DNA motifs in user-provided genomic regions across 30 genomes, validated for disrupting MYC binding sites and affecting gene expression.

The paper identifies causal regulatory elements in complex genetic loci using CRISPR perturbations and shows that many causal variants lack classical epigenetic markers.

The paper identifies target genes and pathways of blood trait loci using CRISPR screens and single-cell RNA sequencing, revealing cis and trans regulatory effects of noncoding variants.

The paper identifies enhancer dependencies in MYC-intact and MYC-rearranged GCB-DLBCL using CRISPRi screens, revealing distinct regulatory mechanisms.

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 analyzes single-cell CRISPR perturbations to show enhancers act multiplicatively with limited evidence for epistatic interactions.

This paper combines CRISPR nucleases to simultaneously knock-in and base edit CAR T cells, reducing translocations to 1.5% and improving safety.

The paper constructs a mobile CRISPRi library in E. coli to study genetic interactions of essential genes by knocking down their expression and analyzing combined effects with non-essential gene deletions.

This paper develops CaRTRIDGE, a system using CRISPR-associated proteins to control mRNA translation, creating orthogonal switches and synthetic circuits in mammalian cells.

The paper designs a diffusion-based molecular communication system using synthetic genetic circuits and introduces a tool to optimize communication parameters for efficient cellular signal transmission.

The paper develops a CRISPR/Cas9-mediated knock-in method in African turquoise killifish for precise genomic modifications and cell-type-specific expression.

This paper develops a compact AAV-delivered dCas9-based repressor system for gene silencing, demonstrating its effectiveness in reducing ApoE expression in vitro and in vivo.

The paper uses base editor mutagenesis to identify activating DNMT3A mutations, revealing hyperactivating variants in the ADD domain that remain functional in the presence of a heterozygous R882H mutation.

The paper identifies enhancers linked to congenital heart defects that, when repressed, impair human cardiomyocyte differentiation.

The paper develops a pooled CRISPR activation screening platform in Drosophila cells to identify rapamycin resistance genes, finding three novel genes involved in RTK-Akt-mTOR pathway activation.

The paper introduces a PCR-RFLP method called PIM-RFLP to efficiently detect CRISPR-induced indels in cell clones and pools.

This paper describes a method to validate sgRNAs that generate RET and NTRK1 fusion oncogenes in murine models, demonstrating their efficacy in creating tumor models responsive to targeted therapies.

CRaTER enriches for on-target gene-edited cells in hiPSCs, enabling efficient generation of variant libraries for studying cardiomyopathy-associated mutations.