Luke A. Gilbert

State, a set-based transformer trained on over 100 million perturbed cells, predicts perturbation responses in new cellular contexts better than mean, linear and deep learning baselines.

This paper develops a virus-like particle-based system for CRISPR gene editing and screening in primary human myeloid cells, identifying TNFAIP3 as a key regulator of inflammatory polarization.

This study identifies FBXO42's role in regulating PPP4C and p53 signaling, showing its importance in cancer cell survival through genetic and proteomic analyses.

This study identifies a multi-subunit autophagic capture complex that degrades ER-stalled MHC-I in pancreatic cancer, reducing immunogenicity.

This paper identifies BisRoc, a dimeric rocaglate ligand that suppresses translation more potently and specifically than monomeric RocA by promoting multivalent eIF4A-RNA assembly.

ProPer-seq is a cost-effective, barcode-free single-cell perturbation profiling method that enables scalable analysis of synthetic biology perturbations and reveals transcriptional control principles.

The paper identifies cis-regulatory elements and transcription factors controlling FOXP3 expression in human Tregs and Tconvs, revealing mechanisms that restrict FOXP3 to Tregs in mice.

This study engineers recombinases to improve DNA insertion efficiency and specificity in human cells, achieving 53% integration and 97% genome-wide specificity.

This study uses CRISPR screens to identify PTGES3 as a novel modulator of AR protein levels and function in prostate cancer, showing its role in therapy resistance.

This study identifies a dependency on lysosomal exocytosis in FA pathway-deficient cells and tumors, revealing a new therapeutic target for FA-related cancers.

The paper shows that ecDNA-borne PVT1 fusions stabilize oncogenic mRNAs by interacting with SRSF1, enhancing RNA stability and supporting MYC dependency in cancer.

The paper introduces COMET, a high-throughput screening platform for identifying transcriptional modulators by testing combinatorial dCas9-based fusion proteins, and finds over 5800 significant hits that modulate transcription.

This study uses in vivo perturb-seq to analyze gene function and radiotherapy responses in glioblastoma by targeting cancer and microenvironment cells.

The paper identifies 245 putative RNA structural switches in the human transcriptome using a computational and experimental approach, validates one with DMS-MaPseq and cryo-EM, and shows its regulation by trans factors and nonsense-mediated decay.

The paper quantifies RNA flow across subcellular compartments using TimeLapse-seq and identifies factors influencing mRNA life cycles.

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.

The paper quantifies how human gene functional connections change under environmental stress, revealing large-scale rewiring of genetic interactions across different conditions.

This paper develops compact CRISPRi sgRNA libraries and optimal effectors to improve knockdown consistency and efficiency in mammalian cells.

This paper compares prime editing efficiency to conventional methods in human pluripotent stem cells, showing higher efficiency with optimized mRNA delivery for mutation correction and introduction.

The paper develops a data integrator to uncover synthetic lethality, sex disparity, and immunotherapy targets in cancer by combining public and custom datasets.

The paper identifies a common genetic architecture that explains context-specific gene essentiality across cell lines using CRISPR screens and machine learning.

The paper explores genetic interaction manifolds using rich phenotypes from Perturb-seq to classify and mechanistically understand genetic interactions.

The paper identifies genetic modifiers of cell growth in response to a PCSK9 translational inhibitor and reveals their roles in ribosome quality control.