Danwei Huangfu

This paper introduces Perturbscape, a framework that uses perturbation-induced gene programs to identify disease-relevant genes and pathways, showing higher heritability informativeness than steady-state approaches.

Open-source STAR binary for five transcriptomic assays runs 3.9- to 6.2-fold faster than Cell Ranger 9.0.1 for scRNA-seq and Perturb-seq, 17- to 41-fold for Flex, with closely concordant counts.

FourC identifies significant and differential contacts in 4C-seq data using a Bayesian model and Gaussian processes to address duplication and model spatial patterns.

The paper identifies pre-established chromatin regions in human ESCs that enable rapid activation of lineage-specific genes during differentiation.

The paper introduces pertTF, a transformer-based model for predicting genetic perturbation responses, showing improved performance in expression prediction and cell identity shifts across cellular contexts.

This paper develops a human organoid model of early PDAC that identifies genetic and epigenetic barriers to lineage plasticity, showing CDKN2A loss is essential with KRAS/TP53 mutations and TET1 suppression links ERK signaling to transcription factor silencing.

CausalGRN infers causal gene regulatory networks from single-cell CRISPR screens and predicts responses to unseen perturbations with improved accuracy.

This study uses a knockout village framework to analyze how mutations in diabetes genes alter pancreatic beta cell development, revealing non-canonical cell fate shifts and identifying ISL1 as a key regulator.

This study investigates the effects of a Dicer1 mutation on miRNA function, showing both loss and gain of miRNA activity through strand switching.

This study uses Perturb-seq to analyze how varying levels of pluripotency regulators affect hESC self-renewal and differentiation through single-cell RNA-seq.

The paper identifies two NANOG enhancers in human embryonic stem cells and shows their critical role in maintaining self-renewal and preventing differentiation.

This study develops a CRISPRa-based method to rapidly verify gene editing in human pluripotent stem cells without differentiation.

This study shows GATA6 regulates WNT and BMP programs in human precardiac mesoderm patterning, and modulating these pathways can rescue cardiomyocyte defects in GATA6 mutants.

ChromaFold predicts 3D chromatin contact maps from scATAC-seq data, outperforming bulk-based methods and enabling cell-type-specific interaction analysis.

The paper uses CRISPR-Cas9 screens to identify genes affecting stem cell fitness versus pluripotency identity, finding distinct and overlapping roles for chromatin and metabolic regulators.

The paper identifies a long-range enhancer for ONECUT1 involved in pancreatic differentiation and links a diabetes risk variant to disrupted transcription factor binding.

The paper introduces a method to quantify diverse perturbation responses and discover novel biological insights in single-cell perturbation datasets.

The paper uses a CRISPRi screen in hESC differentiation to identify enhancers with nonlinear regulatory activity, revealing a CTCF loop-constrained model for improved enhancer prediction.

This study identifies a Pold1 hypomorphic mutation in mice that causes reduced embryo size and morphogenetic defects during gastrulation, highlighting the need for coordinated growth and lineage specification.

The paper identifies HES1 target genes using ChIP-seq and RNA-seq in hESC lines, revealing HES1's role in pancreatic development through Notch pathway regulation and suppression of intestinal gene programs.