Hanwen Zhang

This study examines how different SETD1A mutations and genetic backgrounds affect human hippocampal neurons derived from hiPSCs, revealing divergent molecular and cellular phenotypes and contrasting mutation impacts.

The paper identifies context-specific genetic effects in neuronal activation using single-cell multiomics, revealing NPD risk variants and genes active during stimulation.

The paper investigates XCI erosion in CRISPR-edited female iPSCs and their derived neurons, showing variable erosion in iPSCs and preserved XIST effects on gene expression in neurons.

This study investigates how rare mutations in the SETD1A gene affect human neurons, showing they disrupt synaptic function and may contribute to schizophrenia pathophysiology.

The paper develops a pipeline for efficient loss-of-function mutagenesis in NPD genes using base editing in hiPSCs, achieving high reproducibility and confirming neural phenotypes.

The paper identifies an AD protective allele of CLU that enhances neuronal excitability via lipid-droplet-mediated neuron-glia communication.

The paper identifies OTUD7A loss-of-function mutations in schizophrenia-associated 15q13.3 deletions and shows they impair synapse development and function in human neurons.

The paper identifies multiple genes in cis regulated by a chromatin accessibility variant that contribute to synaptic dysfunction in human neurons associated with schizophrenia.

The paper introduces MetaChrom, a deep transfer learning framework for predicting epigenomic functions of genetic variants in neurodevelopment, showing improved accuracy over existing methods.

The paper presents twelve hiPSC lines with extreme polygenic risk scores for schizophrenia, available for CRISPR-based functional studies.

The paper identifies allele-specific open chromatin (ASoC) variants in human iPSC-derived neurons and shows their strong enrichment in brain disorder risk variants.

The paper deconvolves transcriptional networks in schizophrenia to identify TCF4 as a master regulator potentially dysregulated in the disease.