Howard Y. Chang

The paper uses single-cell epigenomic data to identify functional SNPs associated with Alzheimer's and Parkinson's disease, revealing novel gene-disease associations and regulatory mechanisms.

This study examines B cell clonal expansion and convergent antibody responses in SARS-CoV-2 patients, identifying shared features with SARS-CoV.

This study identifies a primed chromatin state in oligodendroglia that facilitates rapid activation of immune gene programs in multiple sclerosis.

The paper functionally annotates human long non-coding RNAs by systematically knocking down 285 lncRNAs and analyzing molecular phenotypes using CAGE sequencing.

The paper predicts SARS-CoV-2 RNA localization to host mitochondria and nucleolus using machine learning, identifying key regions in viral RNA that drive this localization.

This study shows Spen binds to endogenous retroviral RNAs and recruits chromatin silencing machinery, linking RNA-mediated retrovirus silencing to X chromosome inactivation.

This study uses super-resolution imaging to reveal the 3D structure and organizing mechanism of accessible chromatin domains.

CRISPRpic provides fast and precise mutation calling by counting exact matches and pattern searches in CRISPR sequencing data.

The paper uses scATAC-seq to analyze chromatin accessibility in immune cell development and tumor microenvironments, identifying regulatory elements and trajectories associated with cell differentiation and therapy response.

This paper develops a single-cell multi-omic framework to identify malignant regulatory signatures in mixed phenotype acute leukemia by analyzing transcriptomic and epigenetic data.

EMBLEM uses mitochondrial DNA mutations in ATAC-seq data to track cell lineage with high sensitivity and specificity in acute myeloid leukemia.

The paper maps RNA structuromes in three subcellular compartments and identifies LIN28A as an m6A anti-reader, revealing dynamic RNA structure regulation.

This study examines DNA methylation changes during fibroblast-to-neuron reprogramming, identifying key factors and mechanisms involved in epigenomic remodeling.

The paper identifies lnc-NR2F1 as a pro-neurogenic lncRNA mutated in neurodevelopmental disorders through genetic and functional studies.

Perturb-ATAC combines CRISPR perturbations with single-cell ATAC-seq to identify gene regulatory networks in human cells.

This study investigates the role of Polycomb recruitment in Xist-mediated X chromosome silencing in mouse ES cells, finding that silencing can occur independently of Polycomb complexes.

The paper introduces Pi-ATAC, a method combining single-cell chromatin and proteomic profiling, revealing hypoxia's role in shaping the regulome in tumor cells.

This study identifies factors that determine Satb1 binding-site selectivity, showing its preference for nucleosome-dense regions and its mechanosensitive interactions with DNA.

The paper introduces coupled nonnegative matrix factorizations to integrate single cell RNA-seq and ATAC-seq data by coupling clustering across samples.

The paper identifies genetic variants affecting chromatin accessibility in T cells and links them to gene expression and autoimmune disease.

The paper identifies TFAP2C and p63 as key regulators of epidermal lineage commitment and shows TFAP2C initiates differentiation while p63 drives maturation through chromatin dynamics.

The paper investigates how morphogens and p63 interact to regulate chromatin dynamics during keratinocyte differentiation from hESCs, revealing p63's dependence on morphogenetic signaling for long-range chromatin interactions.

This paper uses HiChIP to map enhancer-promoter interactions in primary human cells, linking disease-associated DNA variants to their target genes.

Omni-ATAC improves ATAC-seq by reducing background noise and enabling analysis of frozen tissues, revealing disease-associated DNA element activities in human brain structures.

The paper uses single-cell chromatin accessibility to map the continuous regulatory variation in human hematopoietic differentiation and identifies epigenomic heterogeneity within cell populations.

HiChIP improves the yield and reduces input requirements of chromatin conformation analysis, revealing multi-scale genome architecture with better signal-to-background.