Qiang Wu

This study shows WAVE2 and REST/NRSF regulate clustered gene expression by maintaining heterochromatin organization through chromatin dynamics and spatial reorganization.

The paper introduces COP, a deep learning framework to predict ZFP genomic enrichments, identifies Wiz as a key regulator of cPcdh genes by affecting CTCF/cohesin loop extrusion.

This study shows that DSB end configuration and 3D genome architecture influence translocation frequency and junctional indel patterns using CRISPR/Cas9.

The paper experimentally measures CTCF-binding affinity across 276,765 human DNA sequences and develops a deep learning model to predict and interpret binding strength based on sequence features.

The paper shows that CTCF's N-terminal domain enhances cohesin processivity, affecting clustered protocadherin gene expression and suggesting a new role for CTCF in 3D genome folding.

The paper identifies a negatively-charged region in CTCF's C-terminal domain that weakens DNA binding and chromatin accessibility through an autoinhibitory mechanism.

The paper develops a computational tool to analyze CRISPR/Cas9-induced chromosomal rearrangements and identifies roles of DNA polymerases in deletion mechanisms and junctional repair.

The paper investigates clustered CTCF TAD boundaries and finds that outward-oriented CBS elements are crucial for intraTAD promoter-enhancer interactions and gene regulation.

This study identifies ZNF143's role in chromatin looping and 3D genome organization by showing its directional recognition of genomic sites and collaboration with CTCF.

The paper investigates STR instability in cultured human cells using sequencing methods and finds STRs are intrinsically unstable during cloning and in cell populations.

The paper identifies an antisense eRNA, PEARL, that regulates Pcdh expression through R-loop formation in the HS5-1 enhancer region.

This study investigates how REST/NRSF regulates clustered protocadherin genes by forming directional base-specific interactions with NRSEs and altering enhancer-promoter interactions.

The paper shows that CTCF-binding sites act as enhancer-blocking insulators and that tandem arrays of these sites balance promoter usage in gene clusters.

This study reveals that Cas9-mediated DNA fragment editing (DFE) can be precise and predictable by manipulating DNA repair genes and PAM configurations, with insertions determined by sequences upstream of both PAM sites.

This study shows that Pyk2 suppresses contextual fear memory independently of its kinase activity, with effects on immediate early genes and neuronal structure.