Qin Li

The paper generates disease-specific genetic effect maps on the blood transcriptome for five glomerular diseases using whole genome and transcriptome sequencing data from the CureGN cohort.

The paper identifies immunogenic endogenous dsRNAs by isolating MDA5 filaments and shows their suppression by ADAR1 and DDX3X.

The paper shows that rDNA breaks generate sense-antisense rRNA transcripts that activate immune signaling via MDA5 and RIG-I.

The paper links ADAR1-mediated RNA editing in smooth muscle cells to regulation of MDA5 activation, showing its role in atherosclerosis progression and vascular calcification.

This study identifies an alternative splicing mechanism in IRF7 that generates a protein isoform with enhanced transcriptional activity, leading to increased resistance to viral infection.

The paper develops a CRISPR-based mutagenesis approach combined with machine learning to model cis-regulatory features of ADAR-mediated RNA editing, explaining over 70% of editing level variation.

The paper identifies Zn72D as a regulator of ADAR-mediated RNA editing in Drosophila neurons and shows its conservation in mammals.

The paper identifies trans regulators of ADAR1 and ADAR2 using BioID and mass-spectrometry, validating novel interactors as RNA editing regulators.

The paper presents a spatial RNA editing map in the Drosophila brain, revealing distinct editing signatures across neuronal populations and identifying novel editing sites in conserved regions of essential neuronal genes.

The paper examines RNA editing changes in schizophrenia by analyzing postmortem brain samples and identifies genetic regulators and associations with schizophrenia GWAS loci.

This study identifies the THO nuclear export complex as critical for synaptic transcript export, synapse development, and neuronal survival in dopaminergic neurons across species.