Yong‐hui Jiang

Epitope-tagged knockin mice show histone H1.4 protein accumulates in postmitotic neurons, shifts toward B-compartment heterochromatin with maturation, and H1f2/H1f4 loss impairs cerebellar granule neuron chromatin compaction.

This study identifies a dysfunctional nucleus accumbens ensemble in Shank3-/- mice that drives social avoidance by hyperresponding to social novelty.

The paper identifies UBE3A-dependent regulation of oligodendroglial homeostasis via estrogen receptor-β signaling as a therapeutic target for Angelman syndrome.

The paper shows that inflammation worsens behavioral issues in mice with partial SHANK3 gene loss, suggesting a mechanism for behavioral regression in human SHANK3-related autism.

This study identifies PAD-associated SNPs with stronger associations with surgical intervention than premature onset using UK Biobank data.

This study identifies a role for Shank3 in regulating affective empathy through cortico-amygdala circuits in a mouse model of autism.

This study shows that reducing Shank3 in the nucleus accumbens decreases social motivation in mice without affecting food reward or anxiety.

This paper develops a non-viral genome-editing method called STEP-RNPs that effectively treats Angelman syndrome in mice and human neurons, showing functional genetic rescue without off-target effects.

This study shows that OPTN dysfunction leads to neuroinflammation and RGC death in glaucoma, independent of IOP, and identifies OPTN-NPY signaling as a potential therapeutic target.

This study identifies ASD-like transcriptomic changes in oligodendrocytes and microglia of C58/J mice amygdala, dependent on sex and sociability, using bulk RNA-Seq and snRNA-Seq.

The paper profiles the SHANK3 transcriptome using cDNA-capture and long-read sequencing, revealing complex transcript variants altered in Shank3 mutants and ASD brains, improving variant detection in neuropsychiatric disorders.

The paper develops a proximity proteomics method in mice to identify protein interactions relevant to autism, revealing new genetic risk factors and functional interactions.

The paper shows that inhibiting TRPV4 rescues social and circuit deficits in Shank3 mutant mice induced by inflammation.

This study uses whole-exome sequencing on products of conception to identify genetic causes of pregnancy loss, finding pathogenic variants in 22% of cases and a higher rate with uncertain variants included.

The paper identifies a brain network encoding socioemotional behavior using machine learning on electrical activity from mice during social interactions.

This study shows that TET1-mediated DNA hydroxy-methylation is essential for adult remyelination, with loss of function leading to impaired myelin repair in aged mice.

This paper identifies a cellular mechanism involving giant ankyrin-B that leads to stochastic axon projections and contributes to neurodiversity and ASD.