Xinyu Zhao

The paper identifies an exitron in UBQLN2 that generates an alternatively spliced isoform with distinct properties linked to ALS.

The paper shows that chronic stress and voluntary running induce distinct molecular programs in parvalbumin interneurons, with stress increasing KAT6A and H3K23 acetylation in the frontal cortex.

SAMS improves spike sorting accuracy and efficiency for hPSC-derived neurons, enabling better disease modeling and drug development.

This study identifies how the coronavirus envelope protein disrupts the TAp73-FDXR axis to cause iron overload, leading to iron deficiency perception and tissue damage, and presents a therapeutic molecule to counteract this effect.

Prime-InDel provides PCR-based InDel markers for fine-mapping in rice, narrowing QTL intervals effectively.

The paper constructs a gene regulatory network resource across species and brain regions to study neurogenesis dynamics and their links to neurodevelopmental disorders.

The paper identifies genes and regulatory networks driving electrophysiological maturation of neurons in primate prefrontal cortex, with implications for autism.

This study identifies an HNF4-TET2-FBP1 axis that regulates gluconeogenesis and shows metformin's effect on this pathway in type 2 diabetes.

The paper investigates how excitatory inputs affect parvalbumin interneurons in different layers of mouse barrel cortex, finding layer-specific differences in response properties.

This study measures conduction velocities between cortical layers and within barrel columns using hVOS imaging in PV interneurons, finding interlaminar conduction is 71% faster than intralaminar.

BOMA identifies conserved and specific developmental gene expression programs between human brains and organoids at cellular resolution.

This study shows that a short Nutlin-3 treatment in young FMR1-deficient mice prevents long-term neurogenic and cognitive deficits in adulthood.

This paper introduces a CRISPR/Cas9 strategy to edit APP and manipulate the amyloid pathway in Alzheimer's disease by reducing β-cleavage and Aβ while increasing α-cleavage.