Wei Wang

This study determines the structural basis for differential inhibition of THIK1 by chemically related inhibitors using cryo-EM, showing how they affect different gates despite sharing a common binding site.

This study shows that short-term gonadal cultures of zebra finch PGCs can produce germline chimeras and validated offspring, despite being heterogeneous, unlike long-term chicken PGC cultures.

The paper identifies four synovial transcriptional clusters in knee OA linked to cartilage degeneration severity through bulk and single-cell RNA-seq analyses.

The paper identifies Optineurin as a key regulator of mitochondrial health and proteostasis in Alzheimer's disease vulnerable neurons, showing its downregulation leads to early dysfunction and neuronal loss.

This study profiles cell-type specific changes in human entorhinal cortex at early Alzheimer's disease stages, identifying dysregulation of Reelin signaling and downregulation of NPTX2 and CBLN4.

This study identifies astrocyte-derived extracellular matrix proteins, particularly SPARC, as regulators of synapse remodeling in stress-induced depression.

The paper identifies DEK as a driver of tau pathology in Alzheimer's disease vulnerable neurons using in silico modeling and experimental validation.

This study identifies neuron-glia signaling mechanisms underlying the delayed antidepressant response to SSRIs in mice using single-cell sequencing.

This study identifies GSAP's role in Alzheimer's disease by showing it regulates mitochondrial function through the MAM and lipid homeostasis, with a SNP linked to increased AD risk.

The paper identifies 6,645 novel lncRNA transcripts in Varroa destructor using high-throughput sequencing, revealing their characteristics and potential roles in biological processes.

The paper identifies translational and splicing differences in dopaminoceptive neurons and highlights PGE2's role in enhancing D2 dopamine receptor function in the dorsal striatum.

This study identifies a functional gene module associated with selective neuronal vulnerability in Alzheimer’s disease using integrated molecular and genetic data from mice and humans.

This study shows that loss of SATB1 in dopaminergic neurons leads to cellular senescence through p21 activation, suggesting a role for senescence in Parkinson's disease pathology.