Malaria remodels the spleen to imprint tolerance and reduce pathology in subsequent infections.

The structure of human PINK1 explains structural regulation and clarity on the impact of loss of function disease-associated mutations, which may stimulate future drug discovery efforts for both familial and idiopathic Parkinson's disease.

Increased excitation and decreased inhibition associated with abnormal neuronal morphology, aberrant ion channel properties, and synaptic dysfunction contribute to hyperexcitability in Alzheimer’s disease hiPSC-derived neuronal cultures and cerebral organoids.

Collaborative transcription factors (TFs) exhibit a dominant pattern of a relaxed range of spacing and substantial tolerance of spacing alterations resulting from naturally occurring insertions and deletions in comparison to genetic variants directly affecting TF binding sites.

Structural, biophysical, and functional analyses reveal that mutations in TREM2 trigger either misfolding or reduced binding to cell-surface glycosaminoglycans, which segregate with neurodegenerative disease link and highlight a functional surface linked to the pathogenesis of Alzheimer's disease.

Alternative first exon usage was the major event observed in macrophages during inflammation, which resulted in the elucidation of a novel isoform and regulatory mechanism of the protein-coding gene, Aim2.

Defective mitochondrial protein import results in protein aggregation and a specific chaperone response in the cytosol, causatively linking mitochondrial function and cellular protein homeostasis disturbances observed in neurodegeneration.

In keratinocytes, the BRAF and RAF1 proteins work independently to balance the activity of mitogenic and stress kinase cascades and uphold the mechanical and immunological barrier functions of the epidermis.

The mathematical modeling approach disentangles the impacts of the COVID-19 pandemic on antibiotic resistance in Streptococcus pneumoniae in the community setting and identifies the three most plausible driving mechanisms responsible for the observed trends in invasive isolates and pneumococcal carriage.

A computer model built on insights gained from comprehensive experimental analysis reveals mechanisms of blood stem cell regulation.