N. Krogan

Circulating cholesterol fuels SARS-CoV-2 replication via ORF3a.

High levels of "bad" cholesterol increase the risk of cardiovascular disease and are also linked to more severe COVID-19, though the reason has been unclear. We show that low-density lipoprotein (LDL) directly enhances SARS-CoV-2 RNA replication, especially in the Beta variant. The viral accessory protein ORF3a is both...

Multi-omics Reveals Divergent Endothelial Molecular Responses to New and Old World Hantaviruses

Whole-exome sequencing in individuals with obsessive-compulsive disorder and chronic tic disorders identifies 36 large-effect risk genes.

Obsessive-compulsive disorder (OCD) and chronic tic disorders (CTDs) are highly heritable. Rare mutations confer large risks for OCD and CTDs but only four high-confidence (hc) genes have been identified. Here we analyzed whole-exome sequencing data from 3,964 individuals with OCD, CTDs or both, including 2,418 trios....

The 4EHP/GIGYF2 translation repressor complex is co-opted by the vaccinia virus K3L protein as a potential mechanism of immunoevasion.

It is demonstrated that the vaccinia virus-encoded K3L protein interacts with 4EHP via its obligatory binding partner GIGYF2 to increase the stability of the 4EHP/GIGYF2 complex and bolsters 4EHP/GIGYF2-mediated mRNA translation repression.

Secreted ORF8 reprograms macrophages to enhance SARS-CoV-2 infection of lung epithelial cells

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily targets the respiratory epithelium, yet severe disease features diffuse lung injury and hyperinflammatory syndromes driven by dysregulated immune activation. Emerging evidence indicates that resident and infiltrating immune cells in the lung can enc...

An operon encoding two secreted nucleases mediates virulence in Methicillin-resistant Staphylococcus aureus

Genetic analysis of the SAUSA300_1739 to SAUSA300_1744 operon across several Staphylococcus aureus strains indicate that the operon is highly conserved, highlighting its importance for virulence.

Autism mutations rewire protein interaction networks to drive neurodevelopmental pathology.

Overall, these findings link genetic variation to protein networks and convergent neurodevelopmental dysfunction in ASD.