N. J. Krogan

This study reveals that Smoothened (SMO) activates GLI transcription factors by sequestering PKA catalytic subunits at the membrane, bypassing traditional GPCR signaling mechanisms.

This study uses proteomics to analyze post-translational modifications in macrophages infected with three intracellular pathogens, revealing pathogen-specific molecular responses and a novel mechanism of virus-bacterial synergy.

This study identifies non-canonical proline-tyrosine interactions in the Ebola virus VP30 protein that regulate viral replication by interacting with multiple host proteins.

This study profiles host cell proteome, ubiquitinome, and phosphoproteome during Legionella pneumophila infection, revealing modulation of mitochondrial stress response pathways.

This paper presents a high-resolution crystal structure of HIV-1 Nef interacting with AP2, revealing how Nef sequesters CD4 for degradation and identifying a dual-function pocket crucial for both MHC recruitment and CD4 binding.

The paper shows that adhesion-mediated mechanosignaling activates a mitochondrial stress response through SLC9A1 and HSF1, altering mitochondrial function in aging and cancer.

The paper identifies a chaperone-mediated process that refuxes properly folded ER proteins to the cytosol during ER stress, functioning parallel to ERAD.

The paper identifies PDHK1 as a synthetic-essential gene in PTEN-deficient cells and cancers, showing its upregulation drives aerobic glycolysis and correlates with poor patient survival.

This study shows that ZIKV infection disrupts the NMD pathway by interacting with UPF1 via its capsid protein, enhancing viral infection and contributing to neuropathology.