John Kuriyan

A rational design strategy and validation for protease-resistant fusion-inhibitor antiviral peptides

This study designs and validates protease-resistant antiviral peptides that inhibit SARS-CoV-2 fusion, showing improved efficacy in vitro and in vivo.

The Central Coupler of ClpXP Controls Intersubunit Communication and Couples Intrasubunit Chemical Energy with Force Generation

Q208A mutations in up to four subunits of the ClpX central coupler barely slow unfolded-substrate translocation but raise ATP spent per step, weaken force generation and can abolish GFP unfolding.

LAT condensation gates PLCγ1 activation via bimodal LAT phosphorylation

This study shows LAT condensation gates PLCγ1 activation through bimodal LAT phosphorylation, enhancing signal amplification and noise suppression in T cells.

Redesign of energetically frustrated regions rescues function in defective T4 clamp loaders

The paper identifies and redesigns energetically frustrated regions in a defective T4 clamp loader to restore function through conformational balance and stability.

Autophosphorylation of the oncogenic protein TEL-ABL confers resistance to the allosteric ABL inhibitor asciminib

The paper shows that phosphorylation of TEL-ABL makes it resistant to asciminib, but dephosphorylation restores sensitivity.

BTK Autoinhibition Analyzed by High-Throughput SH2 Domain Swaps

The paper assesses BTK autoinhibition by substituting SH2 domains and finding that some substitutions enhance fitness by disrupting autoinhibition while maintaining phosphotyrosine targeting.

Ligand-induced CaMKIIα hub Trp403 flip, hub domain stacking and kinase inhibition

This paper investigates how PIPA, a GHB analog, affects CaMKII hub domain conformation and stability, revealing a mechanism involving Trp403 flip and hub domain stacking that reduces kinase activity.

Stimulation of the catalytic activity of the tyrosine kinase Btk by the adaptor protein Grb2

This study shows that Grb2 enhances PIP3-bound Btk activity on membranes by recruiting it to scaffold-mediated signaling clusters.

Breakage of the Oligomeric CaMKII Hub by the Regulatory Segment of the Kinase

The paper shows that the regulatory segment of CaMKII can break the oligomeric hub into smaller assemblies through binding and structural destabilization.