Jay T. Groves

This study shows that Grb2 phosphorylation at Y160 inhibits EGFR condensate formation, thereby reducing Ras activation, and reveals how kinase inhibition can promote Ras signaling under certain conditions.

This study shows ECM stiffness enhances EGFR signaling through integrin-mediated membrane curvature and topography, affecting RTK signaling across scales and potentially explaining resistance to tyrosine kinase inhibitors.

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

This study develops a machine-learning strategy to improve error tolerance in image-based nanoparticle immunoassays for field-based diagnostics.

This paper develops an image-based assay to measure PLCγ1 activity in LAT condensates and finds that condensation does not enhance PLCγ1 activity.

This paper shows eIF2B activates mutant KRAS by forming a complex with SOS at the plasma membrane and regulating glycosphingolipid biosynthesis.

The paper measures how costimulatory and inhibitory signals affect LAT condensate nucleation timing after TCR activation.

This paper develops two models to explain LAT condensate formation in reconstitution experiments, showing that condensate morphologies arise from common dynamics modulated by experimental conditions.

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

This paper proposes a multi-thread kinetic proofreading model for TCR activation, showing that parallel reactions and integration improve discrimination fidelity compared to sequential models.

This paper shows that T-cell receptor signaling uses condensate nucleation to selectively detect single foreign peptides by amplifying weak signals and setting spatial-temporal thresholds.

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

This study investigates whether BTK dimerization via its PH-TH module is required for signaling in B and T cells, finding it is not necessary in B cells but essential in T cells.

This paper introduces a modified Fab'-DNA ligand to study TCR signal integration by controlling kinetic on- and off-rates, revealing how dwell time affects TCR signaling and LAT condensation.

The paper tracks molecular pMHC binding events and LAT condensation in T cells, showing stochastic condensation events drive calcium signal dynamics without cooperativity or oscillation.

The paper shows that Ras signaling bimodality arises from SOS processivity, not kinetic bistability, and is controlled by scaffold protein condensation.

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

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