Susan Serota Taylor

This study identifies a catalytically inactive PKCα mutation that drives chordoid glioma by rewiring cellular interactions and impairing cell junction function.

This study shows that knocking out PKA regulatory subunits RI and RII leads to distinct metabolic and phosphorylation changes, with RI KO increasing Tau phosphorylation linked to Alzheimer's disease.

This study shows that S-nitrosylation of PKA regulatory subunits by SCAN is required for GPCR-induced PKA activation in heart, brain, and fat tissues.

The paper reveals how phosphorylation of SMO in the Hedgehog pathway stabilizes a conformation that inhibits PKA-C, providing a structural mechanism for noncanonical GPCR signaling.

The paper develops a mouse model of SCA14 with a clinically relevant PKCγ mutation, identifies sex-specific disease mechanisms, and highlights potential therapeutic targets for males.

The paper investigates the role of the C-β4 loop in protein kinase structure and dynamics, showing its importance in hydrophobic spine architecture and communication between kinase lobes.

The paper shows how a single amino acid change in PKCβ's C1A domain can switch between cancer-promoting and neurodegenerative effects by altering autoinhibition and degradation.

The paper evaluates centrality metrics in amino acid networks of protein kinase A, showing that traditional network construction methods are less effective than using conserved spatial patterns.

The paper identifies a mechanism by which glutamatergic and dopaminergic signaling integrate to regulate PKA via RII{beta} phosphorylation, affecting synaptic plasticity and stress responses.

The paper maps the subcellular localization of PKA subunits in the retina, revealing distinct patterns and functional nonredundancy, with C{beta} localized to mitochondria and linked to neurodegenerative diseases.