R. L. Wiseman

An mTOR-independent Macroautophagy Activator Ameliorates Tauopathy and Prionopathy Neurodegeneration Phenotypes

The paper identifies CCT020312, an mTOR-independent autophagy activator, which reduces tauopathy and prionopathy neurodegeneration phenotypes by enhancing autophagy flux and clearing protein aggregates.

PERK Signaling Promotes Mitochondrial Elongation By Remodeling Membrane Phosphatidic Acid

The paper shows PERK signaling promotes mitochondrial elongation by remodeling membrane phosphatidic acid during ER stress.

A surface morphometrics toolkit to quantify organellar membrane ultrastructure using cryo-electron tomography

The paper introduces a surface morphometrics toolkit for quantifying organellar membrane ultrastructure using cryo-ET, showing ER stress induces adaptive mitochondrial ultrastructural remodeling.

Amyloidogenic Proteins Drive Hepatic Proteostasis Remodeling in an Induced Pluripotent Stem Cell Model of Systemic Amyloid Disease

This study uses iPSC-derived hepatic cells to show that liver proteostasis factors and UPR signaling correlate with TTR amyloid production and can reduce amyloid secretion through ER stress-independent activation.

Deconvoluting Stress-Responsive Proteostasis Signaling Pathways for Pharmacologic Activation using Targeted RNA-sequencing

The paper develops a targeted RNA-seq assay to screen and deconvolute stress-responsive signaling pathway activation, demonstrating its utility for identifying selective pharmacologic activators.

PERK Signaling Regulates Extracellular Proteostasis of an Amyloidogenic Protein During Endoplasmic Reticulum Stress

This study shows that PERK signaling affects extracellular proteostasis by modulating the secretion of TTR in different conformations during ER stress.

Quantitative Interactome Proteomics Reveals a Molecular Basis for ATF6-Dependent Regulation of a Destabilized Amyloidogenic Protein

The paper identifies how ATF6 activation reduces secretion of a destabilized amyloidogenic protein by enhancing its retention in the ER through specific proteostasis factors.