Peter Walter

This paper identifies ATF6α as a non-transcriptional regulator of peroxisome quality control through its interaction with ABCD3, and shows how this interaction can be modulated by Ceapin to influence cancer-related processes.

This study identifies an allosteric mechanism in eIF2B that regulates the Integrated Stress Response by showing how eIF2-P binding inhibits eIF2B activity through latch-helix dislocation.

The paper identifies a third mode of IRE1 activation called TRES, triggered by reduced protein influx into the ER, leading to a distinct gene expression program to rebalance ER load.

The paper demonstrates that a modified ISRIB analog selectively targets a mutant eIF2B, improving synaptic plasticity and memory in mice, confirming its on-target mechanism.

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

This study investigates how a genetic variant disrupts proteostasis networks, leading to cognitive dysfunction, and identifies a viral protein that can reverse these deficits.

The paper generates a single-cell ISR atlas in a mouse model of persistent ISR activation, identifying cell-type-specific ISR programs and their roles in cognitive decline.

This study shows that activation of the integrated stress response (ISR) drives tumor evolution and therapy resistance by promoting dedifferentiation and stemness in lung adenocarcinoma.

This study shows that ISRIB, a translational modulator, alleviates synaptic and behavioral issues in Fragile X syndrome by rescuing molecular and synaptic deficits in Fmr1 knockout mice.

This study shows that inhibiting the integrated stress response (ISR) after concussive injury reverses cognitive deficits and aberrant cortical spine dynamics in mice.

The paper systematically characterizes gene function in a photosynthetic organism by analyzing mutant phenotypes across diverse conditions and linking them to functional pathways.

The paper shows how a point mutation in eIF2B's β subunit mimics eIF2-P binding, leading to constitutive activation of the integrated stress response through an I-State conformation.

Inhibition of the integrated stress response restores neuronal and immune dysfunction and alleviates memory deficits in aged mice.

This study shows that disrupting IRE1α's kinase domain reduces multiple myeloma tumor growth and enhances treatment efficacy, suggesting it as a therapeutic target.