The glycolytic enzyme PGAM1 functions as a metabolic–autophagy checkpoint to coordinate growth and stress tolerance

Chaperone-mediated autophagy as a regulator of hallmarks of cancer

Current evidence is brought together to provide a comprehensive understanding of how CMA contributes to the Hallmarks of Cancer, including sustained proliferative signaling, resistance to cell death, metabolic reprogramming, invasion and metastasis, immune evasion, and the enabling characteristics of genome instability...

The KAT2/HDACⅡa-PGK-ALDO axis constitutes a dual degradation inhibition cascade links energy stress to glycolytic amplification.

A metazoan-conserved dual degradation inhibition cascade whereby energy stress coordinates acetylation-phosphorylation crosstalk that simultaneously enhances glycolytic output and suppresses two protein degradation systems is reported.

Disruption of Protein Homeostasis by Targeting Autophagosome Formation: A Novel Anticancer Strategy Inducing Cell Death

It is demonstrated that targeting autophagosome formation can block autophagic flux and induce incomplete autophagic cell death, which leads to substrate accumulation and ultimately triggering cell death.

p62/SQSTM1: From an autophagy receptor to a condensate organizer of selective autophagy and stress signaling.

Upon exposure to stress, cells activate a variety of stress-response and quality-control mechanisms to maintain homeostasis. Dysregulation of these processes is implicated in numerous diseases, including cancer, liver disorders, and neurodegenerative diseases. p62/Sequestosome 1 (SQSTM1) is a multifunctional protein th...

Proteome stability and dynamic protein complex profiling identified EEF1A1 as a novel translation regulator of autophagy and mitophagy

This work integrates thermal proteome profiling with co-aggregation analysis to monitor protein thermal stability and complex assembly dynamics in response to two canonical inducers: Torin 1, which activates autophagy via mTOR inhibition, and CCCP, a mitochondrial uncoupler that triggers mitophagy.

PTPRF is a stress-responsive cytoskeletal checkpoint that coordinates metabolic adaptation in hepatocytes and β cells