Associated Papers
p62/SQSTM1 Condensation Modulates Mitochondrial Clustering to Participate in Mitochondrial Quality Control.
Sun S et al.
Aging Cell, 2026
Deleterious Sequestosome 1 mutations G262R and P438L in amyotrophic lateral sclerosis cause autophagy and oxidative stress imbalance.
Singh N et al.
Neuroscience, 2025
Targeting mitophagy in neurodegenerative diseases.
Antico O et al.
Nature Reviews. Drug Discovery, 2025
Genotype-phenotype correlation of SQSTM1 variants in patients with amyotrophic lateral sclerosis.
Wang S et al.
Journal of Medical Genetics, 2024
Urolithin A promotes p62-dependent lysophagy to prevent acute retinal neurodegeneration.
Jiménez-Loygorri JI et al.
Molecular Neurodegeneration, 2024
Mitochondria, a Key Target in Amyotrophic Lateral Sclerosis Pathogenesis.
Genin EC et al.
Genes, 2023
Studies of Genetic and Proteomic Risk Factors of Amyotrophic Lateral Sclerosis Inspire Biomarker Development and Gene Therapy.
Bagyinszky E et al.
Cells, 2023
Emerging Trends in the Field of Inflammation and Proteinopathy in ALS/FTD Spectrum Disorder.
De Marchi F et al.
Biomedicines, 2023
The selective autophagy adaptor p62/SQSTM1 forms phase condensates regulated by HSP27 that facilitate the clearance of damaged lysosomes via lysophagy.
Gallagher ER et al.
Cell Reports, 2023
SQSTM1, a protective factor of SOD1-linked motor neuron disease, regulates the accumulation and distribution of ubiquitinated protein aggregates in neuron.
Mitsui S et al.
Neurochemistry International, 2022
Autophagy Dysfunction in ALS: from Transport to Protein Degradation.
Cozzi M et al.
Journal of Molecular Neuroscience : Mn, 2022
The converging roles of sequestosome-1/p62 in the molecular pathways of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Davidson JM et al.
Neurobiology of Disease, 2022
An ALS-associated variant of the autophagy receptor SQSTM1/p62 reprograms binding selectivity toward the autophagy-related hATG8 proteins.
Brennan A et al.
The Journal of Biological Chemistry, 2022
Phase-separated protein droplets of amyotrophic lateral sclerosis-associated p62/SQSTM1 mutants show reduced inner fluidity.
Faruk MO et al.
The Journal of Biological Chemistry, 2021
DNA damage as a mechanism of neurodegeneration in ALS and a contributor to astrocyte toxicity.
Kok JR et al.
Cellular and Molecular Life Sciences : Cmls, 2021
SQSTM1L341V variant that is linked to sporadic ALS exhibits impaired association with MAP1LC3 in cultured cells.
Nozaki M et al.
Eneurologicalsci, 2021
The role of sequestosome 1/p62 protein in amyotrophic lateral sclerosis and frontotemporal dementia pathogenesis.
Foster AD et al.
Neural Regeneration Research, 2020
p62/SQSTM1, a Central but Unexploited Target: Advances in Its Physiological/Pathogenic Functions and Small Molecular Modulators.
Chen Y et al.
Journal of Medicinal Chemistry, 2020
ALS-FTLD-linked mutations of SQSTM1/p62 disrupt selective autophagy and NFE2L2/NRF2 anti-oxidative stress pathway.
Deng Z et al.
Autophagy, 2020
Misconnecting the dots: altered mitochondrial protein-protein interactions and their role in neurodegenerative disorders.
Zilocchi M et al.
Expert Review of Proteomics, 2020
Mendelian neurodegenerative disease genes involved in autophagy.
Stamatakou E et al.
Cell Discovery, 2020
The role of mitochondria in amyotrophic lateral sclerosis.
Smith EF et al.
Neuroscience Letters, 2019
Structural and functional analysis of the GABARAP interaction motif (GIM).
Rogov VV et al.
Embo Reports, 2017
Pathways to mitochondrial dysfunction in ALS pathogenesis.
Carrì MT et al.
Biochemical and Biophysical Research Communications, 2017
ALS-FTLD associated mutations of SQSTM1 impact on Keap1-Nrf2 signalling.
Goode A et al.
Molecular and Cellular Neurosciences, 2016
Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD.
Goode A et al.
Autophagy, 2016
SQSTM1 mutations--bridging Paget disease of bone and ALS/FTLD.
Rea SL et al.
Experimental Cell Research, 2014
SQSTM1 mutations in Han Chinese populations with sporadic amyotrophic lateral sclerosis.
Chen Y et al.
Neurobiology of Aging, 2014