Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The role of SQSTM1 (p62) in mitochondrial function and clearance in human cortical neurons

22 Apr 2021

Abstract excerpt

Sequestosome-1 (SQSTM1/p62) is involved in cellular processes such as autophagy and metabolic reprogramming. Mutations resulting in the loss of function of SQSTM1 lead to neurodegenerative diseases including frontotemporal dementia. The pathogenic mechanism that contributes to SQSTM1-related neurodegeneration has been linked to its role as an autophagy adaptor, but this is poorly understood, and its precise role...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autophagy in Disease and Therapy
Share to Parkinson's Disease Mechanisms and Treatments
Share to Sirtuins and Resveratrol in Medicine

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 33891871
DOI: 10.1016/j.stemcr.2021.03.030

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The role of SQSTM1 (p62) in mitochondrial function and clearance in human cortical neuronsPMID 33891871Read ↗

Generation and characterization of human-derived induced pluripotent stem cell line (IGIBi010-A) from a patient with neurodegenerative disease phenotype carrying mutation in SQSTM1/p62 gene.Semantic proximity Read ↗

Absence of the Autophagy Adaptor SQSTM1/p62 Causes Childhood-Onset Neurodegeneration with Ataxia, Dystonia, and Gaze Palsy.Semantic proximity Read ↗

SQSTM1/p62-Directed Metabolic Reprogramming Is Essential for Normal NeurodifferentiationSemantic proximity Read ↗

Neuronal mitochondrial dysfunction in sporadic amyotrophic lateral sclerosis is developmentally regulatedSemantic proximity Read ↗

Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1)-dependent ubiquitination of endogenous Parkin attenuates mitophagy: study in human primary fibroblasts and induced pluripotent stem cell-derived neurons.Semantic proximity Read ↗

PARK2 Mutation Causes Metabolic Disturbances and Impaired Survival of Human iPSC-Derived NeuronsSemantic proximity Read ↗

p62/SQSTM1 – steering the cell through health and diseaseSemantic proximity Read ↗

Mitophagy-driven mitochondrial rejuvenation regulates stem cell fateSemantic proximity Read ↗

Decreased Sirtuin Deacetylase Activity in LRRK2 G2019S iPSC-Derived Dopaminergic Neurons.Semantic proximity Read ↗

APP Deficiency Ameliorates FAD Presenilin 1 F105C and A246E Mutations-induced Mitochondrial Dysfunction in Human Cortical Neurons.Semantic proximity Read ↗

p62/SQSTM1 Cooperates with Hyperactive mTORC1 to Regulate Glutathione Production, Maintain Mitochondrial Integrity, and Promote TumorigenesisSemantic proximity Read ↗

SQSTM1/p62 variants in 486 patients with familial ALS from Germany and Sweden.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.