ArticleBiochemical and biophysical research communications2008
p62 serves as a shuttling factor for TrkA interaction with the proteasome.
Article in Biochemical and biophysical research communications, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Benzenesulfonamide Analogs: Synthesis, Anti-GBM Activity and Pharmacoprofiling.International journal of molecular sciences · 2023Article
- Autophagy Dysfunction in ALS: from Transport to Protein Degradation.Journal of molecular neuroscience : MN · 2022Review
- Cross-talk between mutant p53 and p62/SQSTM1 augments cancer cell migration by promoting the degradation of cell adhesion proteins.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Endoplasmic Reticulum Stress-Mediated p62 Downregulation Inhibits Apoptosis via c-Jun Upregulation.Biomolecules & therapeutics · 2021Article
- Akebia Saponin D prevents axonal loss against TNF-induced optic nerve damage with autophagy modulation.Molecular biology reports · 2020Article
- PDLIM7 Synergizes With PDLIM2 and p62/Sqstm1 to Inhibit Inflammatory Signaling by Promoting Degradation of the p65 Subunit of NF-κB.Frontiers in immunology · 2020Article
- SQSTM1/p62: A Potential Target for Neurodegenerative Disease.ACS chemical neuroscience · 2019Review
- Review
- The FMRpolyGlycine Protein Mediates Aggregate Formation and Toxicity Independent of the CGG mRNA Hairpin in a Cellular Model for FXTAS.Frontiers in genetics · 2019Article
- HMGB1-Induced p62 Overexpression Promotes Snail-Mediated Epithelial-Mesenchymal Transition in Glioblastoma Cells via the Degradation of GSK-3β.Theranostics · 2019Article
- Effect of different levels of protein concentrates supplementation on the growth performance, plasma amino acids profile andAsian-Australasian journal of animal sciences · 2018Article
- A Review on Ubiquitination of Neurotrophin Receptors: Facts and Perspectives.International journal of molecular sciences · 2017Review
- Mutations in TrkA Causing Congenital Insensitivity to Pain with Anhidrosis (CIPA) Induce Misfolding, Aggregation, and Mutation-dependent Neurodegeneration by Dysfunction of the Autophagic Flux.The Journal of biological chemistry · 2016Article
- P62/SQSTM1 at the interface of aging, autophagy, and disease.Age (Dordrecht, Netherlands) · 2014Review
- Presenilin-1 regulates the expression of p62 to govern p62-dependent tau degradation.Molecular neurobiology · 2014Article
- Significant role of PB1 and UBA domains in multimerization of Joka2, a selective autophagy cargo receptor from tobacco.Frontiers in plant science · 2014Article
- Behavioral effects of SQSTM1/p62 overexpression in mice: support for a mitochondrial role in depression and anxiety.Behavioural brain research · 2013Article
- The cell biology of TRIM5α.Current HIV/AIDS reports · 2012Review
- TRIM5α associates with proteasomal subunits in cells while in complex with HIV-1 virions.Retrovirology · 2011Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The scaffold protein p62 is involved in internalization and trafficking of TrkA. The receptor is deubiquitinated by the proteasomes prior to degradation by lysosomes. Here we demonstrate that p62 serves as a shuttling protein for interaction of ubiquitinated TrkA with Rpt1, one of the six ATPases of 19S regulatory particle of the 26S proteasome. In p62(-/-) mouse brain TrkA failed to interact with the Rpt1. The interaction of TrkA with Rpt1 was reduced in proteasomes isolated from p62(-/-) brain, but was restored by addition of p62. The UBA domain of p62 interacts with TrkA and its PB1/UbL domain with AAA-ATPase cassette in the C-terminal region of Rpt1. Last, neurotrophin-dependent turnover of TrkA was impaired by reduction in the level of p62. These findings reveal that p62 serves as a shuttling factor for interaction of ubiquitinated substrates with the proteasome and could promote localized protein turnover in neurons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.