ArticleCell chemical biology2016
Stabilizing the Hsp70-Tau Complex Promotes Turnover in Models of Tauopathy.
Article in Cell chemical biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed.
- A Bioinformatic Analysis of BAG Protein Interactors and Pathways in Alzheimer's and Parkinson's Disease.Journal of molecular neuroscience : MN · 2026Review
- Heat shock proteins (Hsp70 and Hsp90) in neurodegeneration: pathogenic roles and therapeutic potential.Frontiers in aging neuroscience · 2026Review
- Polyglutamine expansion induced dynamic misfolding of androgen receptor.Protein science : a publication of the Protein Society · 2025Article
- Hsp70: A Multifunctional Chaperone in Maintaining Proteostasis and Its Implications in Human Disease.Cells · 2025Review
- Advances in the structures, mechanisms and targeting of molecular chaperones.Signal transduction and targeted therapy · 2025Review
- Chaperone-dependent and chaperone-independent functions of carboxylate clamp tetratricopeptide repeat (CC-TPR) proteins.Trends in biochemical sciences · 2025Review
- High-throughput screening identifies a novel small-molecule modulator of Hsp70 that selectively enhances ubiquitination and degradation of misfolded neuronal NO synthase.Molecular pharmacology · 2025Article
- Phosphorylation of tau at a single residue inhibits binding to the E3 ubiquitin ligase, CHIP.Nature communications · 2024Article
- Proteostasis perturbation of N-Myc leveraging HSP70 mediated protein turnover improves treatment of neuroendocrine prostate cancer.Nature communications · 2024Article
- Selenoprotein W modulates tau homeostasis in an Alzheimer's disease mouse model.Communications biology · 2024Article
- The protein phosphatase-2A subunit PR130 is involved in the formation of cytotoxic protein aggregates in pancreatic ductal adenocarcinoma cells.Cell communication and signaling : CCS · 2024Article
- MSUT2 regulates tau spreading via adenosinergic signaling mediated ASAP1 pathway in neurons.Acta neuropathologica · 2024Article
- Bioinformatic analysis of hippocampal histopathology in Alzheimer's disease and the therapeutic effects of active components of traditional Chinese medicine.Frontiers in pharmacology · 2024Article
- DnaJs are enriched in tau regulators.International journal of biological macromolecules · 2023Article
- Article
- The relationship between protein modified folding molecular network and Alzheimer's disease pathogenesis based on BAG2-HSC70-STUB1-MAPT expression patterns analysis.Frontiers in aging neuroscience · 2023Article
- Multivalent protein-protein interactions are pivotal regulators of eukaryotic Hsp70 complexes.Cell stress & chaperones · 2022Review
- Bromo-protopine, a novel protopine derivative, alleviates tau pathology by activating chaperone-mediated autophagy for Alzheimer's disease therapy.Frontiers in molecular biosciences · 2022Article
- The interactions of molecular chaperones with client proteins: why are they so weak?The Journal of biological chemistry · 2021Review
- Review
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Authors and funding
13 authors.
Funding
Abstract
Heat shock protein 70 (Hsp70) is a chaperone that normally scans the proteome and initiates the turnover of some proteins (termed clients) by linking them to the degradation pathways. This activity is critical to normal protein homeostasis, yet it appears to fail in diseases associated with abnormal protein accumulation. It is not clear why Hsp70 promotes client degradation under some conditions, while sparing that protein under others. Here, we used a combination of chemical biology and genetic strategies to systematically perturb the affinity of Hsp70 for the model client, tau. This approach revealed that tight complexes between Hsp70 and tau were associated with enhanced turnover while transient interactions favored tau retention. These results suggest that client affinity is one important parameter governing Hsp70-mediated quality control.
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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.