ReviewInternational journal of molecular sciences2022
DnaJC7 in Amyotrophic Lateral Sclerosis.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- The ALS-associated E425K mutation uncouples DNAJC7 from the Hsp70 chaperone cycle.The FEBS journal · 2026Article
- Holding but not folding: How a single charge flip uncouples the DNAJC7-Hsp70 relay in amyotrophic lateral sclerosis.The FEBS journal · 2026Article
- Differential proteomic responses to short-term heat stress in Vechur and crossbred cattle of Kerala.Tropical animal health and production · 2026Article
- The Hsp40 cochaperone DNAJC7 regulates polyglutamine aggregation and exhibits context-dependent effects on polyglycine aggregation.The Journal of biological chemistry · 2026Article
- Tailoring treatments: pharmacogenomics in the management of neurodegenerative diseases.Acta neurologica Belgica · 2026Review
- Proteome Microarray-Guided Global View: Multiple Pharmacological Targets of Icariin.Drug design, development and therapy · 2026Article
- Increased expression of DNAJC7 promotes the progression of hepatocellular carcinoma by influencing the cell cycle and immune microenvironment.Journal of cancer research and clinical oncology · 2025Article
- The ALS-associated co-chaperone DNAJC7 mediates neuroprotection against proteotoxic stress by modulating HSF1 activity.bioRxiv : the preprint server for biology · 2024Article
- Two novel DnaJ chaperone proteins CG5001 and P58IPK regulate the pathogenicity of Huntington's disease related aggregates.Scientific reports · 2024Article
- Molecular Mechanisms in the Design of Novel Targeted Therapies for Neurodegenerative Diseases.Current issues in molecular biology · 2024Review
- Rare DNAJC7 Variants May Play a Minor Role in Chinese Patients with ALS.Molecular neurobiology · 2024Article
- Genetics screening in an Italian cohort of patients with Amyotrophic Lateral Sclerosis: the importance of early testing and its implication.Journal of neurology · 2024Article
- Characteristics of Sensory Neuron Dysfunction in Amyotrophic Lateral Sclerosis (ALS): Potential for ALS Therapy.Biomedicines · 2023Review
- Amyotrophic lateral sclerosis: translating genetic discoveries into therapies.Nature reviews. Genetics · 2023Review
- DnaJC7 specifically regulates tau seeding.eLife · 2023Article
- Blood T Helper Memory Cells: A Tool for Studying Skin Inflammation in HS?International journal of molecular sciences · 2023Article
- DnaJC7 specifically regulates tau seeding.bioRxiv : the preprint server for biology · 2023Article
- Recent progress of the genetics of amyotrophic lateral sclerosis and challenges of gene therapy.Frontiers in neuroscience · 2023Review
- Machine learning hypothesis-generation for patient stratification and target discovery in rare disease: our experience with Open Science in ALS.Frontiers in computational neuroscience · 2023Article
- Molecular Research on Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Protein misfolding is a common basis of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Misfolded proteins, such as TDP-43, FUS, Matrin3, and SOD1, mislocalize and form the hallmark cytoplasmic and nuclear inclusions in neurons of ALS patients. Cellular protein quality control prevents protein misfolding under normal conditions and, particularly, when cells experience protein folding stress due to the fact of increased levels of reactive oxygen species, genetic mutations, or aging. Molecular chaperones can prevent protein misfolding, refold misfolded proteins, or triage misfolded proteins for degradation by the ubiquitin-proteasome system or autophagy. DnaJC7 is an evolutionarily conserved molecular chaperone that contains both a J-domain for the interaction with Hsp70s and tetratricopeptide domains for interaction with Hsp90, thus joining these two major chaperones' machines. Genetic analyses reveal that pathogenic variants in the gene encoding DnaJC7 cause familial and sporadic ALS. Yet, the underlying ALS-associated molecular pathophysiology and many basic features of DnaJC7 function remain largely unexplored. Here, we review aspects of DnaJC7 expression, interaction, and function to propose a loss-of-function mechanism by which pathogenic variants in
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What OpenQuestion holds
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.