ReviewCurrent opinion in cell biology2011
Chemical and/or biological therapeutic strategies to ameliorate protein misfolding diseases.
Review in Current opinion in cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 68 citations in OpenAlex.
- Idiopathic Pulmonary Fibrosis Caused by Damaged Mitochondria and Imbalanced Protein Homeostasis in Alveolar Epithelial Type II Cell.Advanced biology · 2025Review
- Cellular rejuvenation: molecular mechanisms and potential therapeutic interventions for diseases.Signal transduction and targeted therapy · 2023Review
- Carnitine is a pharmacological allosteric chaperone of the human lysosomalJournal of enzyme inhibition and medicinal chemistry · 2021Article
- Substrate ubiquitination retains misfolded membrane proteins in the endoplasmic reticulum for degradation.Cell reports · 2021Article
- Improved correction of F508del-CFTR biogenesis with a folding facilitator and an inhibitor of protein ubiquitination.Bioorganic & medicinal chemistry letters · 2021Article
- Acute Intermittent Porphyria: An Overview of Therapy Developments and Future Perspectives Focusing on Stabilisation of HMBS and Proteostasis Regulators.International journal of molecular sciences · 2021Review
- The Amyloid Phenomenon and Its Significance in Biology and Medicine.Cold Spring Harbor perspectives in biology · 2020Review
- Targeting IRE1 with small molecules counteracts progression of atherosclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Cell-based high-throughput screening identifies galactocerebrosidase enhancers as potential small-molecule therapies for Krabbe's disease.Journal of neuroscience research · 2016Article
- Neuroprotection by Endoplasmic Reticulum Stress-Induced HRD1 and Chaperones: Possible Therapeutic Targets for Alzheimer's and Parkinson's Disease.Medical sciences (Basel, Switzerland) · 2016Review
- A molecular imaging biosensor detects in vivo protein folding and misfolding.Journal of molecular medicine (Berlin, Germany) · 2016Article
- The Role of Endoplasmic Reticulum Stress and Unfolded Protein Response in Atherosclerosis.International journal of molecular sciences · 2016Review
- The safety dance: biophysics of membrane protein folding and misfolding in a cellular context.Quarterly reviews of biophysics · 2015Article
- Lysosomal storage diseases and the heat shock response: convergences and therapeutic opportunities.Journal of lipid research · 2014Review
- ERdj3 is an endoplasmic reticulum degradation factor for mutant glucocerebrosidase variants linked to Gaucher's disease.Chemistry & biology · 2014Article
- Celastrol increases glucocerebrosidase activity in Gaucher disease by modulating molecular chaperones.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Protein Stability, Folding and Misfolding in Human PGK1 Deficiency.Biomolecules · 2013Article
- A nanobody binding to non-amyloidogenic regions of the protein human lysozyme enhances partial unfolding but inhibits amyloid fibril formation.The journal of physical chemistry. B · 2013Article
- Expanding proteostasis by membrane trafficking networks.Cold Spring Harbor perspectives in biology · 2013Review
- Diversity in the origins of proteostasis networks--a driver for protein function in evolution.Nature reviews. Molecular cell biology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Inheriting a mutant misfolding-prone protein that cannot be efficiently folded in a given cell type(s) results in a spectrum of human loss-of-function misfolding diseases. The inability of the biological protein maturation pathways to adapt to a specific misfolding-prone protein also contributes to pathology. Chemical and biological therapeutic strategies are presented that restore protein homeostasis, or proteostasis, either by enhancing the biological capacity of the proteostasis network or through small molecule stabilization of a specific misfolding-prone protein. Herein, we review the recent literature on therapeutic strategies to ameliorate protein misfolding diseases that function through either of these mechanisms, or a combination thereof, and provide our perspective on the promise of alleviating protein misfolding diseases by taking advantage of proteostasis adaptation.
Indexed as
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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.