ReviewProgress in neurobiology2012
Engineered antibody therapies to counteract mutant huntingtin and related toxic intracellular proteins.
Review in Progress in neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 60 citations in OpenAlex.
- Chaperone-mediated remodelling of mutant huntingtin.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Article
- Advances in Molecular Docking Techniques for Targeting Protein Misfolding in Neurodegenerative Diseases.Current pharmaceutical biotechnology · 2025Review
- Why Is Arginine the Only Amino Acid That Inhibits Polyglutamine Monomers from Taking on Toxic Conformations?ACS chemical neuroscience · 2024Article
- Rapid Generation and Molecular Docking Analysis of Single-Chain Fragment Variable (scFv) Antibody Selected by Ribosome Display Targeting Cholecystokinin B Receptor (CCK-BR) for Reduction of Chronic Neuropathic Pain.International journal of molecular sciences · 2023Article
- Single-Dose P2 X4R Single-Chain Fragment Variable Antibody Permanently Reverses Chronic Pain in Male Mice.International journal of molecular sciences · 2021Article
- A comprehensive comparison between camelid nanobodies and single chain variable fragments.Biomarker research · 2021Review
- Nemo-like kinase reduces mutant huntingtin levels and mitigates Huntington's disease.Human molecular genetics · 2020Article
- Molecular Targets and Therapeutic Strategies in Spinocerebellar Ataxia Type 7.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Single-Domain Antibodies as Therapeutic and Imaging Agents for the Treatment of CNS Diseases.Antibodies (Basel, Switzerland) · 2019Review
- Computational affinity maturation of camelid single-domain intrabodies against the nonamyloid component of alpha-synuclein.Scientific reports · 2018Article
- Evaluating the current state of the art of Huntington disease research: a scientometric analysis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Review
- Recombinant Antibody Fragments for Neurodegenerative Diseases.Current neuropharmacology · 2017Review
- Antibodies inside of a cell can change its outside: Can intrabodies provide a new therapeutic paradigm?Computational and structural biotechnology journal · 2016Review
- Gγ recruitment systems specifically select PPI and affinity-enhanced candidate proteins that interact with membrane protein targets.Scientific reports · 2015Article
- Transcriptional dysregulation of inflammatory/immune pathways after active vaccination against Huntington's disease.Human molecular genetics · 2015Article
- Engineering humoral immunity as prophylaxis or therapy.Current opinion in immunology · 2015Review
- Structure of a single-chain Fv bound to the 17 N-terminal residues of huntingtin provides insights into pathogenic amyloid formation and suppression.Journal of molecular biology · 2015Article
- Differential nuclear localization of complexes may underlie in vivo intrabody efficacy in Huntington's disease.Protein engineering, design & selection : PEDS · 2014Article
- Systemic delivery of P42 peptide: a new weapon to fight Huntington's disease.Acta neuropathologica communications · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The engineered antibody approach to Huntington's disease (HD) therapeutics is based on the premise that significantly lowering the levels of the primary misfolded mutant protein will reduce abnormal protein interactions and direct toxic effects of the misfolded huntingtin (HTT). This will in turn reduce the pathologic stress on cells, and normalize intrinsic proteostasis. Intracellular antibodies (intrabodies) are single-chain (scFv) and single-domain (dAb; nanobody) variable fragments that can retain the affinity and specificity of full-length antibodies, but can be selected and engineered as genes. Functionally, they represent a protein-based approach to the problem of aberrant mutant protein folding, post-translational modifications, protein-protein interactions, and aggregation. Several intrabodies that bind on either side of the expanded polyglutamine tract of mutant HTT have been reported to improve the mutant phenotype in cell and organotypic cultures, fruit flies, and mice. Further refinements to the difficult challenges of intraneuronal delivery, cytoplasmic folding, and long-term efficacy are in progress. This review covers published studies and emerging approaches on the choice of targets, selection and engineering methods, gene and protein delivery options, and testing of candidates in cell and animal models. The resultant antibody fragments can be used as direct therapeutics and as target validation/drug discovery tools for HD, while the technology is also applicable to a wide range of neurodegenerative and other diseases that are triggered by toxic proteins.
Indexed as
Identifiers
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.