ArticleeNeuro
Quantification of Total and Mutant Huntingtin Protein Levels in Biospecimens Using a Novel alphaLISA Assay.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Enhancing the detection of HTT1a with neoepitope antibodies in mouse models of Huntington's disease.Brain communications · 2026Article
- Novel tools to quantify total, phospho-Ser129 and aggregated alpha-synuclein in the mouse brain.NPJ Parkinson's disease · 2024Article
- Mutant huntingtin protein decreases with CAG repeat expansion: implications for therapeutics and bioassays.Brain communications · 2024Article
- Uncovering the universality of self-replication in protein aggregation and its link to disease.Science advances · 2022Article
- Huntingtin Co-Isolates with Small Extracellular Vesicles from Blood Plasma of TgHD and KI-HD Pig Models of Huntington's Disease and Human Blood Plasma.International journal of molecular sciences · 2022Article
- Effects of mutant huntingtin inactivation on Huntington disease-related behaviours in the BACHD mouse model.Neuropathology and applied neurobiology · 2021Article
- What, When and How to Measure-Peripheral Biomarkers in Therapy of Huntington's Disease.International journal of molecular sciences · 2021Review
- Development of novel bioassays to detect soluble and aggregated Huntingtin proteins on three technology platforms.Brain communications · 2021Article
- Assessing average somatic CAG repeat instability at the protein level.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
Abstract
The neurodegenerative Huntington's disease (HD) is caused by a polyglutamine (polyQ) amplification in the huntingtin protein (HTT). Currently there is no effective therapy available for HD; however, several efforts are directed to develop and optimize HTT-lowering methods to improve HD phenotypes. To validate these approaches, there is an immediate need for reliable, sensitive, and easily accessible methods to quantify HTT expression. Using the AlphaLISA platform, we developed two novel sensitive and robust assays for quantification of HTT in biological samples using commercially available antibodies. The first, a polyQ-independent assay, measures the total pool of HTT, while the second, a polyQ-dependent assay, preferentially detects the mutant form of HTT. Using purified HTT protein standards and brain homogenates from an HD mouse model, we determine a lower limit of quantification of 1 and 3 pm and optimal reproducibility with CV values lower than 7% for intra- and 20% for interassay. In addition, we used the assays to quantify HTT in neural stem cells generated from patient-derived induced pluripotent stem cells
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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.