ArticleThe Journal of biological chemistry2010
Huntingtin-associated protein-1 interacts with pro-brain-derived neurotrophic factor and mediates its transport and release.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 77 citations in OpenAlex.
- Huntingtin polyglutamine expansions misdirect axonal transport by perturbing motor and adaptor recruitment.iScience · 2026Article
- Brain-Derived Neurotrophic Factor Trafficking via the Regulated Secretory Pathway: Mechanisms and Disease Implications.Molecular neurobiology · 2025Review
- Research advances in huntingtin-associated protein 1 and its application prospects in diseases.Frontiers in neuroscience · 2024Review
- Apoptosis Genes as a Key to Identification of Inverse Comorbidity of Huntington's Disease and Cancer.International journal of molecular sciences · 2023Article
- Huntingtin-associated protein 1-associated intracellular trafficking in neurodegenerative diseases.Frontiers in aging neuroscience · 2023Review
- Untangling the Conformational Plasticity of V66M Human proBDNF Polymorphism as a Modifier of Psychiatric Disorder Susceptibility.International journal of molecular sciences · 2022Article
- Differential Transcriptome Profiling Unveils Novel Deregulated Gene Signatures Involved in Pathogenesis of Alzheimer's Disease.Biomedicines · 2022Article
- Biological functions and potential therapeutic applications of huntingtin-associated protein 1: progress and prospects.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Mutant Huntingtin Protein Interaction Map Implicates Dysregulation of Multiple Cellular Pathways in Neurodegeneration of Huntington's Disease.Journal of Huntington's disease · 2022Article
- Uncovering a Genetic Polymorphism Located in Huntingtin Associated Protein 1 in Modulation of Central Pain Sensitization Signaling Pathways.Frontiers in neuroscience · 2022Article
- Effect of Interleukin-1β on Gene Expression Signatures in Schwann Cells Associated with Neuropathic Pain.Neurochemical research · 2021Article
- The BDNF Val66Met polymorphism (rs6265) enhances dopamine neuron graft efficacy and side-effect liability in rs6265 knock-in rats.Neurobiology of disease · 2021Article
- Dorsolateral Striatal proBDNF Improves Reversal Learning by Enhancing Coordination of Neural Activity in Rats.Molecular neurobiology · 2020Article
- Peripheral ProBDNF Delivered by an AAV Vector to the Muscle Triggers Depression-Like Behaviours in Mice.Neurotoxicity research · 2020Article
- Proteotoxicity and Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- The adaptor proteins HAP1a and GRIP1 collaborate to activate the kinesin-1 isoform KIF5C.Journal of cell science · 2019Article
- Decreased BDNF Release in Cortical Neurons of a Knock-in Mouse Model of Huntington's Disease.Scientific reports · 2018Article
- The Role of Adenosine Tone and Adenosine Receptors in Huntington's Disease.Journal of caffeine and adenosine research · 2018Review
- HAP1 Is Required for Endocytosis and Signalling of BDNF and Its Receptors in Neurons.Molecular neurobiology · 2018Article
- Activation of the sigma-1 receptor by haloperidol metabolites facilitates brain-derived neurotrophic factor secretion from human astroglia.Neurochemistry international · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Brain-derived neurotrophic factor (BDNF) plays a pivotal role in brain development and synaptic plasticity. It is synthesized as a precursor (pro-BDNF), sorted into the secretory pathway, transported along dendrites and axons, and released in an activity-dependent manner. Mutant Huntingtin with expanded polyglutamine (polyQ) and the V66M polymorphism of BDNF reduce the dendritic distribution and axonal transport of BDNF. However, the mechanism underlying this defective transport remains unclear. Here, we report that Huntingtin-associated protein-1 (HAP1) interacts with the prodomain of BDNF and that the interaction was reduced in the presence of polyQ-expanded Huntingtin and BDNF V66M. Consistently, there was reduced coimmunoprecipitation of pro-BDNF with HAP1 in the brain homogenate of Huntington disease. Pro-BDNF distribution in the neuronal processes and its accumulation in the proximal and distal segments of crushed sciatic nerve and the activity-dependent release of pro-BDNF were abolished in HAP1(-/-) mice. These results suggest that HAP1 may participate in axonal transport and activity-dependent release of pro-BDNF by interacting with the BDNF prodomain. Accordingly, the decreased interaction between HAP1 and pro-BDNF in Huntington disease may reduce the release and transport of BDNF.
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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.