ArticleProceedings of the National Academy of Sciences of the United States of America2003
Stimulation of NeuroD activity by huntingtin and huntingtin-associated proteins HAP1 and MLK2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Pathological and Functional Brain Amyloids: A New Concept Explaining the Differences.International journal of molecular sciences · 2025Review
- Advances in gene and cellular therapeutic approaches for Huntington's disease.Protein & cell · 2025Review
- Elevated SLC7A2 expression is associated with an abnormal neuroinflammatory response and nitrosative stress in Huntington's disease.Journal of neuroinflammation · 2024Article
- Research advances in huntingtin-associated protein 1 and its application prospects in diseases.Frontiers in neuroscience · 2024Review
- Huntingtin S421 phosphorylation increases kinesin and dynein engagement on early endosomes and lysosomes.Biophysical journal · 2023Article
- Huntingtin-associated protein 1-associated intracellular trafficking in neurodegenerative diseases.Frontiers in aging neuroscience · 2023Review
- 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
- Zebrafish an experimental model of Huntington's disease: molecular aspects, therapeutic targets and current challenges.Molecular biology reports · 2021Review
- RNA-seq analysis reveals significant transcriptome changes in huntingtin-null human neuroblastoma cells.BMC medical genomics · 2021Article
- Review
- DNA Damage Repair in Huntington's Disease and Other Neurodegenerative Diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Developmental alterations in Huntington's disease neural cells and pharmacological rescue in cells and mice.Nature neuroscience · 2017Article
- Article
- Review
- Huntingtin Is Required for Neural But Not Cardiac/Pancreatic Progenitor Differentiation of Mouse Embryonic Stem CellsFrontiers in cellular neuroscience · 2017Article
- Physical exercise-induced adult neurogenesis: a good strategy to prevent cognitive decline in neurodegenerative diseases?BioMed research international · 2014Review
- Sp1 regulates human huntingtin gene expression.Journal of molecular neuroscience : MN · 2012Article
- Huntington's disease and the striatal medium spiny neuron: cell-autonomous and non-cell-autonomous mechanisms of disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2012Review
- Longitudinal behavioral, cross-sectional transcriptional and histopathological characterization of a knock-in mouse model of Huntington's disease with 140 CAG repeats.Experimental neurology · 2011Article
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Authors and funding
3 authors.
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Abstract
NeuroD (ND) is a basic helix-loop-helix transcription factor important for neuronal development and survival. By using a yeast two-hybrid screen, we identified two proteins that interact with ND, huntingtin-associated protein 1 (HAP1) and mixed-lineage kinase 2 (MLK2), both of which are known to interact with huntingtin (Htt). Htt is a ubiquitous protein important for neuronal transcription, development, and survival, and loss of its function has been implicated in the pathogenesis of Huntington's disease, a neurodegenerative disorder. However, the mechanism by which Htt exerts its neuron-specific function at the molecular level is unknown. Here we report that Htt interacts with ND via HAP1, and that MLK2 phosphorylates and stimulates the activity of ND. Furthermore, we show that Htt and HAP1 facilitate the activation of ND by MLK2. To our knowledge, ND is the first example of a neuron-specific transcription factor involved in neuronal development and survival whose activity is modulated by Htt. We propose that Htt, together with HAP1, may function as a scaffold for the activation of ND by MLK2.
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