ArticleNature communications2021
Cerebellar Kv3.3 potassium channels activate TANK-binding kinase 1 to regulate trafficking of the cell survival protein Hax-1.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Adipose Tissue Epigenetic Profile in Obesity-Related Dysglycemia - A Systematic Review.Frontiers in endocrinology · 2021Pooled it
- A novel early onset spinocerebellar ataxia 13 BAC mouse model with cerebellar atrophy, tremor, and ataxic gait.Experimental animals · 2025Article
- KCNC3 as a prognostic indicator and a predictive marker for immunotherapy in colorectal cancer.Journal of gastrointestinal oncology · 2025Article
- The role of autophagy in the pathogenesis and treatment of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).Autophagy reports · 2025Review
- Biogenesis and secretion of mitovesicles, small extracellular vesicles of mitochondrial origin at the crossroads between brain health and disease.Current opinion in physiology · 2024Article
- Plasma extracellular vesicle tau and TDP-43 as diagnostic biomarkers in FTD and ALS.Nature medicine · 2024Article
- Apolipoprotein E2 Expression Alters Endosomal Pathways in a Mouse Model With Increased Brain Exosome Levels During Aging.Traffic (Copenhagen, Denmark) · 2024Article
- Mitovesicles secreted into the extracellular space of brains with mitochondrial dysfunction impair synaptic plasticity.Molecular neurodegeneration · 2024Article
- The EIF3H-HAX1 axis increases RAF-MEK-ERK signaling activity to promote colorectal cancer progression.Nature communications · 2024Article
- Voltage-gated potassium channels as a potential therapeutic target for the treatment of neurological and psychiatric disorders.Frontiers in cellular neuroscience · 2024Review
- A novelFrontiers in cellular neuroscience · 2024Article
- The endolysosomal pathway and ALS/FTD.Trends in neurosciences · 2023Review
- Interactome profiling of Crimean-Congo hemorrhagic fever virus glycoproteins.Nature communications · 2023Article
- Kv3-Expressing Cells Present More Elaborate N-Glycans with Changes in Cytoskeletal Proteins, Neurite Structure and Cell Migration.COJ biomedical science & research · 2023Article
- Cocaine perturbs mitovesicle biology in the brain.Journal of extracellular vesicles · 2023Article
- Isolation of mitochondria-derived mitovesicles and subpopulations of microvesicles and exosomes from brain tissues.Nature protocols · 2022Review
- Cocaine Modulates the Neuronal Endosomal System and Extracellular Vesicles in a Sex-Dependent Manner.Neurochemical research · 2022Article
- Suppression of Kv3.3 channels by antisense oligonucleotides reverses biochemical effects and motor impairment in spinocerebellar ataxia type 13 mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Mutations in KCNC3, which encodes the Kv3.3 potassium channel, cause degeneration of the cerebellum, but exactly how the activity of an ion channel is linked to the survival of cerebellar neurons is not understood. Here, we report that Kv3.3 channels bind and stimulate Tank Binding Kinase 1 (TBK1), an enzyme that controls trafficking of membrane proteins into multivesicular bodies, and that this stimulation is greatly increased by a disease-causing Kv3.3 mutation. TBK1 activity is required for the binding of Kv3.3 to its auxiliary subunit Hax-1, which prevents channel inactivation with depolarization. Hax-1 is also an anti-apoptotic protein required for survival of cerebellar neurons. Overactivation of TBK1 by the mutant channel leads to the loss of Hax-1 by its accumulation in multivesicular bodies and lysosomes, and also stimulates exosome release from neurons. This process is coupled to activation of caspases and increased cell death. Our studies indicate that Kv3.3 channels are directly coupled to TBK1-dependent biochemical pathways that determine the trafficking of cellular constituents and neuronal survival.
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