ArticleActa neuropathologica communications2014
Abundant kif21b is associated with accelerated progression in neurodegenerative diseases.
Article in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Systematic review of human post-mortem immunohistochemical studies and bioinformatics analyses unveil the complexity of astrocyte reaction in Alzheimer's disease.Neuropathology and applied neurobiology · 2022Pooled it
- Myelin Dynamics at the Axon-Oligodendrocyte Interface: Adaptive Conduction Homeostasis in Demyelination, Remyelination and White Matter Repair.International journal of molecular sciences · 2026Review
- Article
- An activity-modulated transport route across myelin (TRAM) for motor-driven organelle transfer in oligodendrocytes.Nature neuroscience · 2026Article
- Microtubule Engagement by the WD40-Containing Tail of Kinesin-4 KIF21B.bioRxiv : the preprint server for biology · 2026Article
- Kif15 orchestrates neuronal-microglial communication via CX3CL1 to impede nerve regeneration.The Journal of biological chemistry · 2026Article
- Research progress of kinesin family in neurological diseases.Frontiers in cellular neuroscience · 2025Review
- A novel in-frame deletion in KIF5C gene causes infantile onset epilepsy and psychomotor retardation.MedComm · 2024Article
- Unraveling the interplay of kinesin-1, tau, and microtubules in neurodegeneration associated with Alzheimer's disease.Frontiers in cellular neuroscience · 2024Review
- Interaction of Tau with Kinesin-1: Effect of Kinesin-1 Heavy Chain Elimination on Autophagy-Mediated Mutant Tau Degradation.Biomedicines · 2023Article
- Recent advances in novel mutation genes of Parkinson's disease.Journal of neurology · 2023Review
- Differential splicing of neuronal genes in a Trem2*R47H mouse model mimics alterations associated with Alzheimer's disease.BMC genomics · 2023Article
- Article
- Targeting kinesin family member 21B by miR-132-3p represses cell proliferation, migration and invasion in gastric cancer.Bioengineered · 2022Article
- Reduction of kinesin I heavy chain decreases tau hyperphosphorylation, aggregation, and memory impairment in Alzheimer's disease and tauopathy models.Frontiers in molecular biosciences · 2022Article
- A novel age-informed approach for genetic association analysis in Alzheimer's disease.Alzheimer's research & therapy · 2021Article
- Article
- Normal levels of KIF5 but reduced KLC1 levels in both Alzheimer disease and Alzheimer disease in Down syndrome: evidence suggesting defects in anterograde transport.Alzheimer's research & therapy · 2021Article
- Kinesin-4 KIF21B limits microtubule growth to allow rapid centrosome polarization in T cells.eLife · 2020Article
- KIF21B Expression in Osteosarcoma and Its Regulatory Effect on Osteosarcoma Cell Proliferation and Apoptosis Through the PI3K/AKT Pathway.Frontiers in oncology · 2020Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kinesin family member 21b (kif21b) is one of the few multiple sclerosis (MS) risk genes with a presumed central nervous system function. Kif21b belongs to the kinesin family, proteins involved in intracellular transport of proteins and organelles. We hypothesised that kif21b is involved in the neurodegenerative component of MS and Alzheimer's (AD) disease. Post-mortem kinesin expression was assessed in 50 MS, 58 age and gender matched non-demented controls (NDC) and 50 AD. Kif21b expression was five-fold increased in AD compared to MS and NDC aged below 62 years (p = 8*10(-5)), three-fold between 62-72 years (p = 0.005) and not different above 72 years. No significant differences were observed between MS and NDC. In AD, kif21b expression was two-fold increased in Braak stage 6 (scoring for density of neurofibrillary tangles) compared with stage 5 (p = 0.003). In MS patients, kif21b correlated with the extent of grey matter demyelination (Spearman's rho = 0.31, p = 0.03). Abundant kif21b, defined as expression above the median, was associated with a two-fold accelerated development of the Kurtzke Expanded Disability Status Scale (EDSS) 6.0 (median time in low kif21b group 16 years vs. high kif21b 7.5 years, log-rank test p = 0.04) in MS. Given the genetic association of kif21b with MS, the results were stratified according to rs12122721[A] single nucleotide polymorphism (SNP). No association was found between kif21b expression or the time to EDSS 6 in kif21b risk SNP carriers compared to non-risk carriers. Kif21b was expressed in astrocytes in addition to neurons. Upon astrocyte activation, kif21b increased nine-fold. Abundant kif21b expression is associated with severe MS and AD pathology and with accelerated neurodegeneration independent of the kif21b risk SNP.
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