ArticleNature communications2026
Intellectual disability-causing mutations in KIF11 impair microtubule dynamics and dendritic arborization.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Kif15 orchestrates neuronal-microglial communication via CX3CL1 to impede nerve regeneration.The Journal of biological chemistry · 2026Article
- The Long Haul: Microtubule Motors as the Essential Supply Line for Neuronal Longevity.Journal of neurochemistry · 2026Review
- Non-transport functions of motor proteins in corticogenesis.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Microcephaly with or without chorioretinopathy, lymphedema, or intellectual disabilities (MCLID) is a rare disease caused by mutations in the mitotic motor KIF11. However, the specific neuronal functions of KIF11, its mechanisms of microtubule (MT) regulation, and the impact of MCLID mutations on KIF11 function remain underexplored. Here, using live-imaging, we find that KIF11 depletion in postmitotic neurons increases minus-end-out MT dynamics in both axons and dendrites. Introducing MCLID-associated KIF11 mutations, KIF11
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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 Socratic graph.