ArticleFrontiers in molecular neuroscience2019
Multiple Functions of KBP in Neural Development Underlie Brain Anomalies in Goldberg-Shprintzen Syndrome.
Article in Frontiers in molecular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- A systems-level proteomic analysis identifies kinesin targets of KIFBP during neuronal development.bioRxiv : the preprint server for biology · 2026Article
- Rules of the road: how to turn off kinesin motors.The Biochemical journal · 2026Review
- CITK modulates BRCA1 recruitment at DNA double strand breaks sites through HDAC6.Cell death & disease · 2025Article
- Analysis of Neuronal Morphology by Two-Photon Microscopy.Methods in molecular biology (Clifton, N.J.) · 2024Article
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- Goldberg-Shprintzen Syndrome Associated with a Novel Variant in theMolecular syndromology · 2021Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kinesin-binding protein (KBP; KIF1BP; KIAA1279) functions as a regulator for a subset of kinesins, many of which play important roles in neural development. Previous studies have shown that KBP is expressed in nearly all tissue with cytoplasmic localization. Autosomal recessive mutations in KIAA1279 cause a rare neurological disorder, Goldberg-Shprintzen syndrome (GOSHS), characterized by microcephaly, polymicrogyria, intellectual disability, axonal neuropathy, thin corpus callosum and peripheral neuropathy. Most
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Registered trials
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