Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

KBP is essential for axonal structure, outgrowth and maintenance in zebrafish, providing insight into the cellular basis of Goldberg-Shprintzen syndrome.

Development (Cambridge, England) - 1 Feb 2008

Lyons David A, Naylor Stephen G, Mercurio Sara, Dominguez Claudia, Talbot William S

Abstract excerpt

Mutations in Kif1-binding protein/KIAA1279 (KBP) cause the devastating neurological disorder Goldberg-Shprintzen syndrome (GSS) in humans. The cellular function of KBP and the basis of the symptoms of GSS, however, remain unclear. Here, we report the identification and characterization of a zebrafish kbp mutant. We show that kbp is required for axonal outgrowth and maintenance. In vivo time-lapse analysis of...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Axons
Share to Body Patterning

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cytoskeleton

Share to Enteric Nervous System

Share to Microtubules

Share to Myelin Sheath

Share to Synaptic Vesicles

Share to Zebrafish Proteins

Source

Identifiers

PMID: 18192286
DOI: 10.1242/dev.012377

Genes

GSS

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

KBP is essential for axonal structure, outgrowth and maintenance in zebrafish, providing insight into the cellular basis of Goldberg-Shprintzen syndrome.PMID 18192286Read ↗

Axonal transport deficit in a KIF5A –/– mouse modelSemantic proximity Read ↗

A systems-level proteomic analysis identifies kinesin targets of KIFBP during neuronal developmentSemantic proximity Read ↗

KBP-cytoskeleton interactions underlie developmental anomalies in Goldberg-Shprintzen syndrome.Semantic proximity Read ↗

Disease-associated mutations hyperactivate KIF1A motility and anterograde axonal transport of synaptic vesicle precursorsSemantic proximity Read ↗

Traffic Jams in the Brain: How Kinesin Dysfunction Shapes Neurodevelopmental DisordersSemantic proximity Read ↗

Mutations in dock1 disrupt early Schwann cell development.Semantic proximity Read ↗

Identification of an axonal kinesin-3 motor for fast anterograde vesicle transport that facilitates retrograde transport of neuropeptides.Semantic proximity Read ↗

Kinesins in Caenorhabditis elegans neuronal morphogenesis.Semantic proximity Read ↗

Going Too Far Is the Same as Falling Short†: Kinesin-3 Family Members in Hereditary Spastic ParaplegiaSemantic proximity Read ↗

Impaired motor unit recovery and maintenance in a knock-in mouse model of ALS-associated Kif5a variantSemantic proximity Read ↗

KIF5A regulates axonal repair and time-dependent axonal transport of SFPQ granules and mitochondria in human motor neuronsSemantic proximity Read ↗

Abnormal neurofilament transport caused by targeted disruption of neuronal kinesin heavy chain KIF5A.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.