ArticleNeural development2022
Primary neurons lacking the SNAREs vti1a and vti1b show altered neuronal development.
Article in Neural development, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Multiple overlapping SNARE complexes drive endosome maturation in Drosophila nephrocytes.Nature communications · 2026Article
- Article
- Alterations in bone malformation in the absence of the endosomal SNAREs Vti1a and Vti1b.PloS one · 2026Article
- The Neuronal Golgi Network and Its Acolytes.Sub-cellular biochemistry · 2026Review
- Formation, Organization, and Maintenance of Synaptic Vesicle Pools: From Molecules to Structure and Dynamics.Advances in neurobiology · 2026Review
- Article
- Prediction of mild cognitive impairment using blood multi-omics data.Frontiers in genetics · 2025Article
- Genomic variations associated with risk and protection against vincristine-induced peripheral neuropathy in pediatric cancer patients.NPJ genomic medicine · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeurons are highly specialized cells with a complex morphology generated by various membrane trafficking steps. They contain Golgi outposts in dendrites, which are formed from somatic Golgi tubules. In trafficking membrane fusion is mediated by a specific combination of SNARE proteins. A functional SNARE complex contains four different helices, one from each SNARE subfamily (R-, Qa, Qb and Qc). Loss of the two Qb SNAREs vti1a and vti1b from the Golgi apparatus and endosomes leads to death at birth in mice with massive neurodegeneration in peripheral ganglia and defective axon tracts.
methodsHippocampal and cortical neurons were isolated from Vti1a
resultsGolgi outposts were present in Vti1a
conclusionThe absence of Golgi outposts did not affect the amount of AMPA and NMDA receptors in postsynaptic densities. Even though TrkB was enriched, BDNF was not able to stimulate neurite elongation in Vti1a
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Registered trials
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