ArticleJournal of neurophysiology2015
Syntaxin 1B is important for mouse postnatal survival and proper synaptic function at the mouse neuromuscular junctions.
Article in Journal of neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Crotonylation of STXBP1 exacerbates seizure susceptibility by impairing GABAergic synaptic transmission.Cell death and differentiation · 2026Article
- STX1B variant-specific synaptic dysfunction is associated with network hyperexcitability in human iPSC-derived neurons.EBioMedicine · 2026Article
- Lipid Disorder and PIP2-Regulated Clustering of Syntaxin-1 JMD-TMD Regions Govern Membrane Fusion Competence.International journal of molecular sciences · 2026Article
- Bltp1 Is Required for Survival and Normal Development and Function of the Neuromuscular Junction in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Cholesterol-Lowering Treatment Suppresses Neuromuscular Transmission Via Presynaptic Mechanism at the Mouse Diaphragm Muscle.Neurochemical research · 2025Article
- The sodium leak channel NALCN is regulated by neuronal SNARE complex proteins.Science advances · 2025Article
- Article
- Functional regulation of syntaxin-1: An underlying mechanism mediating exocytosis in neuroendocrine cells.Frontiers in endocrinology · 2023Review
- Syntaxin-1 is necessary for UNC5A-C/Netrin-1-dependent macropinocytosis and chemorepulsion.Frontiers in molecular neuroscience · 2023Article
- Vesicle trafficking with snares: a perspective for autism.Molecular biology reports · 2022Review
- Article
- Synaptopathies in Developmental and Epileptic Encephalopathies: A Focus on Pre-synaptic Dysfunction.Frontiers in neurology · 2022Review
- Loss of MUNC18-1 leads to retrograde transport defects in neurons.Journal of neurochemistry · 2021Article
- SNAP23 deficiency causes severe brain dysplasia through the loss of radial glial cell polarity.The Journal of cell biology · 2021Article
- Epileptic Phenotypes Associated With SNAREs and Related Synaptic Vesicle Exocytosis Machinery.Frontiers in neurology · 2021Review
- SNARE Regulatory Proteins in Synaptic Vesicle Fusion and Recycling.Frontiers in molecular neuroscience · 2021Review
- Maternal Immune Activation Induces Neuroinflammation and Cortical Synaptic Deficits in the Adolescent Rat Offspring.International journal of molecular sciences · 2020Article
- Article
- A conserved role for Syntaxin-1 in pre- and post-commissural midline axonal guidance in fly, chick, and mouse.PLoS genetics · 2018Article
- SNARE complex in axonal guidance and neuroregeneration.Neural regeneration research · 2018Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STX1 is a major neuronal syntaxin protein located at the plasma membrane of the neuronal tissues. Rodent STX1 has two highly similar paralogs, STX1A and STX1B, that are thought to be functionally redundant. Interestingly, some studies have shown that the distribution patterns of STX1A and STX1B at the central and peripheral nervous systems only partially overlapped, implying that there might be differential functions between these paralogs. In the current study, we generated an STX1B knockout (KO) mouse line and studied the impact of STX1B removal in neurons of several brain regions and the neuromuscular junction (NMJ). We found that either complete removal of STX1B or selective removal of it from forebrain excitatory neurons in mice caused premature death. Autaptic hippocampal and striatal cultures derived from STX1B KO mice still maintained efficient neurotransmission compared with neurons from STX1B wild-type and heterozygous mice. Interestingly, examining high-density cerebellar cultures revealed a decrease in the spontaneous GABAergic transmission frequency, which was most likely due to a lower number of neurons in the STX1B KO cultures, suggesting that STX1B is essential for neuronal survival in vitro. Moreover, our study also demonstrated that although STX1B is dispensable for the formation of the mouse NMJ, it is required to maintain the efficiency of neurotransmission at the nerve-muscle synapse.
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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 OpenQuestion graph.