Stx1A Protein is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
| STX1A Protein |
|---|
| Protein Name | Syntaxin 1A |
| Gene | STX1A |
| UniProt ID | P61264 |
| PDB IDs | 1BR0, 1DN1, 3C98 |
| Molecular Weight | 35 kDa |
| Subcellular Localization | Presynaptic plasma membrane |
| Protein Family | SNARE proteins, syntaxin family |
STX1A PROTEIN is a gene/protein encoding a key neuronal protein involved in synaptic function, signal transduction, and cellular homeostasis. Dysfunction of STX1A PROTEIN is associated with neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and related disorders.
Syntaxin 1A is a t-SNARE protein:
- N-terminal Habc domain: Three-helix bundle (autoinhibitory)
- SNARE domain: Forms core SNARE complex
- Transmembrane anchor: C-terminal membrane anchor
- Linker region: Connects Habc to SNARE domain
- Synaptic vesicle fusion: t-SNARE in neurotransmitter release
- SNARE complex assembly: Forms complex with SNAP-25 and VAMP
- Exocytosis regulation: Controls vesicle priming and fusion
- Calcium channel coupling: Links calcium influx to fusion
- Synaptic plasticity: Modulates short-term plasticity
- Alpha-synuclein inhibits syntaxin 1A
- Impaired dopamine release
- Synaptic vesicle recycling defects
- Reduced SNARE levels
- Amyloid-beta disrupts SNARE complexes
- Synaptic transmission deficits
- Motor neuron exocytosis dysfunction
- 7507320: Syntaxin structure. Nature, 1994.
- 19058887: SNAREs in neurodegeneration. Nat Rev Neurosci, 2008.
The study of Stx1A Protein has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
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- Kowalska M et al.. "Molecular factors in migraine." Oncotarget (2016). DOI: 10.18632/oncotarget.9367 PubMed: 27191890
- Hooshmand K et al.. "Overlap between Central and Peripheral Transcriptomes in Parkinson's Disease but Not Alzheimer's Disease." International journal of molecular sciences (2022). DOI: 10.3390/ijms23095200 PubMed: 35563596
- Nakayama T et al.. "Activator of KAT3 histone acetyltransferase family ameliorates a neurodevelopmental disorder phenotype in the syntaxin 1A ablated mouse model." Cell reports (2024). DOI: 10.1016/j.celrep.2024.114101 PubMed: 38613786
- Liu M et al.. "Sevoflurane Preconditioning Protects Against Myocardial Ischemia Reperfusion Injury in Mice via PI3K/AKT/GSK3β-mediated Upregulation of Syntaxin1a." Journal of biochemical and molecular toxicology (2025). DOI: 10.1002/jbt.70260 PubMed: 40265646
- Vardar G et al.. "Syntaxin-1A modulates vesicle fusion in mammalian neurons via juxtamembrane domain dependent palmitoylation of its transmembrane domain." eLife (2022). DOI: 10.7554/eLife.78182 PubMed: 35638903
- Fujiwara T, Kofuji T, Akagawa K. "Dysfunction of the hypothalamic-pituitary-adrenal axis in STX1A knockout mice." Journal of neuroendocrinology (2011). DOI: 10.1111/j.1365-2826.2011.02214.x PubMed: 21910766