Anti-Syntaxin antibody [EPR15140(B)]

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Syntaxin also known as HPC-1 or STX1A functions as an important component in the vesicle docking and fusion process particularly in neuronal exocytosis. This protein weighs approximately 33 kDa and has a significant presence in the brain especially in the synapses. Syntaxin belongs to the SNARE protein family and plays a pivotal role in facilitating the fusion of synaptic vesicles with the presynaptic membrane allowing neurotransmitter release. Its expression is not limited to nervous tissue but occurs in various other tissues reflecting its versatile roles in cellular activities.

Biological function summary

Syntaxin interacts with other SNARE proteins such as SNAP-25 and VAMP to form the SNARE complex essential for synaptic vesicle fusion and neurotransmitter release. This complex mediates the membrane fusion process vital for effective neuronal communication. Syntaxin exhibits interaction with several regulatory proteins like Munc18 which stabilizes its closed conformation critical in maintaining a reservoir of readily releasable vesicles. Its involvement in the SNARE complex marks its importance in cellular exocytosis and endocytosis.

Pathways

Syntaxin participates prominently in the neurotransmission and secretion pathways. It interacts within the neurotransmission pathway by associating with SNAP-25 and VAMP facilitating rapid neurotransmitter release in synaptic transmission. Additionally in the secretion pathway Syntaxin involvement extends to insulin release interacting with proteins like Munc18 and enhancing vesicular transport processes. Its action in these pathways demonstrates its fundamental role in cellular signaling and material transport.

Syntaxin's dysfunction has links to neurological conditions such as Alzheimer's disease and botulism. In Alzheimer's disease abnormal Syntaxin interaction may impair synaptic function and neurotransmitter release leading to cognitive deficits. Botulism caused by botulinum toxin disrupts Syntaxin-mediated vesicle docking leading to muscular paralysis. Related proteins like SNAP-25 also play a role in these conditions emphasizing the complex network within the SNARE pathway that Syntaxin operates within highlighting its significance in maintaining cellular homeostasis and function.