Syntaxin1A Antibody [L16C23] Datasheet

Biological Description

Specificity	Syntaxin1A Antibody [L16C23] detects endogenous levels of total Syntaxin1A protein.
Background	Syntaxin‑1A (STX1A/STX1B) is a presynaptic plasma membrane Q‑SNARE that forms the core of the synaptic vesicle fusion machinery and acts as a principal organizer of fast, Ca²⁺‑triggered neurotransmitter release at central synapses. The protein has an N‑terminal Habc regulatory domain that folds into a three‑helix bundle, a central SNARE (H3) helix that contributes one of the four helices of the SNARE core complex, and a C‑terminal transmembrane segment that anchors syntaxin‑1 in the presynaptic active zone membrane, creating a topology that allows the cytosolic domains to engage vesicular v‑SNARE synaptobrevin‑2 (VAMP2) and plasma‑membrane SNAP‑25 into a parallel four‑helix bundle driving membrane apposition and fusion. Syntaxin‑1 exists in a dynamic equilibrium between a closed conformation, in which the Habc domain packs back onto the H3 helix and masks the SNARE‑binding surface, and an open conformation, in which H3 is exposed and competent for SNARE‑complex assembly; both conformations bind the Sec1/Munc18 family chaperone Munc18‑1 at distinct interfaces, with closed syntaxin‑1–Munc18‑1 complexes stabilizing syntaxin at the plasma membrane and open syntaxin‑1–Munc18‑1 complexes participating directly in the fusion‑competent SNARE ensemble. A conformational switch from closed to open syntaxin‑1 gates the initiation of synaptic vesicle fusion: knock‑in expression of a constitutively open syntaxin‑1B variant reduces Munc18‑1 binding, decreases the readily releasable pool size, and dramatically accelerates the rate of evoked fusion, demonstrating that closed syntaxin‑1 sets a threshold for vesicle priming and that progression to the open state allows rapid SNARE zippering and exocytosis. Syntaxin‑1 also has essential functions in vesicle docking and neuronal maintenance that are partially separable from full fusion: loss of syntaxin‑1 abolishes fusion‑competent vesicles and severely impairs vesicle docking and neurotransmission, whereas a SNARE‑motif mutant that supports partial SNARE assembly rescues vesicle docking and neuronal survival but fails to restore exocytosis, indicating that syntaxin‑1‑dependent SNARE nucleation is required for docking while complete four‑helix bundle formation is necessary for membrane fusion.

Specificity

Syntaxin1A Antibody [L16C23] detects endogenous levels of total Syntaxin1A protein.

Background

Syntaxin‑1A (STX1A/STX1B) is a presynaptic plasma membrane Q‑SNARE that forms the core of the synaptic vesicle fusion machinery and acts as a principal organizer of fast, Ca²⁺‑triggered neurotransmitter release at central synapses. The protein has an N‑terminal Habc regulatory domain that folds into a three‑helix bundle, a central SNARE (H3) helix that contributes one of the four helices of the SNARE core complex, and a C‑terminal transmembrane segment that anchors syntaxin‑1 in the presynaptic active zone membrane, creating a topology that allows the cytosolic domains to engage vesicular v‑SNARE synaptobrevin‑2 (VAMP2) and plasma‑membrane SNAP‑25 into a parallel four‑helix bundle driving membrane apposition and fusion. Syntaxin‑1 exists in a dynamic equilibrium between a closed conformation, in which the Habc domain packs back onto the H3 helix and masks the SNARE‑binding surface, and an open conformation, in which H3 is exposed and competent for SNARE‑complex assembly; both conformations bind the Sec1/Munc18 family chaperone Munc18‑1 at distinct interfaces, with closed syntaxin‑1–Munc18‑1 complexes stabilizing syntaxin at the plasma membrane and open syntaxin‑1–Munc18‑1 complexes participating directly in the fusion‑competent SNARE ensemble. A conformational switch from closed to open syntaxin‑1 gates the initiation of synaptic vesicle fusion: knock‑in expression of a constitutively open syntaxin‑1B variant reduces Munc18‑1 binding, decreases the readily releasable pool size, and dramatically accelerates the rate of evoked fusion, demonstrating that closed syntaxin‑1 sets a threshold for vesicle priming and that progression to the open state allows rapid SNARE zippering and exocytosis. Syntaxin‑1 also has essential functions in vesicle docking and neuronal maintenance that are partially separable from full fusion: loss of syntaxin‑1 abolishes fusion‑competent vesicles and severely impairs vesicle docking and neurotransmission, whereas a SNARE‑motif mutant that supports partial SNARE assembly rescues vesicle docking and neuronal survival but fails to restore exocytosis, indicating that syntaxin‑1‑dependent SNARE nucleation is required for docking while complete four‑helix bundle formation is necessary for membrane fusion.

Usage Information

Application

WB, IP, IHC, ELISA

Dilution

WB	IHC
1 : 1000 - 1 : 10000	1 : 500

Reactivity

Human, Rat, Mouse, Mammals, Chicken, Zebrafish, Leech

Source

Mouse Monoclonal Antibody

MW

33 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

References

https://pubmed.ncbi.nlm.nih.gov/27466336/
https://pubmed.ncbi.nlm.nih.gov/18703708/

Application Data

WB

Validated by Selleck

Lane 1: Mouse brain, Lane 2: Rat brain