ACHE Antibody (YA3883)(PBS only)
(Synonyms: YT; ACEE; ARACHE; N-ACHE)ACHE Antibody (YA3883) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to ACHE.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, IHC-P, FC
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Reactivity :
Human, Mouse, Monkey, Rat
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Formulation:
Supplied in PBS, pH 7.4.
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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FC
FC: Flow Cytometry
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|---|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:200-1:1000 | 1:200-1:400 |
Product Details
ACHE Antibody (YA3883) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to ACHE.
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Host Mouse
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Species ReactivityHuman, Mouse, Monkey, Rat
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Observed Molecular WeightObserved band size: 68 kDaNote: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 68 kDa
Purified recombinant fragment of human ACHE aa 587-611(KLH).
affinity purified.
Non-conjugated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS, pH 7.4.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
Acetylcholinesterase (AChE) is the principal cholinergic enzyme that rapidly hydrolyzes acetylcholine at cholinergic synapses and neuromuscular junctions, thereby terminating neurotransmission and maintaining synaptic signaling fidelity[1]. Mechanistically, AChE regulates cholinergic pathway activity through efficient acetylcholine clearance, a process that is essential for normal neuronal communication and neuromuscular function[1]. Beyond its catalytic role, AChE displays multiple molecular forms and has been implicated in cellular interactions, neuronal activity modulation, and pathological states, supporting broader biological functions outside classical neurotransmission[1]. In neurodegenerative disease models, particularly Alzheimer’s disease (AD), altered cholinergic signaling is closely associated with cognitive impairment, and cholinesterase inhibition remains a major symptomatic therapeutic strategy[2][3]. Compared with the related isoform butyrylcholinesterase (BChE), AChE is the predominant cholinesterase in the brain and plays a primary role in synaptic acetylcholine hydrolysis, whereas BChE may compensate when AChE activity is reduced and exhibits distinct pathological changes during AD progression[3][4]. For experimental and translational applications, reversible and dual AChE/BChE inhibitors, including rivastigmine, are widely used to enhance cholinergic neurotransmission and investigate mechanisms underlying neurodegeneration and cognitive dysfunction[2][3].
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Subcellular Localization
Synapse; Secreted; Cell membrane; Peripheral membrane protein; Nucleus; Cell membrane; Lipid-anchor, GPI-anchor; Extracellular side
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Expression
Tissue_specificity:Isoform H is highly expressed in erythrocytes -
Isoforms & Post-Translational Modification
P22303 has 4 isomers: P22303-1: 67796 Da (predicted); P22303-2: 67376 Da (predicted); P22303-4: 65560 Da (predicted); P22303-3: 58352 Da (predicted).
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Subunit
Interacts with PRIMA1. The interaction with PRIMA1 is required to anchor it to the basal lamina of cells and organize into tetramers (By similarity). Isoform H generates GPI-anchored dimers; disulfide linked. Isoform T generates multiple structures, ranging from monomers and dimers to collagen-tailed and hydrophobic-tailed forms, in which catalytic tetramers are associated with anchoring proteins that attach them to the basal lamina or to cell membranes. In the collagen-tailed forms, isoform T subunits are associated with a specific collagen, COLQ, which triggers the formation of isoform T tetramers, from monomers and dimers. Isoform R may be monomeric
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SwissProt ID
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Synonyms
YT; ACEE; ARACHE; N-ACHE
Documentation
References
[1]. Massoulié J, et al. Structure and functions of acetylcholinesterase and butyrylcholinesterase. Prog Brain Res. 1993;98:139-46. [Content Brief]
[2]. Walczak-Nowicka ŁJ, et al. Acetylcholinesterase Inhibitors in the Treatment of Neurodegenerative Diseases and the Role of Acetylcholinesterase in their Pathogenesis. Int J Mol Sci. 2021 Aug 27;22(17):9290. [Content Brief]
[3]. Nordberg A, et al. A review of butyrylcholinesterase as a therapeutic target in the treatment of Alzheimer's disease. Prim Care Companion CNS Disord. 2013;15(2):PCC.12r01412. [Content Brief]
[4]. Geula C, et al. Butyrylcholinesterase, cholinergic neurotransmission and the pathology of Alzheimer's disease. Drugs of Today (Barcelona, Spain : 1998). 2004 Aug;40(8):711-721. [Content Brief]