anti-AchE (Acetylcholinesterase), mAb (3A5)

CHF 315.00
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YIF-LF-MA0283100 µlCHF 315.00
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Product Details
Synonyms ACHE; AChE; EC=; Acetylcholinesterase
Product Type Monoclonal Antibody
Clone 3A5
Isotype Mouse IgG1 κ
Immunogen/Antigen Recombinant human His-DJ-AChE protein purified from E. coli.

Western Blot (1:2,000)

Crossreactivity Human
Purity Detail Ammonium sulfate precipitation.
Formulation Liquid. HEPES with 0.15M NaCl, 0.01% BSA, 0.03% sodium azide, and 50% glycerol.
Isotype Negative Control

Mouse IgG1 Isotype Control

Other Product Data

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Declaration Manufactured by AbFrontier
Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage -20°C
Use/Stability Stable for at least 1 year after receipt when stored at -20°C.
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Product Specification Sheet
Datasheet Download PDF

Acetylcholinesterase hydrolyzes the neurotransmitter acetylcholine at neuromuscular junctions and brain cholinergic synapses, and thus terminates signal transmission. In addition, acetylcholinesterase contributes to various physiological processes through its involvement in the regulation of cell proliferation, differentiation and survival. Because of alternative splicing at the C-terminus of acetylcholinesterase mRNA, it has three different isoforms: synaptic (S), erythrocytic (E) and read-through (R). These acetylcholinesterase variants selectively participate in the processes involved in promoting or attenuating cell death that accompany changes in expression, distribution and balance among the enzyme variants. Impairment of cholinergic neurotransmission is a well-established fact in Alzheimer’s disease (AD). AD is characterized by a loss of cholinergic neurons and their cortical projections from the nucleus basalis and associated areas in the basal forebrain. The cholinesterase inhibitors (ChE-Is) attenuate the cholinergic deficit underlying the cognitive and neuropsychiatric dysfunctions in patients with AD. Inhibition of brain acetylcholinesterase (AChE) has been the major therapeutic target of cholinesterase inhibitor treatment strategies for Alzheimer's disease (AD). Terminates signal transduction at the neuromuscular junction by rapid hydrolysis of the acetylcholine released into the synaptic cleft. Role in neuronal apoptosis.

Product References

1) Jiang H and Zhang XJ. (2008) FEBS J. 275(4):612-617 (General)
2) Herholz K, (2008) Eur J Nucl Med Mol Imaging. 35 Suppl 1:S25-29 (General)
3) Lane RM et al. (2006) Int J Neuropsychopharmacol. 9(1):101-124 (General)

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