|Application ||WB, ICC/IF|
|Description||Rabbit Anti-Human Choline Acetyltransferase Polyclonal|
|Target/Specificity||Predicted molecular weight at ~82.5kDa. Observed molecular weights between 68-70kDa.|
|Other Names||CHAT_Human Antibody, Acetyl CoA choline O Acetyltransferase Antibody, Choline Acetylase Antibody, CLAT_Human Antibody, CMS1A Antibody|
|Immunogen||Synthetic peptide from the N-terminal to the mid-protein of human Choline O-Acetyltrasferase|
|Purification||Peptide Affinity Purified|
|Storage Buffer||PBS, 50% glycerol, 0.09% sodium azide|
|Shipping Temperature||Blue Ice or 4ºC|
|Certificate of Analysis||A 1:1000 dilution of SPC-706 was sufficient for detection of Choline Acetyltransferase on mouse brain lysates using Goat anti-rabbit IgG:HRP as the secondary antibody.|
|Cellular Localization||Cytoplasm | Cytosol | Mitochondrion | Nucleus|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Acetylcholine (ACh) is a common neurotransmitter for motoneurons, preganglionic autonomic neurons, postganglionic parasympathetic neurons, a variety of brain regions and some emerging neuron-like stem cells. The metabolism of Ach is relatively simple, involving only two enzymes: choline acetyltransferase (ChAT) for synthesis and acetylcholinesterase (AChE) for degradation. Further, acetylcholine has little function in neurons other than neurotransmission and seems to be neuron specific. It seems that only cholinergic neurons have significant amounts of ChAT making anti-choline acetyltransferase a useful specific marker. ChAT is a valuable marker for diseases associated with decreased cholinergic function such as Schizophrenia, Alzheimer disease and Down syndrome (1-3).
1. Houser C.R., Crawford G.D., Barber R.P., Salvaterra P.M., Vaughn J.E. (1983) Brain Research. 266(1): 97-119.
2. Karson C.N., Casanova M.F., Kleinman J.E.m Griffin W.S. (1993) Am J Psychiatry. 150: 454-459.
3. Baskins D.S., et al. (1999) Arch Neurol. 56: 1121-1123.
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