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MAB5270

Sigma-Aldrich

Anti-Choline Acetyltransferase Antibody, clone 1.B3.9B3

clone 1.B3.9B3, Chemicon®, from mouse

Synonym(s):

ChAT

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

1.B3.9B3, monoclonal

species reactivity

human, rat, pig

manufacturer/tradename

Chemicon®

technique(s)

ELISA: suitable
immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
western blot: suitable

isotype

IgG1

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... CHAT(1103)
pig ... Chat(396896)
rat ... Chat(290567)

Specificity

Reacts with choline acetyltransferase (ChAT)-positive cells from humans, rats and pigs (Ostermann-Fatif et al., 1992a,b).

Immunogen

Highly purified ChAT obtained from porcine brain (Ostermann-Fatif et al., 1990).

Application

Research Category
Neuroscience
Research Sub Category
Neurotransmitters & Receptors
This Anti-Choline Acetyltransferase Antibody, clone 1.B3.9B3 is validated for use in ELISA, IH, IH(P), WB for the detection of Choline Acetyltransferase.
Western blot

ELISA

Immunohistochemistry: 10-20 μg/mL in paraffin embedded sections {See Ratcliffe et al. 1998}

Optimal working dilutions and protocols must be determined by end user.

Target description

69 kDa

Physical form

Format: Purified
Protein A purified
Purified immunoglobulin. Lyophilized from 0.02 M Phosphate buffer, 0.25 M NaCl with 0.1% sodium azide. Reconstitute to 100 μg/mL with sterile distilled water.

Storage and Stability

Maintain lyophilized antibody at 2–8°C in undiluted aliquots for up to 6 months. Maintain reconstituted antibody at -20°C in undiluted aliquots for up to 6 months.

Analysis Note

Control
Brain tissue

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Angela Marina Montalbano et al.
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IL-17A is overexpressed in the lung during acute neutrophilic inflammation. Acetylcholine (ACh) increases IL-8 and Muc5AC production in airway epithelial cells. We aimed to characterize the involvement of nonneuronal components of cholinergic system on IL-8 and Muc5AC production in bronchial
Julio Santos-Torres et al.
Journal of neurotrauma, 26(9), 1593-1607 (2009-06-16)
Lesions in specific areas of the rat motor cortex generate deficits related to fine movement performance affecting the forelimb. We have previously shown that transplants of embryonic frontal cortex ameliorate these motor deficits. Amelioration has been associated with a functional
Lydia Lebenheim et al.
Molecular psychiatry (2020-11-16)
The striatum is the main input structure of the basal ganglia. Distinct striatal subfields are involved in voluntary movement generation and cognitive and emotional tasks, but little is known about the morphological and molecular differences of striatal subregions. The ventrolateral
Xue-Lian Qi et al.
Cell reports, 36(5), 109469-109469 (2021-08-05)
Acetylcholine plays a critical role in the neocortex. Cholinergic agonists and acetylcholinesterase inhibitors can enhance cognitive functioning, as does intermittent electrical stimulation of the cortical source of acetylcholine, the nucleus basalis (NB) of Meynert. Here we show in two male
Y-Y Lai et al.
Neuroscience, 154(2), 431-443 (2008-05-20)
There is no adequate animal model of restless legs syndrome (RLS) and periodic leg movements disorder (PLMD), disorders affecting 10% of the population. Similarly, there is no model of rapid eye movement (REM) sleep behavior disorder (RBD) that explains its

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