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Key Documents

MAB1852

Sigma-Aldrich

Anti-Macrophages/Monocytes Antibody, clone MOMA-2

clone MOMA-2, Chemicon®, from rat

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About This Item

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

biological source

rat

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

MOMA-2, monoclonal

species reactivity

mouse

manufacturer/tradename

Chemicon®

technique(s)

flow cytometry: suitable
immunohistochemistry: suitable

isotype

IgG2b

shipped in

wet ice

target post-translational modification

unmodified

Related Categories

Specificity

Recognizes an intracellular antigen of mouse macrophages and monocytes. It reacts strongly with macrophages in lymphoid organs such as tingible body macrophages and macrophages in T cell dependent areas and is extremely useful in immunohistochemistry. Reacts on all mouse strains tested.

Application

Detect Macrophages/Monocytes using this Anti-Macrophages/Monocytes Antibody, clone MOMA-2 validated for use in FC, IH.
Flow Cytometry: membrane permeabilization is recommended for this application.

Immunohistology: FRESH frozen sections at 1:25. The epitope recognized by MAB1852 is formaline sensitive. Fixation in fresh, acetone at 4°C or colder is strongly recommended. Specimens must be completely air dried after acetone fixation. Formalin or PFA fixation is not recommended.

Because of the lower titer, enhanced detection systems such as our poly-HRP secondaries or biotin labelled secondary antibodies followed by SA-FITC are recommended.



Optimal working dilutions must be determined by end user.
Research Category
Inflammation & Immunology
Research Sub Category
Inflammation & Autoimmune Mechanisms

Physical form

Format: Purified
Protein A Purified mouse immunoglobulin in 10 mM sodium phosphate buffer (pH 7.4), 0.15 M NaCl, and 0.1% sodium azide as a preservative..
Protein A purified

Storage and Stability

Maintain for 1 year at 2–8°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Analysis Note

Control
Macrophages, monocytes, lymphoid organs

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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Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


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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Macrophages in T and B cell compartments and other tissue macrophages recognized by monoclonal antibody MOMA-2. An immunohistochemical study.
Kraal, G, et al.
Scandinavian Journal of Immunology, 26, 653-661 (1987)
Morphologic and electroretinographic phenotype of SR-BI knockout mice after a long-term atherogenic diet.
Provost AC, Vede L, Bigot K, Keller N, Tailleux A, Jais JP, Savoldelli M, Ameqrane I et al.
Investigative Ophthalmology & Visual Science null
Cannabinoid receptor type 2 (CB2) deficiency alters atherosclerotic lesion formation in hyperlipidemic Ldlr-null mice.
Courtney D Netherland,Theresa G Pickle,Alicia Bales,Douglas P Thewke
Atherosclerosis null
Yujiao Zhang et al.
Nature communications, 14(1), 4622-4622 (2023-08-02)
Caspase recruitment-domain containing protein 9 (CARD9) is a key signaling pathway in macrophages but its role in atherosclerosis is still poorly understood. Global deletion of Card9 in Apoe-/- mice as well as hematopoietic deletion in Ldlr-/- mice increases atherosclerosis. The
Johannes Schödel et al.
Atherosclerosis, 206(2), 383-389 (2009-04-11)
We previously reported that deletion of brain type neuronal nitric oxide synthase-alpha (nNOS-alpha) accelerates atherosclerosis in apolipoproteinE (apoE) knockout (ko) mice. The regulation of nNOS expression is complex, involving the generation of mRNA splice variants. The current study investigates occurrence

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