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MAB1852

Sigma-Aldrich

Anti-Macrophages/Monocytes Antibody, clone MOMA-2

clone MOMA-2, Chemicon®, from rat

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About This Item

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

Origine biologica

rat

Livello qualitativo

Forma dell’anticorpo

purified immunoglobulin

Tipo di anticorpo

primary antibodies

Clone

MOMA-2, monoclonal

Reattività contro le specie

mouse

Produttore/marchio commerciale

Chemicon®

tecniche

flow cytometry: suitable
immunohistochemistry: suitable

Isotipo

IgG2b

Condizioni di spedizione

wet ice

modifica post-traduzionali bersaglio

unmodified

Specificità

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.

Applicazioni

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

Stato fisico

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

Stoccaggio e stabilità

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.

Risultati analitici

Control
Macrophages, monocytes, lymphoid organs

Altre note

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

Note legali

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

Esclusione di responsabilità

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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Codice della classe di stoccaggio

12 - Non Combustible Liquids

Classe di pericolosità dell'acqua (WGK)

WGK 2

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

Cerca il Certificati d'analisi (COA) digitando il numero di lotto/batch corrispondente. I numeri di lotto o di batch sono stampati sull'etichetta dei prodotti dopo la parola ‘Lotto’ o ‘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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