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MAB19292

Sigma-Aldrich

Anti-ADAM2 Antibody, clone 9D2.2

clone 9D2.2, Chemicon®, from mouse

Synonyme(s) :

Fertilin beta

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About This Item

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

Source biologique

mouse

Niveau de qualité

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

9D2.2, monoclonal

Espèces réactives

mouse

Fabricant/nom de marque

Chemicon®

Technique(s)

ELISA: suitable
western blot: suitable

Isotype

IgG2b

Adéquation

not suitable for immunohistochemistry

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

wet ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... ADAM2(2515)

Spécificité

Recognizes mouse fertilin beta by immunoblot, staining of bands in a 46-48 kDa range (multiple bands are due to variable protein glycosylation).

Immunogène

Recombinant mouse fertilin produced by baculovirus expressin in SF9 cells.

Application

Research Category
Cell Structure
Research Sub Category
ECM Proteins

MMPs & TIMPs
This Anti-ADAM2 Antibody, clone 9D2.2 is validated for use in ELISA, WB for the detection of ADAM2.
Western blot: 1:500 - 1:1,000 dilution for detected against sperm lysates, using standard alkaline phosphatase with NBT/BCIP detection. Chemiluminescent detection may permit higher dilutions.

Not effective for immunohistochemistry.

Optimal working dilutions must be determined by end user.

Forme physique

Format: Purified
Liquid at 1 mg/mL in 0.02M phosphate buffer, pH 7.6, 0.25M NaCl, and 0.1% sodium azide

Stockage et stabilité

Maintain refrigerated at 2-8°C in undiluted aliquots for up to 12 months.

Informations légales

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

Clause de non-responsabilité

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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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

WGK 2

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

H Nishimura et al.
Developmental biology, 233(1), 204-213 (2001-04-26)
We produced mice lacking the sperm surface protein cyritestin (ADAM 3) and found mutant males are infertile. Similar to fertilin beta (ADAM 2) null sperm (C. Cho et al., 1998, Science 281, 1857-1859), cyritestin null sperm are drastically deficient in
Ryo Yamaguchi et al.
Biology of reproduction, 75(5), 760-766 (2006-07-28)
Male mice deficient for the calmegin (Clgn) or the angiotensin-converting enzyme (Ace) gene show impaired sperm migration into the oviduct and loss of sperm-zona pellucida binding ability in vitro. Since CLGN is a molecular chaperone for membrane transport of target
Ryo Yamaguchi et al.
Genes to cells : devoted to molecular & cellular mechanisms, 13(8), 851-861 (2008-09-11)
CD52 is a glycosylphosphatidylinositol (GPI)-anchored antigen expressed on lymphocytes and in epididymal epithelial cells. CD52 is also known as "maturation-associated sperm antigen" but its function is unknown. We therefore generated Cd52 disrupted mice. The resulting Cd52 null mice were healthy
Yasutaka Ueda et al.
The Journal of biological chemistry, 282(42), 30373-30380 (2007-08-23)
A palmitate linked to the inositol in glycosylphosphatidylinositol (GPI) is removed in the endoplasmic reticulum immediately after the conjugation of GPI with proteins in most cells. Previously, we identified PGAP1 (post GPI attachment to proteins 1) as a GPI inositoldeacylase
Kathryn K Stein et al.
Biology of reproduction, 73(5), 1032-1038 (2005-07-15)
Adam2-null and Adam3-null male mice exhibit reduced levels of one or more ADAM proteins on mature sperm, in addition to the loss of the genetically targeted protein. ADAM protein loss was believed to occur posttranslationally, although the timing of loss

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