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MAB19292

Sigma-Aldrich

Anti-ADAM2 Antibody, clone 9D2.2

clone 9D2.2, Chemicon®, from mouse

Synonym(s):

Fertilin beta

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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

9D2.2, monoclonal

species reactivity

mouse

manufacturer/tradename

Chemicon®

technique(s)

ELISA: suitable
western blot: suitable

isotype

IgG2b

suitability

not suitable for immunohistochemistry

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... ADAM2(2515)

Specificity

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

Immunogen

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.

Physical form

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

Storage and Stability

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

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 Code

12 - Non Combustible Liquids

WGK

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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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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