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Key Documents

HPA001399

Sigma-Aldrich

Anti-ADA antibody produced in rabbit

enhanced validation

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

Synonym(s):

Anti-Adenosine aminohydrolase antibody produced in rabbit, Anti-Adenosine deaminase antibody produced in rabbit

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About This Item

MDL number:
UNSPSC Code:
12352203
Human Protein Atlas Number:
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

product line

Prestige Antibodies® Powered by Atlas Antibodies

form

buffered aqueous glycerol solution

species reactivity

human

enhanced validation

independent
orthogonal RNAseq
Learn more about Antibody Enhanced Validation

technique(s)

immunoblotting: 0.04-0.4 μg/mL
immunohistochemistry: 1:5000-1:10000

immunogen sequence

GDETIPGSSLLPGHVQAYQEAVKSGIHRTVHAGEVGSAEVVKEAVDILKTERLGHGYHTLEDQALYNRLRQENMHFEICPWSSYLTGAWKPDTEHAVIRLKNDQANYSLNTDDPLIFKSTLDTDYQMTKRDMGFTEEE

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... ADA(100)

Immunogen

Adenosine deaminase recombinant protein epitope signature tag (PrEST)

Application

Anti-ADA antibody produced in rabbit is suitable for use as an antibody suspension bead array in affinity proteomic array to explore the potentiality of the human proteins in plasma to predict disease status during malaria infections.
Anti-ADA antibody produced in rabbit, a Prestige Antibody, is developed and validated by the Human Protein Atlas (HPA) project . Each antibody is tested by immunohistochemistry against hundreds of normal and disease tissues. These images can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. The antibodies are also tested using immunofluorescence and western blotting. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.

Biochem/physiol Actions

ADA (adenosine deaminase) gene encodes an enzyme that catalyzes the hydrolysis of adenosine to inosine. It is involved in the maintenance of adenosine homeostasis and plays a role in purine metabolism. It interacts with CD26 and mediates epithelial and lymphocyte cell adhesion. It also transduces co-stimulatory signals in T cells by interacting with CD26, an integral membrane protein. Defects in this gene can cause a deficiency of ADA resulting in severe combined immunodeficiency disease (SCID) with dysfunction of both B and T lymphocytes, impaired cellular immunity and decreased production of immunoglobulins. Overexpression of this enzyme can lead to congenital hemolytic anemia.

Features and Benefits

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

Linkage

Corresponding Antigen APREST78236

Physical form

Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide

Legal Information

Prestige Antibodies 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

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

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 Kanno et al.
The Japanese journal of experimental medicine, 58(1), 1-8 (1988-02-01)
We report the fourth case of adenosine deaminase (ADA) overproduction associated with hereditary nonspherocytic hemolytic anemia and the molecular analysis of this anomaly. The proband was a 10-year-old Japanese boy, who had an episode of erythroblastosis fetalis during the perinatal
Yue Hu et al.
Cell reports. Medicine, 5(5), 101530-101530 (2024-05-01)
Chimeric antigen receptor (CAR) T cell therapy is hindered in solid tumor treatment due to the immunosuppressive tumor microenvironment and suboptimal T cell persistence. Current strategies do not address nutrient competition in the microenvironment. Hence, we present a metabolic refueling approach using
Adenosine deaminase (ADA) isoenzymes ADA1 and ADA2: diagnostic and biological role.
C Gakis
The European respiratory journal, 9(4), 632-633 (1996-04-01)
I De Meester et al.
European journal of immunology, 24(3), 566-570 (1994-03-01)
The relationship between CD26/dipeptidyl peptidase IV, an ectopeptidase involved in T cell activation, and the binding protein for adenosine deaminase (ADAbp) was studied. Monoclonal antibodies (mAb) against CD26 and ADAbp, respectively, showed a similar binding profile on various lymphocyte subsets
D T Bonthron et al.
The Journal of clinical investigation, 76(2), 894-897 (1985-08-01)
Deficiency of adenosine deaminase (ADA) is the cause of an autosomal recessive form of immunodeficiency. We sought to define, at a molecular level, the mutations responsible for ADA deficiency in the cell line GM-1715, derived from an immunodeficient patient. Full-length

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