Primary Antibodies  >  Cancer Research Antibodies

NAG-1 H Variant Antibody

Mouse Monoclonal 7C12.B3.F2 IgG2b kappa
JCYIA Product
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  • Anti-NAG-1 (H variant specific) Monoclonal Antibody - Western Blot
100 µg
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NAG-1 H Variant Antibody Properties

Anti-NAG-1 (H variant specific) (MOUSE) Monoclonal Antibody - 200-301-B08
Target Species
Known Cross Reactivity
Monoclonal 7C12.B3.F2 IgG2b kappa
ELISA : 1:150,000
Western Blot : 1:1,000
Other Dilution: User Optimized
Physical State
Liquid (sterile filtered)
Shipping Condition
Dry Ice
1.30 mg/mL by UV absorbance at 280 nm
0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2
0.01% (w/v) Sodium Azide
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NAG-1 H Variant Antibody Description

Non-steroidal anti-inflammatory drug (NSAID) activated gene (NAG-1) is a member of the transforming growth factor-beta (TGF-beta) superfamily. NAG-1 is also known as Macrophage Inhibitory Cytokine-1 (MIC-1), Growth Differentiation Factor 15 (GDF15), Placental Bone Morphogenetic Protein (PLAB), or Prostate Derived Factor (PDF). NAG-1 is expressed in human placenta, prostate and colon. It possesses antitumorigenic and proapoptotic activities. NAG-1 expression is dramatically increased in inflammation, injury and malignancy. Increase of NAG-1 expression is a feature of many cancers including breast, colon, pancreas and prostate. In a number of studies, NAG-1 expression was increased by a number of NSAIDs. This increase in expression may correlate with the chemopreventive effect NSAIDs seem to have with certain cancers. NAG-1 expression is also induced by PPAR gamma ligands and by several dietary compounds such as conjugated linoleic acids (CLAs), naturally occurring fatty acids in ruminant food products, indoles, epicatechin gallate, and genistein. Induced expression of NAG-1 results in stimulation of apoptosis and inhibition of cell growth. Inhibition of NAG-1 induced expression by small interference RNA (siRNA) results in repression of induced apoptosis. NAG-1 expression is regulated by a numbers of transcription factors such as ERG-1 and Sp1. EGR-1 may be necessary for NSAID-induced NAG-1 expression. The study of expression of NAG-1 proteins, including variants, is important to define their potential role as serum biomarkers for cancer diagnosis, treatment monitoring, epidemiology study, and nutrition surveys.
mouse anti-NAG1 Antibody, NAG-1, GDF15, MIC-1, nonsteroidal anti-inflammatory drug-activated gene, NSAID-activated gene 1 protein, growth differentiation factor 15, macrophage inhibitory compound 1, prostate-derived factor
This Protein A purified antibody was prepared by repeated immunizations with a synthetic peptide corresponding to a region near the amino terminal end of human NAG-1 protein.  A residue of cysteine was added to facilitate coupling to KLH.
Immunogen Type
Storage Condition
Store vial at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use.
Application Note
This Protein A purified antibody is suitable for ELISA and western blotting of human NAG-1 protein.  This reagent is particularly useful to differentiate polymorphic forms of NAG-1 protein present in human serum samples.  This antibody is useful in dual antibody immunometric assays (EIA).  Expect bands in Western blots of approximately 14 and 28 kDa in size corresponding to NAG-1 monomer and dimer, respectively, using the appropriate cell lysate or extract. Specific conditions for reactivity should be optimized by the end user.
This product was purified from concentrated tissue culture supernatant Protein A chromatography.  This antibody specifically reacts with an H variant sequence of human NAG-1 protein from human tissues.  A BLAST analysis was used to suggest partial reactivity with NAG-1 from chimpanzee and macaque based on a 92% homology.  Cross-reactivity with NAG-1 from other sources has not been determined.
Disclaimer Note-General
This product is for research use only and is not intended for therapeutic or diagnostic applications. Please contact a technical service representative for more information. All products of animal origin manufactured by Rockland Immunochemicals are derived from starting materials of North American origin. Collection was performed in United States Department of Agriculture (USDA) inspected facilities and all materials have been inspected and certified to be free of disease and suitable for exportation. All properties listed are typical characteristics and are not specifications. All suggestions and data are offered in good faith but without guarantee as conditions and methods of use of our products are beyond our control. All claims must be made within 30 days following the date of delivery. The prospective user must determine the suitability of our materials before adopting them on a commercial scale. Suggested uses of our products are not recommendations to use our products in violation of any patent or as a license under any patent of Rockland Immunochemicals, Inc. If you require a commercial license to use this material and do not have one, then return this material, unopened to: Rockland Inc., P.O. BOX 5199, Limerick, Pennsylvania, USA.
General Reference
Baek, S.J., Eling, T.E. (2006) Changes in gene expression contribute to cancer prevention by COX inhibitors. Prog Lipid Res. 45(1):1-16. Lindmark, F., Zheng, S.L., Wiklund, F., Bensen, J., Balter, K.A., Chang, B., Hedelin, M., Clark, J., Stattin, P., Meyers, D.A., Adami, H-O., Isaacs, W., Gronberg, H. and Xu, J. (2004) H6D Polymorphism in Macrophage-Inhibitory Cytokine-1 Gene Associated With Prostate Cancer J Natl Cancer Inst. 96(16): 1248-1254.
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