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Growth Differentiation Factor 15 (GDF15) (C-Term) antibody

Details for Product No. ABIN453961, Supplier: Login to see
Antigen
  • GDF15
  • GDF-15
  • MIC-1
  • MIC1
  • NAG-1
  • PDF
  • PLAB
  • PTGFB
  • SBF
Epitope
C-Term
79
52
17
16
15
13
11
7
6
5
5
5
4
3
2
2
2
1
1
1
1
1
1
1
1
1
1
1
Reactivity
Chimpanzee, Human, Macaque, Mouse (Murine), Rat (Rattus)
263
79
38
6
6
2
2
Host
Rabbit
231
30
20
5
Clonality
Polyclonal
Conjugate
Un-conjugated
34
28
13
5
5
5
1
1
1
1
1
1
1
1
1
Application
Enzyme Immunoassay (EIA), Western Blotting (WB)
241
208
80
25
23
11
11
6
5
4
1
1
Supplier
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Immunogen Synthetic peptide corresponding to the C-terminal sequence of NAG-1 protein. A residue of cysteine was added to facilitate coupling
Isotype IgG
Specificity This antibody reacts with the C-terminus of endogenous NAG-1 protein.
Cross-Reactivity (Details) Species reactivity (expected):Chimpanzee, Macaque, Mouse, Rat.
Species reactivity (tested):Human.
Purification Affinity chromatography
Alternative Name GDF15 (GDF15 Antibody Abstract)
Background The non-steroidal antiinflammatory 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. The induced expression of NAG-1 results in a 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.Synonyms: GDF-15, Growth/differentiation factor 15, MIC-1, MIC1, Macrophage inhibitory cytokine 1, NAG-1, NRG-1, NSAID-activated gene 1 protein, NSAID-regulated gene 1 protein, PDF, PLAB, PTGFB, Placental TGF-beta, Placental bone morphogenetic protein, Prostate differentiation factor
Gene ID 9518
NCBI Accession NP_004855
UniProt Q99988
Research Area Cardiovascular, Hypertrophy, Extracellular Matrix
Pathways
Application Notes ELISA: 1/300,000. Western Blot: 2,000 - 10,000.
Restrictions For Research Use only
Format Liquid
Concentration 1.0 mg/mL (by UV absorbance at 280 nm)
Buffer 0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2 containing 0.09 % (w/v) Sodium
Preservative Sodium azide
Precaution of Use This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Handling Advice Avoid repeated freezing and thawing.
Storage -20 °C
Supplier Images
 image for anti-Growth Differentiation Factor 15 (GDF15) (C-Term) antibody (ABIN453961) anti-Growth Differentiation Factor 15 (GDF15) (C-Term) antibody
Background publications Baek, Eling: "Changes in gene expression contribute to cancer prevention by COX inhibitors." in: Progress in lipid research, Vol. 45, Issue 1, pp. 1-16, 2006 (PubMed).

Lindmark, Zheng, Wiklund et al.: "H6D polymorphism in macrophage-inhibitory cytokine-1 gene associated with prostate cancer." in: Journal of the National Cancer Institute, Vol. 96, Issue 16, pp. 1248-54, 2004 (PubMed).