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Anti-NAG-1 (N-terminal specific) (RABBIT) Antibody
NAG-1 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Host | Rabbit |
|---|---|
| Conjugate | Unconjugated |
| Target Species | Human |
| Reactivity | Human |
| Clonality | Polyclonal |
Application 
| WB, IHC, E, I, LCI |
| Application Note | This affinity purified antibody is tested for ELISA and western blotting of human NAG-1 protein. For detection of NAG-1 in human serum, a sandwich ELISA is suggested using this antibody in combination with anti-NAG-1/GDF15 C-terminal specific antibodies. This antibody is useful in dual antibody immunometric assays (EIA). Specific conditions for reactivity should be optimized by the end user. Expect bands in western blots of approximately 14 kDa in size corresponding to NAG-1 monomer using the appropriate cell lysate or extract. |
| Physical State | Liquid (sterile filtered) |
| Buffer | 0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2 |
| Immunogen | This affinity 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. |
| Preservative | 0.01% (w/v) Sodium Azide |
| Gene ID | 9518 |
|---|---|
| Other Names | 9518 |
| Purity | This product was affinity purified from monospecific antiserum by immunoaffinity chromatography. This antibody specifically reacts with the amino terminal end 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. Multimeric forms of NAG-1 may be detected. Cross-reactivity with NAG-1 from other sources has not been determined. |
| 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. |
| Precautions Note | This product is for research use only and is not intended for therapeutic or diagnostic applications. |
| Name | GDF15 {ECO:0000303|PubMed:23468844, ECO:0000312|HGNC:HGNC:30142} |
|---|---|
| Function | Hormone produced in response to various stresses to confer information about those stresses to the brain, and trigger an aversive response, characterized by nausea, vomiting, and/or loss of appetite (PubMed:23468844, PubMed:24971956, PubMed:28846097, PubMed:28846098, PubMed:28846099, PubMed:28953886, PubMed:29046435, PubMed:30639358, PubMed:31875646, PubMed:33589633, PubMed:38092039). The aversive response is both required to reduce continuing exposure to those stresses at the time of exposure and to promote avoidance behavior in the future (PubMed:30639358, PubMed:33589633, PubMed:38092039). Acts by binding to its receptor, GFRAL, activating GFRAL-expressing neurons localized in the area postrema and nucleus tractus solitarius of the brainstem (PubMed:28846097, PubMed:28846098, PubMed:28846099, PubMed:28953886, PubMed:31535977). It then triggers the activation of neurons localized within the parabrachial nucleus and central amygdala, which constitutes part of the 'emergency circuit' that shapes responses to stressful conditions (PubMed:28953886). The GDF15-GFRAL signal induces expression of genes involved in metabolism, such as lipid metabolism in adipose tissues (PubMed:31402172). Required for avoidance behavior in response to food allergens: induced downstream of mast cell activation to promote aversion and minimize harmful effects of exposure to noxious substances (By similarity). In addition to suppress appetite, also promotes weight loss by enhancing energy expenditure in muscle: acts by increasing calcium futile cycling in muscle (By similarity). Contributes to the effect of metformin, an anti-diabetic drug, on appetite reduction and weight loss: produced in the kidney in response to metformin treatment, thereby activating the GDF15-GFRAL response, leading to reduced appetite and weight (PubMed:31875646, PubMed:37060902). The contribution of GDF15 to weight loss following metformin treatment is however limited and subject to discussion (PubMed:36001956). Produced in response to anticancer drugs, such as camptothecin or cisplatin, promoting nausea, vomiting and contributing to malnutrition (By similarity). Overproduced in many cancers, promoting anorexia in cancer (cachexia) (PubMed:32661391). Responsible for the risk of nausea and vomiting during pregnancy: high levels of GDF15 during pregnancy, mostly originating from the fetus, are associated with increased nausea and vomiting (PubMed:38092039). Maternal sensitivity to nausea is probably determined by pre-pregnancy exposure to GDF15, women with naturally high level of GDF15 being less susceptible to nausea than women with low levels of GDF15 before pregnancy (PubMed:38092039). Promotes metabolic adaptation in response to systemic inflammation caused by bacterial and viral infections in order to promote tissue tolerance and prevent tissue damage (PubMed:31402172). Required for tissue tolerance in response to myocardial infarction by acting as an inhibitor of leukocyte integring activation, thereby protecting against cardiac rupture (By similarity). Inhibits growth hormone signaling on hepatocytes (By similarity). |
| Cellular Location | Secreted Note=Secreted in the plasma. |
| Tissue Location | Detected in plasma (at protein level) (PubMed:28572090, PubMed:29046435). Highly expressed in placenta, with lower levels in prostate and colon and some expression in kidney (PubMed:37060902, PubMed:9348093). |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
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.
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