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GDF15 Antibody
Purified Mouse Monoclonal Antibody (Mab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | Q99988 |
| Reactivity | Human |
| Predicted | Human |
| Host | Mouse |
| Clonality | monoclonal |
| Isotype | IgG1,κ |
| Clone/Animal Names | 2182CT228.18.8 |
| Calculated MW | 34140 Da |
| Gene ID | 9518 |
|---|---|
| Other Names | Growth/differentiation factor 15, GDF-15, Macrophage inhibitory cytokine 1, MIC-1, NSAID-activated gene 1 protein, NAG-1, NSAID-regulated gene 1 protein, NRG-1, Placental TGF-beta, Placental bone morphogenetic protein, Prostate differentiation factor, GDF15 (HGNC:30142) |
| Target/Specificity | This GDF15 antibody is generated from a mouse immunized with a recombinant protein from the human GDF15. |
| Dilution | WB~~1:4000 |
| Format | Purified monoclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, followed by dialysis against PBS. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | GDF15 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| 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
Regulates food intake, energy expenditure and body weight in response to metabolic and toxin-induced stresses (PubMed:28953886, PubMed:28846097, PubMed:28846098, PubMed:28846099, PubMed:23468844, PubMed:29046435). Binds to its receptor, GFRAL, and activates GFRAL-expressing neurons localized in the area postrema and nucleus tractus solitarius of the brainstem (PubMed:28953886, PubMed:28846097, PubMed:28846098, PubMed:28846099). It then triggers the activation of neurons localized within the parabrachial nucleus and central amygdala, which contitutes part of the 'emergency circuit' that shapes feeding responses to stressful conditions (PubMed:28953886). On hepatocytes, inhibits growth hormone signaling (By similarity).
References
Hromas R.,et al.Biochim. Biophys. Acta 1354:40-44(1997).
Yokoyama-Kobayashi M.,et al.J. Biochem. 122:622-626(1997).
Bootcov M.R.,et al.Proc. Natl. Acad. Sci. U.S.A. 94:11514-11519(1997).
Paralkar V.M.,et al.J. Biol. Chem. 273:13760-13767(1998).
Kalnine N.,et al.Submitted (MAY-2003) to the EMBL/GenBank/DDBJ databases.
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