Glucagon ELISA Kit (DEIABL230)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
2x96T
Sample
biological matrices
Species Reactivity
human
Intended Use
The Glucagon ELISA assay employs the quantitative sandwich enzyme immunoassay technique using two monoclonal antibodies specific for pancreatic glucagon. This user-friendly assay design utilizes a pair of antibodies that allows the detection of the whole pancreatic glucagon molecule in biological matrices with minimal or no cross reactivity to other form of glucagon molecules.
Storage
Store the unopened kit at 2-8°C.
Precision
Intra-assay precision (CV%): 3% - 7%. Inter-assay precision (CV%): 9%.
Detection Limit
11.7 pg/mL

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References


Insights into the potential benefits of black soybean (Glycine maxL.) polyphenols in lifestyle diseases

FOOD & FUNCTION

Authors: Yamashita, Yoko; Sakakibara, Hiroyuki; Toda, Toshiya; Ashida, Hitoshi

Black soybean (Glycine maxL.), a cultivar containing abundant polyphenols in its seed coat such as anthocyanins and flavan-3-ols, has been reported to possess various health benefits toward lifestyle diseases. In this review article, the safety evaluation of polyphenol-rich black soybean seed coat extract (BE) and absorption of BE polyphenols are summarized. Additionally, we describe the antioxidant activity of BE polyphenols and their ability to induce antioxidant enzymes. The health benefits of BE and its polyphenols, such as anti-obesity and anti-hyperglycemic activities through the activation of AMP-activated protein kinase and translocation of glucose transporter 4, respectively, are also discussed. Furthermore, we found that black soybean polyphenols were involved in the improvement of vascular function. These emerging data require further investigation in scientific studies and human trials to evaluate the prevention of lifestyle diseases using black soybean polyphenols.

Regulation of Metabolism by an Ensemble of Different Ion Channel Types: Excitation-Secretion Coupling Mechanisms of Adipokinetic Hormone Producing Cells in Drosophila

FRONTIERS IN PHYSIOLOGY

Authors: Perry, Rebecca J.; Saunders, Cecil J.; Nelson, Jonathan M.; Rizzo, Michael J.; Braco, Jason T.; Johnson, Erik C.

Adipokinetic Hormone (AKH) is the primary insect hormone that mobilizes stored energy and is functional equivalent to mammalian glucagon. While most studies have focused on exploring the functional roles of AKH, relatively little is known about how AKH secretion is regulated. We assessed the AKH cell transcriptome and mined the data set for specific insight into the identities of different ion channels expressed in this cell lineage. We found reliable expression of multiple ion channel genes with multiple members for each ionic species. Specifically, we found significant signals for 39 of the either known or suspected ion channel genes within the Drosophila genome. We next performed a targeted RNAi screen aimed to identify the functional contribution of these different ion channels that may participate in excitation-secretion coupling in AKH producing cells (APCs). We assessed starvation survival, because changes in AKH signaling have previously been shown to impact starvation sensitivity. Genetic knockdown of three genes (Ca-Beta, Sur, and sei), in AKH producing cells caused highly significant changes (P < 0.001) in both male and female lifespan, and knockdown of six other genes (Shaw, cac, Ih, NaCP60E, stj, and TASK6) caused significant changes (P < 0.05) in only female lifespan. Specifically, the genetic knockdown of Ca-Beta and Sur led to increases in starvation lifespan, whereas the knockdown of sei decreased starvation survivorship. Focusing on these three strongest candidates from the behavioral screen, we assessed other AKH-dependent phenotypes. The AKH hormone is required for starvation-induced hyperactivity, and we found that these three ion channel gene knockdowns changed activity profiles and further suggest a modulatory role of these channels in AKH release. We eliminated the possibility that these genetic elements caused AKH cell lethality, and using independent methods, we verified expression of these genes in AKH cells. Collectively, these results suggest a model of AKH-cell excitability and establish an experimental framework for evaluating intrinsic mechanisms of AKH release.

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