Sandwich ELISA, Biotin-labelled antibody
mouse samples: 7 µl/well
rat samples: 50 µl/well
At ambient temperature. Upon receipt, store the product at the temperature recommended below.
Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).
Limit of Detection
mouse samples CV = 8.4%
rat samples CV = 8.5%
mouse samples CV = 8.7%
rat samples CV = 6%
mouse samples 98.9%
rat samples 104.5
mouse samples 99.8%
rat samples 103.7%
- bovine Weak reactivity (recom. dilution 1:3)
- cat Yes (recommended dilution 1:3)
- dog Non-detectable
- horse Non-detectable
- goat Yes (recommended dilution 1:6)
- hamster Yes (recommended dilution 1:12)
- human Non-detectable
- monkey Non-detectable
- rabbit Non-detectable
- chicken Not tested
- mouse Yes
- rat Yes
- sheep Yes (recommended dilution 1:3)
- pig Yes (recommended dilution 1:3)
Diabetology - Other Relevant Products, Energy metabolism and body weight regulation, Animal studies
The FGFs are a family of more than 20 small (~17–26 kDa) secreted peptides. The initial characterization of these proteins focused on their ability to stimulate fibroblast proliferation. This mitogenic activity was mediated through FGF receptors (FGFRs) 1, 2, or 3. A fourth closely related tyrosine kinase receptor (FGFR4) was able to bind the FGFs but did not lead to a mitogenic response.
FGFs modulate cellular activity via at least 5 distinct subfamilies of high-affinity FGF receptors (FGFRs): FGFR-1, –2, –3, and –4, all with intrinsic tyrosine kinase activity and, except for FGFR-4, multiple splice isoforms, and FGFR-5, which lacks an intracellular kinase domain. There is growing evidence that FGFRs can be important for regulation of glucose and lipid homeostasis. The overexpression of a dominant negative form of FGFR-1 in β cells leads to diabetes in mice, which thus implies that proper FGF signaling is required for normal β cell function and glycemia maintenance. FGFR-2 appears to be a key molecule during pancreatic development. Moreover, FGFR-4 has been implicated in cholesterol metabolism and bile acid synthesis.
FGF-19, has been shown to cause resistance to diet-induced obesity and insulin desensitization and to improve insulin, glucose, and lipid profiles in diabetic rodents. Since these effects, at least in part, are mediated through the observed changes in metabolic rates, FGF-19 can be considered as a regulator of energy expenditure.
FGF-21 is preferentially expressed in liver, but an exact knowledge of FGF-21 bioactivity and its mode of action have been lacking to date. FGF-21 is a potent activator of glucose uptake on adipocytes, protects animals from diet-induced obesity when overexpressed in transgenic mice, and lowers blood glucose and triglyceride levels when therapeutically administered to diabetic rodents.