Mouse Fibroblast growth factor 15(FGF15) ELISA kit

Code CSB-EL522052MO
Size 96T,5×96T,10×96T
Price Request a Quote or Start an on-line Chat
Trial Size 24T ELISA Kit Trial Size (Only USD$150/ kit)
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Product Details

Alternative Names
FGF-15 ELISA Kit; Fgf15 ELISA Kit; FGF15_MOUSE ELISA Kit; FGF19 ELISA Kit; Fibroblast growth factor 15 ELISA Kit
Abbreviation
FGF15
Uniprot No.
Species
Mus musculus (Mouse)
Sample Types
serum, plasma, tissue homogenates, cell lysates
Detection Range
15.6 pg/ml - 1000 pg/ml
Sensitivity
3.9 pg/ml
Assay Time
1-5h
Sample Volume
50-100ul
Detection Wavelength
450 nm
Research Area
Signal Transduction
Assay Principle
quantitative
Measurement
Sandwich
Materials provided
    • A micro ELISA plate --- The 96-well plate has been pre-coated with an anti-human FGF15 antibody. This dismountable microplate can be divided into 12 x 8 strip plates.
    • Two vials lyophilized standard ---Dilute a bottle of the standard at dilution series, read the OD values, and then draw a standard curve.
    • One vial Biotin-labeled FGF15 antibody (100 x concentrate) (120 μl/bottle) ---Act as the detection antibody.
    • One vial HRP-avidin (100 x concentrate) (120 μl/bottle) ---Bind to the detection antibody and react with the TMB substrate to make the solution chromogenic.
    • One vial Biotin-antibody Diluent (15 ml/bottle) ---Dilute the Biotin-antibody.
    • One vial HRP-avidin Diluent (15 ml/bottle) ---Dilute the HRP-avidin solution.
    • One vial Sample Diluent (50 ml/bottle)---Dilute the sample to an appropriate concentration.
    • One vial Wash Buffer (25 x concentrate) (20 ml/bottle) ---Wash away unbound or free substances.
    • One vial TMB Substrate (10 ml/bottle) ---Act as the chromogenic agent. TMB interacts with HRP, eliciting the solution turns blue.
    • One vial Stop Solution (10 ml/bottle) ---Stop the color reaction. The solution color immediately turns from blue to yellow.
    • Four Adhesive Strips (For 96 wells) --- Cover the microplate when incubation.
    • An instruction manual
Materials not provided
    • A microplate reader capable of measuring absorbance at 450 nm, with the correction wavelength set at 540 nm or 570 nm.
    • An incubator can provide stable incubation conditions up to 37°C±5°C.
    • Centrifuge
    • Vortex
    • Squirt bottle, manifold dispenser, or automated microplate washer
    • Absorbent paper for blotting the microtiter plate
    • 50-300ul multi-channel micropipette
    • Pipette tips
    • Single-channel micropipette with different ranges
    • 100ml and 500ml graduated cylinders
    • Deionized or distilled water
    • Timer
    • Test tubes for dilution
Troubleshooting
and FAQs
Storage
Store at 2-8°C. Please refer to protocol.
Lead Time
3-5 working days after you place the order, and it takes another 3-5 days for delivery via DHL or FedEx
Description

The Mouse Fibroblast growth factor 15 (FGF15) ELISA Kit is used for the quantitative detection of mouse FGF15 in many biological fluids, including serum, plasma, and tissue homogenates. The kit has high sensitivity, excellent specificity, good linearity, precision low than 10%, high recovery, good lot-to-lot consistency. Get access to more details from the product instructions.

This assay employs the Sandwich-ELISA technique, in which FGF15 in the samples or standards is sandwiched between pre-coated anti-human FGF15 and Biotin-labeled FGF15 antibody. The Ag-Ab-Ag immune complex is labeled with HRP-avidin and then develops a color reaction after the addition of the TMB substrate. The intensity of the color is positively correlated to the amount of FGF15 in the sample.

Mouse FGF15, an ortholog of human FGF19, is a bile acid (BA)-induced late fed-state gut hormone that mediates postprandial metabolic responses in the liver. It plays a key role in the bile acid-driven enterohepatic signaling. After a meal, the intestinal farnesoid X receptor (FXR) senses elevated bile acids to induce the expression of mouse FGF15. Secreted FGF15 acts on FGFR/KLB receptor complexes via repress CYP7A1 decrease BA synthesis, to stimulate glycogen synthase (GS) activity and glycogen production through inactivation of GSK3, and to inhibits gluconeogenesis by blocking the phosphorylation and activation of CREB. FGF15 thus acts after insulin in the transition from the fed to the fasted state.

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Target Background

Function
(From Uniprot)
Involved in the suppression of bile acid biosynthesis through down-regulation of CYP7A1 expression.
Gene References into Functions
  1. Taken together, these results suggested that FGF19, through the anti-oxidative defense system, attenuated the development of diabetic cardiomyopathy and restored cardiac function. PMID: 29778534
  2. ileal FGF15/19 to hepatic FGFR4 axis is activated and promotes liver regeneration (LR) after partial hepatectomy (PH) in mice, supporting the potential of ileal FGF15/19 to hepatic FGFR4 axis-targeted therapy to enhance LR after PH PMID: 29468415
  3. FRS2alpha-mediated pathways are essential for the FGF15/FGF19-FGFR4 signaling axis to control bile acid homeostasis. PMID: 25056539
  4. Together, our results show that SuFu promotes cerebellar radial precursor differentiation to neurons. SuFu function is mediated in part by GLI3R and down-regulation of Fgf15 expression. PMID: 28560839
  5. Results show a reciprocal regulation of adiponectin and FGF19 gene expression in mice. PMID: 27666676
  6. Tumorigenicity was assessed in three mouse models (db/db, diet-induced obese, and multi-drug resistance 2 [Mdr2]-deficient) following continuous exposure to FGF19 or FGF15 via adeno-associated viral-mediated gene delivery. PMID: 28189755
  7. These data identify hypothalamic Fgf15 as a regulator of glucagon secretion. PMID: 27829151
  8. Intestinal sensing of highly elevated levels of conjugated bile acids in blood promotes FGF15 signaling, reducing hepatic bile acid synthesis and modulating bile acid transporters. PMID: 28498614
  9. Fgf15 is the sonic hedgehog downstream signal to control thalamic regionalization, neurogenesis, and neuronal differentiation by regulating the expression and mutual segregation of neurogenic and proneural regulatory genes. PMID: 26311466
  10. human microbiota was able to reduce the levels of tauro-beta-muricholic acid and induce expression of FXR target genes Fgf15 and Shp in ileum after long-term colonization. We show that a human microbiota can change BA composition and induce FXR signaling in colonized mice, but the levels of secondary BAs produced are lower than in mice colonized with a mouse microbiota PMID: 27956475
  11. FGF15 improves lipid homeostasis and reduces bile acid synthesis, but promotes fibrosis during the development of non-alcoholic steatohepatitis PMID: 28673684
  12. This study demonstrates that the FGF19-SHP-LSD1 axis maintains homeostasis by suppressing unnecessary autophagic breakdown of cellular components, including lipids, under nutrient-rich postprandial conditions. PMID: 28446510
  13. The elevation in circulating levels of adiponectin and Fgf15 led to normalized hepatic and serum levels of bile acids, limited hepatic accumulation of toxic bile, attenuated inflammation, and amelioration of liver injury in the ethanol-fed mNT knockout mice. PMID: 27573244
  14. This study reveals SHP as a global transcriptional partner of SREBP-2 in regulation of sterol biosynthetic gene networks and provides a potential mechanism for cholesterol-lowering action of FGF19. PMID: 26634251
  15. we suggest that considerable mechanistic differences exist between humans and mice with regard to the nuclear receptors controlling the VitA-FGF15/19 axis. PMID: 26723851
  16. Ileal Fgf15 expression is a potent inhibitor of bile acid synthesis. PMID: 26040986
  17. Protective effects of farnesoid X receptor on hepatic lipid accumulation are mediated by hepatic FXR and are independent of intestinal FGF15 signaling. PMID: 25156247
  18. In mice with humanized livers human hepatocytes do not recognize FGF-15 produced by mouse intestine, resulting in up-regulation of bile acid synthesis enlargement of the bile acid pool, affecting the hepatostat. PMID: 26028580
  19. Intestinal PPARalpha-UDP- Glucuronyltransferases and downstream FXR-FGF15 signalling play vital roles in control of bile acid homeostasis and the pathological development of colitis. PMID: 25183423
  20. Sstudy shows an important contribution of ileal FGF15 to hepatocarcinogenesis in a clinically relevant mouse model where lack of Fgf15 resulted in reduced tumor burden and attenuated tumor progression. PMID: 25346390
  21. results suggest that FGF15 deficiency severely impairs liver regeneration in mice after PHx. The underlying mechanism is likely the result of disrupted bile acid homeostasis and impaired priming of hepatocyte proliferation. PMID: 24699334
  22. a direct role of intestinal FGF15/19 in the regulation of SI P450 expression and may have profound implications for the prediction of drug exposure in patients with compromised hepatic P450 function PMID: 24184963
  23. findings implicate the brain in the antidiabetic action of systemic FGF19 and establish the brain's capacity to rapidly, potently, and selectively increase insulin-independent glucose disposal PMID: 24084738
  24. Total ileal FGF15 expression was elevated almost 20-fold in Ostalpha(-/-) mice as a result of increased villus epithelial cell number and ileocyte FGF15 protein expression PMID: 22542490
  25. generated a variant of FGF19, FGF19-7, that has altered receptor specificity with a strong bias toward FGFR1c PMID: 22457778
  26. Differential specificity of endocrine FGF19 and FGF21 to FGFR1 and FGFR4 in complex with KLB. PMID: 22442730
  27. Mouse Fgf15 and human FGF19 play key roles in enterohepatic signaling, regulation of liver bile acid biosynthesis, gallbladder motility and metabolic homeostasis PMID: 22396169
  28. Pregnane X receptor activation induces FGF19-dependent tumor aggressiveness in humans and mice PMID: 21747170
  29. mice lacking FGF15 (FGF19) fail to maintain blood concentrations of glucose and normal postprandial liver glycogen; FGF19 activates a physiologically important, insulin-independent endocrine pathway that regulates hepatic protein and glycogen metabolism PMID: 21436455
  30. Fgf15 is a crucial signaling molecule regulating the postmitotic transition of dorsal neural progenitors and thus the initiation and proper progression of dorsal midbrain neurogenesis in the mouse. PMID: 21172336
  31. the physiological relevance of the contribution of the intestinal FXR-Fgf15 signalling pathway in control of hepatic bile acid synthesis PMID: 20531290
  32. the structure-function relationship of FGF19/FGF21 and the structural basis underpinning the distinct proliferative feature of FGF19 compared with FGF21 PMID: 20660733
  33. activation of FGFR4 is the mechanism whereby FGF19 can increase hepatocyte proliferation and induce hepatocellular carcinoma formation. PMID: 20018895
  34. Fgf15 is expressed in the optic vesicle, a subset of progenitor cells of neural retina, and emerging ganglion and amacrine cells during retinogenesis PMID: 15465490
  35. Fgf15 is directly regulated by Shh signaling through Gli proteins in the developing diencephalon and midbrain PMID: 15614767
  36. in the mouse, loss of FG15 gene function results in high penetrant VSDs and alignment defects of the aorta and pulmonary trunk PMID: 15789410
  37. fibroblast growth factor 15 (FGF15) signals from intestine to liver to repress the gene encoding cholesterol 7alpha-hydroxylase (CYP7A1), which catalyzes the first and rate-limiting step in the classical bile acid synthetic pathway PMID: 16213224
  38. identified two enhancers: one directed lacZ expression in the hindbrain/spinal cord and the other in the posterior midbrain (pmb), rhombomere1 (r1) and pharyngeal epithelia PMID: 16930954
  39. compare the expression pattern during neural development of chick Fgf19 with mouse Fgf15. PMID: 17654705
  40. These findings suggest that the repressor form of Gli2 preferentially binds to the GliREs to control Fgf15 expression. PMID: 18279667
  41. FGF15 and FGF8 have distinct signaling properties, and opposite effects on neocortical patterning and differentiation PMID: 18625063
  42. The results of this study indicate that both beta-Klotho and FGF-15/19 repress the apical sodium-dependent bile acid transporter in enterocytes and cholangiocytes. PMID: 18772362
  43. FGF15/FGFR4 integrates growth factor signaling with hepatic bile acid metabolism and insulin action PMID: 19237543
  44. Results suggest that FGF19-regulated liver bile acid metabolism could be independent of its glucose-lowering effect, and direct FGFR activation in adipose tissue may play an important role in the regulation of glucose homeostasis. PMID: 19706524

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Subcellular Location
Secreted.
Protein Families
Heparin-binding growth factors family
Tissue Specificity
Expressed in the developing brain.
Database Links
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