Human FGF20 (Fibroblast growth factor 20) ELISA Kit (DEIA-FN493)

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

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serum, plasma, cell culture supernatants, tissue homogenate
Species Reactivity
Intended Use
For quantitative detection of Human FGF20 (Fibroblast growth factor 20) in serum, plasma, tissue homogenates and other biological fluids.
Contents of Kit
1. 96-well strip plate (Dismountable), 1 plate
2. Lyophilized Standard, 2 vials
3. Sample/Standard dilution buffer, 20 mL
4. Biotin-detection antibody (Concentrated), 120 uL
5. Antibody dilution buffer, 10 mL
6. HRP-Streptavidin Conjugate(SABC), 120 uL
7. SABC dilution buffer, 10 mL
8. TMB substrate, 10 mL
9. Stop solution, 10 mL
10. Wash buffer (25X), 30 mL
11. Plate Sealer, 5 pieces
12. Product Manual, 1 copy
Store the unopened product at 2 - 8 °C. Do not use past expiration date.
Intra-Assay: CV<8%
Inter-Assay: CV<10%
Detection Range
15.6-1000 pg/mL
9.375 pg/mL
Standard Curve


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Fibroblast growth factor 9 (FGF9) inhibits myogenic differentiation of C2C12 and human muscle cells


Authors: Huang, Jian; Wang, Kun; Shiflett, Lora A.; Brotto, Leticia; Bonewald, Lynda F.; Wacker, Michael J.; Dallas, Sarah L.; Brotto, Marco

Osteoporosis and sarcopenia (osteosarcopenia (OS)) are twin-aging diseases. The biochemical crosstalk between muscle and bone seems to play a role in OS. We have previously shown that osteocytes produce soluble factors with beneficial effects on muscle and vice versa. Recently, enhanced FGF9 production was observed in the OmGFP66 osteogenic cell line. To test its role in myogenic differentiation, C2C12 myoblasts were treated with recombinant FGF9. FGF9 as low as 10 ng/mL inhibited myogenic differentiation, suggesting that FGF9 might be a potential inhibitory factor produced from bone cells with effects on muscle cells. FGF9 (10-50 ng/mL) significantly decreased mRNA expression of MyoG and Mhc while increasing the expression of Myostatin. Consistent with the phenotype, RT-qPCR array revealed that FGF9 (10 ng/mL) increased the expression of Icam1 while decreased the expression of Wnt1 and Wnt6 decreased, respectively. FGF9 decreased caffeine-induced Ca2+ release from the sarcoplasmic reticulum (SR) of C2C12 myotubes and reduced the expression of genes (i.e. Cacna1s, RyR2, Naftc3) directly associated with intracellular Ca2+ homeostasis. Myogenic differentiation in human skeletal muscle cells was similarly inhibited by FGF9 but required higher doses of 200 ng/mL FGF9. FGF9 was also shown to stimulate C2C12 myoblast proliferation. FGF2 and the FGF9 subfamily members FGF16 and FGF20 also inhibited C2C12 myoblast differentiation and enhanced proliferation. Intriguingly, the differentiation inhibition was independent of proliferation enhancement. These findings suggest that FGF9 may modulate myogenesis via a complex signaling mechanism.

Depressive symptoms are associated with a functional polymorphism in a miR-433 binding site in the FGF20 gene


Authors: Jimenez, Karen M.; Pereira-Morales, Angela J.; Adan, Ana; Lopez-Leon, Sandra; Forero, Diego A.

Genetic studies of major depressive disorder and its associated endophenotypes are useful for the identification of candidate genes. In recent years, variations in non-coding RNA genes, such as miRNAs, have been explored as novel candidates for psychiatric disorders and related endophenotypes. The aim of the present study was to evaluate the possible association between a functional polymorphism (rs12720208) in the FGF20 gene, which regulates its modulation by miR-433, and depressive symptoms in young adults. A sample of 270 participants from Colombia were evaluated with the Hospital Anxiety and Depression Scale - Depression Subscale (HADS-D) and genotyped for the rs12720208 polymorphism using a TaqMan assay. A lineal regression analysis was used. A statistically significant association of the functional polymorphism in the FGF20 gene (rs12720208) with depressive symptoms was found. It was observed that individuals with the G/A genotype had higher scores for the HADS-D subscale. Our results are the first description in the scientific literature about a significant association between a functional polymorphism in the FGF20 gene, which regulates its modulation by miR-433, and depressive symptoms.

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