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obesity appears as the predominant determinant of the abnormalities in FGF21 (show FGF21 ELISA Kits) and FGF19 (show FGF19 ELISA Kits) levels. Opposite changes in beta-Klotho expression in fat and liver indicate potential tissue-specific alterations in the responsiveness to endocrine FGFs in obesity
ATF4 (show ATF4 ELISA Kits) signaling pathway is essential for mediating the effect of ER stress on beta-klotho expression.
Variants in genes involved in feedback regulation of bile acid synthesis (KLB, P=0.06 and FGFR4 (show FGFR4 ELISA Kits), P=0.09) were potentially associated with the irritable bowel syndrome-diarrhea subgroup with elevated serum C4.
In-depth DNA sequencing identified additional genetic coding and noncoding variants in KLB that are associated with fecal bile acids excretion or colonic transit in Irritable bowel syndrome-diarrhea.
betaKlotho suppresses tumor growth in hepatocellular carcinoma by regulating Akt (show AKT1 ELISA Kits)/GSK-3beta/cyclin D1 (show CCND1 ELISA Kits) signaling pathway.
KLB and FGFR1 (show FGFR1 ELISA Kits) form a 1:1 heterocomplex independent of the galectin lattice that transitions to a 1:2 complex upon the addition of FGF21 (show FGF21 ELISA Kits).
KLB-silencing in Huh7 cells decreased cell proliferation and suppressed FGFR4 (show FGFR4 ELISA Kits) downstream signaling.
Differential specificity of endocrine FGF19 (show FGF19 ELISA Kits) and FGF21 (show FGF21 ELISA Kits) to FGFR1 (show FGFR1 ELISA Kits) and FGFR4 (show FGFR4 ELISA Kits) in complex with KLB.
Deletion of the D1 and the D1-D2 linker (the D1/linker region) from FGFR1c led to beta-Klotho-independent receptor activation by FGF21 (show FGF21 ELISA Kits), suggesting that there may be a direct interaction between FGF21 (show FGF21 ELISA Kits) and the D1/linker region-deficient FGFR1c.
Polymorphism KLB rs4975017 may influence the colonic transit response to colesevelam in female patients with irritable bowel syndrome with diarrhea.
Data show that enhancing beta-klotho (KLB) expression in adipose may sensitize to endogenous fibroblast growth factor 21 (FGF21 (show FGF21 ELISA Kits)), thus representing a novel strategy to combat metabolic disease.
Klotho (show KL ELISA Kits) is a novel player in the retina, with a clear connection to photoreceptor cell death as well as with an influence on retinal organization.
Mice lacking the FGF21 (show FGF21 ELISA Kits) co-receptor, beta-Klotho, in the suprachiasmatic nucleus are refractory to the inhibitory effect of FGF21 (show FGF21 ELISA Kits) on female fertility.
The effects of FGF21 (show FGF21 ELISA Kits) are mediated through beta-Klotho expression in the suprachiasmatic nucleus of the hypothalamus and the dorsal vagal complex of the hindbrain.
betaKlotho is required for fibroblast growth factor 21 (show FGF21 ELISA Kits) effects on growth and metabolism.
demonstrate the first manifest evidence revealing that whereas alpha-Kl (show KL ELISA Kits) and beta-Kl are required for FGF23 (show FGF23 ELISA Kits) and FGF15/hFGF19-mediated signaling pathways in vivo, respectively, beta-Kl appears not to be essential for FGF21 (show FGF21 ELISA Kits)-mediated signal transduction in vivo.
In contrast to wild-type FGF23 (show FGF23 ELISA Kits), FGF23 (show FGF23 ELISA Kits)-21c (a variant of FGF23 (show FGF23 ELISA Kits) where the C-terminal domain of FGF23 (show FGF23 ELISA Kits) was replaced with the corresponding regions from FGF21 (show FGF21 ELISA Kits)), FGF23 (show FGF23 ELISA Kits)-21c gained the ability to activate FGFR1c and FGFR2c in the presence of betaKlotho.
Contributes to the transcriptional repression of cholesterol 7-alpha-hydroxylase (CYP7A1), the rate-limiting enzyme in bile acid synthesis. Probably inactive as a glycosidase. Increases the ability of FGFR1 and FGFR4 to bind FGF21 (By similarity).
, klotho beta like
, klotho beta-like protein
, klotho beta, pseudogene 1