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These results provide evidence that changes in KL gene expression with age may, at least in part, be the result of epigenetic changes to the 5' regulatory region.
a disrupted FGF19/FGFR4/betaKL signaling pathway may play a role in the development of thyroid cancers.
The betaKlotho gene expression might be involved in endometrioid endometrial cancer tumorgenesis. The betaKlotho may in future be used as an useful indicator for endometrial cancer, although further studies are needed
Knockdown of beta-Klotho produced the opposite effects. In conclusion, beta-Klotho inhibits EMT and plays a tumorsuppressive role in prostate cancer (PCa) , linking FGF/FGFR/beta-Klotho signaling to the regulation of PCa progression.
crystal structures of free and ligand-bound beta-klotho extracellular regions that reveal the molecular mechanism that underlies the specificity of FGF21 towards beta-klotho and demonstrate how the FGFR is activated in a klotho-dependent manner
the metabolic FGF21/KLB/FGFR1 pathway is involved in congenital hypogonadotropic hypogonadism (CHH) Genetic screening of 334 CHH patients identified seven heterozygous loss-of-function KLB mutations in 13 patients (4%). Most patients with KLB mutations (9/13) exhibited metabolic defects.
We conducted a genome-wide association meta-analysis and replication study among >105,000 individuals of European ancestry and identified beta-Klotho (KLB) as a locus associated with alcohol consumption (rs11940694; P = 9.2 x 10(-12)).
Our results suggest that KLbeta plays important roles in tumor invasion and progression, and its concentration may be a valuable urinebased marker for the detection of bladder cancer.
obesity appears as the predominant determinant of the abnormalities in FGF21 and FGF19 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 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, 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/GSK-3beta/cyclin D1 signaling pathway.
KLB and FGFR1 form a 1:1 heterocomplex independent of the galectin lattice that transitions to a 1:2 complex upon the addition of FGF21.
KLB-silencing in Huh7 cells decreased cell proliferation and suppressed FGFR4 downstream signaling.
Differential specificity of endocrine FGF19 and FGF21 to FGFR1 and FGFR4 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, suggesting that there may be a direct interaction between FGF21 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 suggest that KLB is an important regulator in the immortalization of HCECs by facilitating FGF19 growth factor signaling.
Sulfated glycosaminoglycans are required for specific and sensitive fibroblast growth factor (FGF) 19 signaling via FGF receptor 4 and betaKlotho.
Downregulation of beta-klotho expression is not the major mechanism of impaired FGF21 signaling in white adipose tissue.
liver FGF21-betaKlotho pathway sufficient and necessary to repress mTOR/S6K activity
The study supports a pro-adipogenic role for betaKlotho in skeletal muscle fibro/adipogenesis and calls for further research on involvement of the FGF-FGFR-betaKlotho axis in the fibro/adipogenic infiltration associated with functional deterioration of skeletal muscle in aging and muscular dystrophy.
Data show that enhancing beta-klotho (KLB) expression in adipose may sensitize to endogenous fibroblast growth factor 21 (FGF21), thus representing a novel strategy to combat metabolic disease.
beta-Kl in hepatocytes is necessary and sufficient for lipid homeostasis, whereas nonhepatic beta-Kl regulates energy metabolism.
Klotho 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 co-receptor, beta-Klotho, in the suprachiasmatic nucleus are refractory to the inhibitory effect of FGF21 on female fertility.
The effects of FGF21 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 effects on growth and metabolism.
demonstrate the first manifest evidence revealing that whereas alpha-Kl and beta-Kl are required for FGF23 and FGF15/hFGF19-mediated signaling pathways in vivo, respectively, beta-Kl appears not to be essential for FGF21-mediated signal transduction in vivo.
In contrast to wild-type FGF23, FGF23-21c (a variant of FGF23 where the C-terminal domain of FGF23 was replaced with the corresponding regions from FGF21), FGF23-21c gained the ability to activate FGFR1c and FGFR2c in the presence of betaKlotho.
function of Klotho family proteins
These results indicate that betaKlotho and FGFRs form the cognate FGF-21 receptor complex, mediating FGF-21 cellular specificity and physiological effects.
Metabolic regulator betaKlotho interacts with fibroblast growth factor receptor 4 (FGFR4) to induce apoptosis and inhibit tumor cell proliferation.
betaKlotho functions as a cofactor essential for fibroblast growth factor 21 activity
Data suggested that betaKlotho expression is a crucial determinant of the FGF21 specificity of the target cells upon which it acts in an endocrine fashion.
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.
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