Klotho converts canonical FGF receptor into a specific receptor for FGF23

By I. Urakawa, Y. Yamazaki, T. Shimada, K. Iijima, H. Hasegawa, K. Okawa, T. Fujita, S. Fukumoto, T. Yamashita. Nature, 2006

1,831 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Nephrology

View Paper: https://www.semanticscholar.org/paper/8a8b9c258c560515a60f701ccbc744676c679144

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. M. Mohammadi
2. M. Kuro-o
3. N. Itoh
4. D. Ornitz
5. D. Basile
6. T. Sutton
7. J. Lo
8. Chi-yuan Hsu

In Molecular Biology

1. Ryuji Hamamoto
2. M. Mohammadi
3. M. Kuro-o
4. N. Itoh
5. D. Ornitz
6. S. Hayami
7. Syuzo Kaneko
8. Masaaki Komatsu

In Nephrology

1. M. Mohammadi
2. D. Basile
3. T. Sutton
4. Harold I. Feldman
5. J. Kusek
6. Melissa D. Anderson
7. D. Bikle

Citations in the corpus

• Fibroblast growth factors: from molecular evolution to roles in development, metabolism and disease. (2011, background): “aKlotho most efficiently binds to and activates FGFR1c among several isoforms of FGFRs in cultured cells (27), suggesting the FGFR1c can transduce an FGF23/aKlotho signal.”
• FGF23, PTH and Phosphorus Metabolism in the Chronic Renal Insufficiency Cohort (2011, background): “FGF23 achieves its cellular specificity in the kidney and parathyroid glands by binding the co-receptor klotho, which increases the affinity of FGF23 for ubiquitously expressed FGF receptors.(3) In patients with chronic kidney disease (CKD), FGF23 levels are thought to increase as a compensatory res”
• Vitamin D Metabolism, Mechanism of Action, and Clinical Applications (2014, positive): “This signaling activates the mitogen-activated protein kinase (MAPK) cascade, but its role in CYP27B1 expression remains unclear (Urakawa et al., 2006).”
• Fibroblast Growth Factor 23 and Risks of Mortality and End-Stage Renal Disease in Patients with Chronic Kidney Disease (2011, background): “Finally, the lack of a validated assay in chronic kidney disease precluded us from measuring circulating levels of the soluble form of klotho, the FGF-23 coreceptor that is expressed in the kidneys and parathyroid glands and that demonstrates antiaging and vascular-protective effects.(29,30) Future ”
• Klotho is a substrate for a-, - and ?-secretase (2009, background): “form of Kl is a co-receptor for FGF-receptor 1, which converts that receptor into a specific receptor for FGF23 [6,7].”
• Programming the magnitude and persistence of antibody responses with innate immunity (2011, neutral): “vector RIG 0 2 4 6 vector KLm (1-1012) KLs (1-549) KLsss (34-549)”
• Pathophysiology of Acute Kidney Injury (2012, positive): “Although not clearly established, Klotho, a senescence related molecule appears to interact with various FGFs; Klotho facilitates the binding of FGF23 to the FGF-R1 in kidney (565).”
• Research resource: Comprehensive expression atlas of the fibroblast growth factor system in adult mouse. (2010, background): “Klotho is expressed at high levels in the kidney, where it serves as a coreceptor for FGF23 (15, 16).”
• Vitamin D and human health: lessons from vitamin D receptor null mice. (2008, background): “Klotho is a transmembrane protein that enhances FGF23 binding to its receptor complex, implicating Klotho as a cofactor in FGF23-FGF receptor interaction (232).”
• FGF/FGFR signaling in health and disease (2020, background): “Several OGD patients caused by activating mutations of FGFR1 present hypophosphatemia and increased serum level of FGF23.”
• Deregulation of the Histone Lysine-Specific Demethylase 1 Is Involved in Human Hepatocellular Carcinoma (2019, background): “Klotho is essential for endogenous FGF23 function as it converts FGFR1c into a specific FGF23 receptor [5,6].”