Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 281, Issue 10, Pages 6120-6123Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.C500457200
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Funding
- Div Of Information & Intelligent Systems
- Direct For Computer & Info Scie & Enginr [0829438] Funding Source: National Science Foundation
- NIA NIH HHS [R01AG19712, R01AG25326, R01 AG019712, R01 AG025326-03, R01 AG019712-05, R01 AG025326] Funding Source: Medline
- NIDDK NIH HHS [R01DK065842, R01 DK065842] Funding Source: Medline
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The aging suppressor gene Klotho encodes a single-pass transmembrane protein. Klotho-deficient mice exhibit a variety of aging-like phenotypes, many of which are similar to those observed in fibroblast growth factor-23 (FGF23)-deficient mice. To test the possibility that Klotho and FGF23 may function in a common signal transduction pathway(s), we investigated whether Klotho is involved in FGF signaling. Here we show that Klotho protein directly binds to multiple FGF receptors (FGFRs). The Klotho-FGFR complex binds to FGF23 with higher affinity than FGFR or Klotho alone. In addition, Klotho significantly enhanced the ability of FGF23 to induce phosphorylation of FGF receptor substrate and ERK in various types of cells. Thus, Klotho functions as a cofactor essential for activation of FGF signaling by FGF23.
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