1Kuro - o M, Matsumura Y, Aizawa H, et al. Mutation of the mouse klotho gene leads to a syndromeresembling ageing. Nature, 1997,390:45 - 51. [ PubMed : 9363890 ].
2Ming - Chang Hu, Makoto Kuro - o, Orson W. Moe, J Nephrol, 2010,23 ( Suppl 16) : S136 - S144.
3Isolde R. Fibroblast g rowth factor 23 and its role in phosphate ho- meostasis. European Journal of Endocrinology ,2010 :1610 - 1621.
4Hemando N, Biber J, Forster I, et al. Recent advances in renal phosphate tramport [ J ]. Ther Apher Dial, 2005,9 ( 4 ) : 323 - 327.
5Segawa H, Yamanaka S, Ohno Y, et al. Correlation between hy- perphosphatemia and type II Na -Picotransporter activity in klotho mice. Am J Physiol Renal Physiol, 2007,292 : F769 - F779. [ PubMed : 16985213 ].
6Urakawa I, Yamazaki Y, Shimada T, et al. Klotho converts canonical FGF receptor into a specific receptor for FGF23. Nature ,2006,444 (7120) :770 -774.
7Shimada T, gakitani M, Yamazaki Y, et al. Targeted ablation of FGF23 demonstrates fill essential physiological role of FGF23 in phosphate and vitamin Dmetabolism. J Clin Invest ,2004,113 (4) : 561 - 568.
8Nakatani T, Sarraj B, Ohnishi M, et al. In vivo genetic evidence for klotho - dependent, fibroblast growth factor 23 (Fgf23) - me- diated regulation of systemic phosphate homeostasis. FASEB J, 2009,23:433 -441. [ PubMed: 18835926].
9Nakatani T, Ohnishi M, Razzaque MS. Inactivation of klotho func- tion induces hyperphosphatemia even in presence of high serum fi-broblast growth factor 23 levels in a genetically engineered hy- pophosphatemic (Hyp) mouse model. FASEB J,2009,23:3702 - 3711. [ PubMed: 19584304].
