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Publication : Overexpression of klotho protein modulates uninephrectomy-induced compensatory renal hypertrophy by suppressing IGF-I signals.

First Author  Nagasu H Year  2011
Journal  Biochem Biophys Res Commun Volume  407
Issue  1 Pages  39-43
PubMed ID  21354104 Mgi Jnum  J:171953
Mgi Id  MGI:5002435 Doi  10.1016/j.bbrc.2011.02.089
Citation  Nagasu H, et al. (2011) Overexpression of klotho protein modulates uninephrectomy-induced compensatory renal hypertrophy by suppressing IGF-I signals. Biochem Biophys Res Commun 407(1):39-43
abstractText  The klotho gene is highly expressed in the distal convoluted tubule of the kidney, while its encoded protein has many physiological and pathophysiological renal roles. We investigated the effect of klotho protein on physiological compensatory renal hypertrophy after nephrectomy in klotho transgenic (KLTG) mice. Renal hypertrophy was suppressed in KLTG mice compared with wild-type mice, and this was associated with suppression of insulin growth factor-1 (IGF-1) signaling by klotho protein. In vitro, IGF-1 signaling was suppressed in human proximal tubular cells transfected with the klotho plasmid. Our data suggest that klotho modulates compensatory renal hypertrophy after nephrectomy via suppression of the IGF-1 signaling pathway, indicating a novel physiological role for klotho protein in the kidney.
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