Calbindin D9k knockout mice are indistinguishable from wild-type mice in phenotype and serum calcium level

Since the discovery of calbindin D 9k , its role in intestinal calcium absorption has remained unsettled. Further, a wide distribution of calbindin D 9k among tissues has argued for its biological importance. We discovered a frameshift deletion in the calbindin D 9k gene in an ES cell line, E14.1, t...

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Published in:Proceedings of the National Academy of Sciences - PNAS 2006-08, Vol.103 (33), p.12377-12381
Main Authors: Kutuzova, Galina D., Akhter, Shirin, Christakos, Sylvia, Vanhooke, Janeen, Kimmel-Jehan, Christine, DeLuca, Hector F.
Format: Article
Language:English
Subjects:
Biological Sciences
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Summary:Since the discovery of calbindin D 9k , its role in intestinal calcium absorption has remained unsettled. Further, a wide distribution of calbindin D 9k among tissues has argued for its biological importance. We discovered a frameshift deletion in the calbindin D 9k gene in an ES cell line, E14.1, that originated from 129/OlaHsd mice. We produced mice with the mutant calbindin D 9k gene by injecting the E14.1 ES cell subline into the C57BL/6 host blastocysts and proved that these mice lack calbindin D 9k protein. Calbindin D 9k knockout mice were indistinguishable from wild-type mice in phenotype, were able to reproduce, and had normal serum calcium levels. Thus, calbindin D 9k is not required for viability, reproduction, or calcium homeostasis. vitamin D3 E14ES cells calcium homeostasis
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0605252103