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Calbindin D(9k) knockout mice are indistinguishable from wild-type mice in phenotype and serum calcium level.


ABSTRACT: 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.

SUBMITTER: Kutuzova GD 

PROVIDER: S-EPMC1567887 | biostudies-literature | 2006 Aug

REPOSITORIES: biostudies-literature

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Calbindin D(9k) knockout mice are indistinguishable from wild-type mice in phenotype and serum calcium level.

Kutuzova Galina D GD   Akhter Shirin S   Christakos Sylvia S   Vanhooke Janeen J   Kimmel-Jehan Christine C   Deluca Hector F HF  

Proceedings of the National Academy of Sciences of the United States of America 20060808 33


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 ca  ...[more]

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