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Calbindin D sub(9k) knockout mice are indistinguishable from wild-type mice in phenotype and serum calcium level
Since the discovery of calbindin D sub(9k), its role in intestinal calcium absorption has remained unsettled. Further, a wide distribution of calbindin D sub(9k) among tissues has argued for its biological importance. We discovered a frameshift deletion in the calbindin D sub(9k) gene in an ES cell...
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Published in: | Proceedings of the National Academy of Sciences - PNAS 2006-08, Vol.103 (33), p.12377-12381 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | Since the discovery of calbindin D sub(9k), its role in intestinal calcium absorption has remained unsettled. Further, a wide distribution of calbindin D sub(9k) among tissues has argued for its biological importance. We discovered a frameshift deletion in the calbindin D sub(9k) gene in an ES cell line, E14.1, that originated from 129/OlaHsd mice. We produced mice with the mutant calbindin D sub(9k) gene by injecting the E14.1 ES cell subline into the C57BL/6 host blastocysts and proved that these mice lack calbindin D sub(9k) protein. Calbindin D sub(9k) knockout mice were indistinguishable from wild-type mice in phenotype, were able to reproduce, and had normal serum calcium levels. Thus, calbindin D sub(9k) is not required for viability, reproduction, or calcium homeostasis. |
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ISSN: | 0027-8424 1091-6490 |