Calbindin D(9k) 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, 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.
Kutuzova
Galina D
GD
Department of Biochemistry, University of Wisconsin, 433 Babcock Drive, Madison, WI 53706-1544, USA.
Akhter
Shirin
S
Christakos
Sylvia
S
Vanhooke
Janeen
J
Kimmel-Jehan
Christine
C
Deluca
Hector F
HF
D000818:Animals; D001483:Base Sequence; D064026:Calbindins; D002118:Calcium / Q000097:blood*; D002460:Cell Line; D016368:Frameshift Mutation; D051379:Mice; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D008969:Molecular Sequence Data; D010641:Phenotype; D064030:S100 Calcium Binding Protein G / Q000235:genetics / Q000378:metabolism*
D064026:Calbindins; D064030:S100 Calcium Binding Protein G; D002118:Calcium