Renal Ca2+ wasting, hyperabsorption, and reduced bone thickness in mice lacking TRPV5
J. Clin. Invest. Joost G.J. Hoenderop, et al. 112:1906 doi:10.1172/JCI19826 [
Go to this article.]
Figure 1Creation of null mutant mice for the
TRPV5 gene locus. (
a) Targeted inactivation of the
TRPV5 gene. Top, exon 13, encoding the pore-forming unit of TRPV5, is flanked by
loxP sites. Middle, recombined TRPV5
loxneo locus. Bottom, targeted allele in which exon 13 is deleted by Cre recombinase. Black boxes indicate exons; probe and genotype primers (A–D) are depicted. neo
R, neomycin resistance cassette. (
b) Representative Southern blot analysis of
BamHI-digested tail-derived DNA isolated from
TRPV5+/+,
TRPV5+/–, and
TRPV5–/– mice. (
c) Identification of mouse genotype by PCR analysis of tail-derived DNA. The PCR product in the upper gel shows the presence of the wild-type allele (+/+) using primers C and D; the lower gel shows the knockout allele (–/–) using primers A and B. Both alleles are detected in heterozygous animals (+/–). (
d) TRPV5 (top images) and kallikrein (lower images) immunohistochemical costaining of kidney cortex from
TRPV5+/+ and
TRPV5–/– mice. (
e) Immunopositive TRPV6 staining of renal distal tubules from
TRPV5+/+ and
TRPV5–/– mice. A color version of this figure is available online as Supplementary Figure
1 (http://www.jci.org/cgi/content/full/112/12/1906/DC1).
