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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(APOE-cre)VITew
transgene insertion VI, Thomas E Willnow
MGI:2449766
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Clcn7tm3.1Tjj/Clcn7tm3.1Tjj
Tg(APOE-cre)VITew/0
B6.Cg-Clcn7tm3.1Tjj Tg(APOE-cre)VITew MGI:4414638
cn2
Clcn5tm1Tjj/Clcn5+
Clcn7tm3.1Tjj/Clcn7tm3.1Tjj
Tg(APOE-cre)VITew/0
involves: 129/Sv * 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J MGI:4414640
cn3
Lrp2tm1Tew/Lrp2tm1Tew
Tg(APOE-cre)VITew/0
Not Specified MGI:2667817


Genotype
MGI:4414638
cn1
Allelic
Composition
Clcn7tm3.1Tjj/Clcn7tm3.1Tjj
Tg(APOE-cre)VITew/0
Genetic
Background
B6.Cg-Clcn7tm3.1Tjj Tg(APOE-cre)VITew
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Clcn7tm3.1Tjj mutation (0 available); any Clcn7 mutation (40 available)
Tg(APOE-cre)VITew mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• degradation of the endocytosed protein in proximal tubule cells of the kidneys is disrupted compared to in wild-type mice

renal/urinary system




Genotype
MGI:4414640
cn2
Allelic
Composition
Clcn5tm1Tjj/Clcn5+
Clcn7tm3.1Tjj/Clcn7tm3.1Tjj
Tg(APOE-cre)VITew/0
Genetic
Background
involves: 129/Sv * 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Clcn5tm1Tjj mutation (0 available); any Clcn5 mutation (17 available)
Clcn7tm3.1Tjj mutation (0 available); any Clcn7 mutation (40 available)
Tg(APOE-cre)VITew mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:2667817
cn3
Allelic
Composition
Lrp2tm1Tew/Lrp2tm1Tew
Tg(APOE-cre)VITew/0
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lrp2tm1Tew mutation (0 available); any Lrp2 mutation (260 available)
Tg(APOE-cre)VITew mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• on a vitamin D-depleted diet, mutant mice exhibit an appropriate increase in circulating PTH levels in reponse to hypocalcemia
• on a vitamin D-depleted diet, mutant mice exhibit hypocalcemia due to hypovitaminosis D
• on a normal (vitamin D-repleted) diet, urinary loss of 25-OH vitamin D3 coincides with a 50% reduction in the plasma levels of 25-OH vitamin D3 and of 1,25-(OH)2 D3 while serum calcium, phosphorus, and PTH levels remain unchanged relative to homozygous Lrp2tm1Tew control mice
• on a vitamin D-depleted diet, the plasma levels of 25-OH vitamin D3 and of 1,25-(OH)2 D3 are reduced to the lowest detection levels along with a marked reduction in serum calcium levels and an increase in PTH levels
• a 5- to 6-fold increase in urinary excretion of 125I-labeled vitamin D-binding protein (DBP) and 3H-25-OH vitamin D3 is observed relative to homozygous Lrp2tm1Tew control mice
• mutant kidneys display impaired retrieval of plasma proteins from the glomerular filtrate and excrete increased amounts of low molecular weight proteins into the urine, including vitamin D-binding protein (DBP) and retinol-binding protein (RBP)

skeleton
• the total bone mineral content in femur and tibia is drastically decreased relative to control mice
• on a vitamin D-deficient chow, mutant verebrates exhibit a highly abnormal and unmineralized bone surface that is mostly covered by osteoid (uncalcified matrix)
• a significant increase in osteoid surface, osteoid width, and osteoid volume and a concomittant reduction in the mineralizing bone surfaces are observed
• after 6 weeks on a vitamin D-deficient chow, mutant mice exhibit true severe osteomalacia (softening of the bones) as a result of hypovitaminosis D
• osteopathy is characterized by a reduction in bone mineral content, an increase in osteoid surfaces, and a lack of mineralizing activity
• on a normal diet, mutant lumbar vertebral bodies show a moderate but consistent increase in resorptive cavities and osteoid-covered surfaces, indicating increased resorption and remodeling activity
• a modest increase in resorptive surface area is observed, as 67% of osteoid surfaces block access of osteoclasts to the bones

renal/urinary system
• a 5- to 6-fold increase in urinary excretion of 125I-labeled vitamin D-binding protein (DBP) and 3H-25-OH vitamin D3 is observed relative to homozygous Lrp2tm1Tew control mice
• mutant kidneys display impaired retrieval of plasma proteins from the glomerular filtrate and excrete increased amounts of low molecular weight proteins into the urine, including vitamin D-binding protein (DBP) and retinol-binding protein (RBP)





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last database update
09/03/2024
MGI 6.24
The Jackson Laboratory