About   Help   FAQ
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 (42 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 (42 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 (261 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)





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
11/12/2024
MGI 6.24
The Jackson Laboratory