About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Kcnn4tm1Rklr
targeted mutation 1, Ralf Kohler
MGI:3722942
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Kcnn4tm1Rklr/Kcnn4tm1Rklr B6.129S-Kcnn4tm1Rklr MGI:5435602
hm2
Kcnn4tm1Rklr/Kcnn4tm1Rklr involves: 129S/SvEv * C57BL/6 MGI:3723135


Genotype
MGI:5435602
hm1
Allelic
Composition
Kcnn4tm1Rklr/Kcnn4tm1Rklr
Genetic
Background
B6.129S-Kcnn4tm1Rklr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kcnn4tm1Rklr mutation (0 available); any Kcnn4 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• at 14 days after unilateral ureteral obstruction (UUO), renal interstitial fibrosis is significantly attenuated in obstructed mutant kidneys relative to wild-type controls
• after UUO, chronic tubulointerstitial damage is reduced by ~48%, interstitial collagen I/III deposition by ~30%, and cells staining positive for (myo)fibroblast marker alphaSMA by ~45%

homeostasis/metabolism
• at 14 days after UUO, mutant obstructed kidneys exhibit significantly less chronic tubulointerstitial damage, reduced collagen deposition, fewer alphaSMA-positive cells, a higher % of preserved proximal tubules and increased width of functional renal parenchyma relative to wild-type obstructed kidneys
• however, no significant difference in mononuclear cell infiltration is observed between genotypes




Genotype
MGI:3723135
hm2
Allelic
Composition
Kcnn4tm1Rklr/Kcnn4tm1Rklr
Genetic
Background
involves: 129S/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kcnn4tm1Rklr mutation (0 available); any Kcnn4 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• heart weight to body weight is increased (4.9+/-0.1 mg/g compared to 4.4+/-0.1 mg/g in wild-type mice)
• left ventricular cross-section area is increased (22.4+/-1.8 mm2 compared to 18.0+/-0.9 mm2 in wild-type mice)
• mean arterial blood pressure is increased (119+/-3 mm Hg compared to 105+/-2 mmHg in wild-type mice)
• diastolic blood pressure is increased (96+/-3 mm Hg compared to 84+/-3 mm Hg in wild-type mice)
• systolic blood pressure is increased (142+/-3 mm Hg compared to 129+/-3 mm Hg in wild-type mice)
• acetylcholine-induced dilations in the carotid artery and resistance-sized vessels are impaired
• endothelium-derived hyperpolarizing factor-inducing dilations in the carotid artery and resistance-sized vessels are impaired

growth/size/body
• heart weight to body weight is increased (4.9+/-0.1 mg/g compared to 4.4+/-0.1 mg/g in wild-type mice)
• at 2 months, mice develop splenomegaly that progresses with age
• at 2 months

hematopoietic system
• at 2 months, mice develop splenomegaly that progresses with age
• at 2 months
• in young mice
• 10% in mature mice
• red blood cells exhibit deformability and 30% reduced filterability compared to wild-type cells
• mild
• at 2 to 3 months, mice exhibit a 7-fold increase in iron depositions in the red pulp of the spleen compared to in wild-type mice
• red blood cells exhibit impaired osmotic tolerance compared to wild-type cells

homeostasis/metabolism
• at 2 to 3 months, mice exhibit a 7-fold increase in iron depositions in the red pulp of the spleen compared to in wild-type mice

immune system
• at 2 months, mice develop splenomegaly that progresses with age
• at 2 months
• at 2 to 3 months, mice exhibit a 7-fold increase in iron depositions in the red pulp of the spleen compared to in wild-type mice

muscle
• acetylcholine-induced dilations in the carotid artery and resistance-sized vessels are impaired
• endothelium-derived hyperpolarizing factor-inducing dilations in the carotid artery and resistance-sized vessels are impaired





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