Search Criteria: Research Area is "Developmental Biology Research: Internal/Organ Defects (kidney)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 007846 | 129S-Pdgfrbtm1Sor/J | Repository- Live |
| One third of homozygous embryos, aged E16 to E18.5, exhibit purpura and edema with some embryos in this group dying at this stage. Homozygous embryos delivered by Caesarean section at E18.5 die within minutes. Homozygotes exhibit anemia, elevated numbers of nucleated erythrocytes, polychromasia, irregularly shaped mature erythrocytes (anisocytosis), and hemorrhaging. Glomerular capillary tufts are absent and the capsule space is filled with blood cells. No gene product (protein) is detected by Western blot analysis of total protein. A truncated transcript presumed to be due to exon skipping is detected by Northern blot analysis. This mutant mouse strain may be useful in studies of hematopoiesis, kidney development and and cellular signaling during development. | ||
| 007199 | 129S-Sgpl1Gt(ROSA)78Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth and do not survive past 8 weeks of age. Homozygotes occur at a lower than Mendelian ratio (19%) from heterozygote X heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern in adult intestinal epithelial cells. Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mutant mice are anemic (low hemoglobin concentration, reduced red blood cell count, low hematocrit). Mutants exhibit polychromasia (abnormally high number of immature blood cells), kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells) and abnormalities in palate bone fusion. Homozygotes are infertile. Heterozygote
..... For more information please see the full descriiption on the strain data sheet | ||
| 008101 | B6.129S6(FVB)-Ptgs2tm1.1Fun/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Female homozygotes are not fertile. The protein gene product does not have cyclooxygenase activity while the peroxidase activity is normal as measured by LPS induction of macrophages derived from mutant mice. Mutant mice are more sensitive to collagen treatment resulting in reduction of platelet numbers (indicating enhanced thrombogenesis) and exhibit a higher frequency of sudden death due to thromboxane receptor agonist treatment. No prolonged bleeding time from LPS administration is observed. Prostaglandin E metabolite levels are diminished in urine. Three month old mutant mice have elevated systolic blood pressure (measured by the tail cuff method). Homozygotes exhibit undersize, pale kidneys with atrophic cortices, interstitial inflammation, hypoplastic glomeruli and glomerulosclerosis.
This mutant mouse strain may be useful in studies of
..... For more information please see the full descriiption on the strain data sheet | ||
| 007204 | B6;129S4-2610005L07RikGt(ROSA)73Sor/J | Repository- Live |
| Mice homozygous for this mutant allele (called BC058969 in the primary publication) are viable and fertile, with greater than 50% embryonic lethality observed in homozygous embryos. Homozygotes occur at a lower than Mendelian ratio (9%) from heterozygote x heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects (sternum and calvarial bones). Notably, 100% incidence of calvarial bones defects is reported. Additionally, homozygotes are reported to have low β-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These BC058969-mutant (2610005L07Rik-mutant) mice may be useful in studying cellular signal
..... For more information please see the full descriiption on the strain data sheet | ||
| 007200 | B6;129S4-Arid5bGt(ROSA)75Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth, occur at lower than Mendelian ratio (16%) and 46% die within 3 weeks of age. Homozygotes are fertile when they survive to adulthood. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit kidney defects (abnormally high blood urea nitrogen level, mutant kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells in glomeruli), and abnormalities in palate bone fusion. These Arid5b-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 007206 | B6;129S4-TiparpGt(ROSA)79Sor/J | Repository- Live |
| Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells); kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled, degraded glomeruli are often observed, increased number of vascular smooth muscle cells partially filling the glomeruli space); and abnormalities in palate bone fusion. Homozygotes occur at lower than Mendelian ratio (22%), and 32% die by age 2 week. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Tiparp-mutant mice may be useful in studying kidney development, vascular development, hematopoiesis and cellular signaling during development and in adult mice; specifically receptor tyrosine
..... For more information please see the full descriiption on the strain data sheet | ||
| 007562 | D2.B6-Ins2Akita/MatbJ | Repository- Live |
| DBA/2J mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe and progressive in the males than in the females and include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. Obesity and insulitis do not accompany diabetes. Litter sizes range from 2-8 pups. Heterozygous Akita males develop albuminuria at two months of age. The albuminuria is progressive such that by 6 months of age albumin/creatine levels are approximately 600ug/mg. Additionally, it has been reported that DBA/2J heterozygous mutant mice develop diabetic nephropathy.
Although not studied in the DBA/2J heterozygotes, C57BL/6 heterozygous mutant mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as
..... | ||
| 003301 | (C57BL/6J x C3H-Eya1bor)F1/J | Repository-Cryopreserved |
| The human Branchio-Oto-Renal Syndrome is generally a dominant disorder with incomplete penetrance and variable expressivity resulting from null mutations in the EYA1 gene. The mouse Eya1bor allele is primarily a recessive hypomorphic mutation. Nevertheless, homozygous mice with this hypomorphic allele offer a good model for Branchio-Oto-Renal Syndrome. The phenotype of Eya1bor/Eya1bor mice parallels that of the human Branchio-Oto-Renal Syndrome and both are thought to result from reduced gene dosage. The Eya1bor/Eya1bor mice are deaf and their behavior is marked by circling and head-bobbing. They lack all but the most basal one-quarter of the cochlea, and the organ of Corti is completely absent. They have foreshortened, narrower semicircular canals and in some the common crus is incomplete. Their kidneys are absent or dysmorphic with greater severity generally on the left side. Fewe
..... For more information please see the full descriiption on the strain data sheet | ||
| 002866 | 129-Wnt4tm1Amc/J | Repository-Cryopreserved |
| 000212 | 129P4.Cg-Axin1Fu/J | Repository-Cryopreserved |
| The fused mutation is dominant and generally more severe in homozygotes, but has highly varying penetrance in both the heterozygote and homozygote, to the extent that some homozygotes do not have an abnormal phenotype. Phenotypic traits of mice carrying the Axin1Fu allele include shortened, bifurcated, or absent tails, kinked tails with fused vertebrae, other asymmetrical fusions of vertebrae, axial duplications, and ribs fused at the proximal ends. Imperforate anus, anemia at birth, waltzing movement, deafness, and missing or abnormal kidneys have also been reported. Both heterozygotes and homozygotes are generally fertile although female carriers transmit with a lower penetrance than males do. (Reed, 1936; Dunn and Gluecksohn-Waelsch, 1954; Theiler and Gluecksohn-Waelsch, 1956.) | ||
| 000277 | ATEB/LeJ | Repository-Cryopreserved |
| Mice homozygous for the atrichosis spontaneous mutation (at) are characterized by sparsely distributed hair, especially on the trunk. The amount of hair varies, but affected mice can be easily recognized at 8 to 10 days old. Both sexes are sterile and have very small gonads with few germ cells. There is a great deficiency of primary spermatogonia in the testes. A quantitative study of maturation of ovarian oocytes showed that the proportion of resident oocytes recruited into the first wave of growth was much higher than in phenotypically normal heterozygous controls (J.J. Eppig, personal communication). This strain is also segregating for the eye blebs spontaneous mutation (Grip1eb). | ||
| 000152 | B6(Cg)-Cys1cpk/J | Repository-Cryopreserved |
| 004478 | B6.129-Foxd1tm1Lai/J | Repository-Cryopreserved |
| 002612 | B6.129S2-Bmp4tm1Blh/J | Repository-Cryopreserved |
| Mice homozygous for the Bmp4tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities. | ||
| 003742 | B6.129S6-Cdh6tm1Sma/J | Repository-Cryopreserved |
| The Cdh6 gene product is a transmembrane protein that is expressed during the earliest stages of nephrogenesis. Mice that are homozygous-null for this gene are viable and fertile with no detectable gene Cdh6 product. They possess only two-thirds the normal number of formed, fully functioning nephrons seen in adult wildtype mice. This diminished number of nephrons is thought to result from delayed epithelialization in the developing kidneys. | ||
| 003783 | B6.129S7-Bmp7tm1Kry/J | Repository-Cryopreserved |
| Mice homozygous for the null Bmp7 allele die within 48 hours after birth and appear smaller in size when compared to wildtype litter mates. Most display polydactyly in the hindlimbs and exhibit skeletal abnormalities involving the rib cage and skull. Unilateral or bilateral eye defects are present in a majority of the null animals. This defect occurs variably, ranging from a complete absence of eye structures to eyes of normal size. Autopsies on newborn null pups reveal the presence of dysgenic kidneys with hydroureters. Histological examination indicates that homozygous null kidneys possess less than 3 percent of the wildtype number of glomeruli, suggesting that Bmp7 plays a critical role during nephrogenesis. Heterozygous animals appear to display a wildtype phenotype. | ||
| 003336 | B6.129S7-Cdkn1ctm1Sje/J | Repository-Cryopreserved |
| Mice lacking the Cdkn1c gene have altered cell proliferation and differentiation, leading to abdominal muscle defects; cleft palate; endochrondral bone ossification defects with incomplete differentiation of hypertrophic chondrocytes; renal medullary dysplasia; adrenal cortical hyperplasia and cytomegaly; lens cell hyperproliferation and apoptosis. The targeted gene is imprinted. The phenotype differs depending on whether the targeted allele is transmitted from the dam or the sire; maternal inheritance of the null allele is lethal. This is a model for the human Beckwith-Wiedemann syndrome. | ||
| 001271 | B6.RBF-Nek1kat/J | Repository-Cryopreserved |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J
..... For more information please see the full descriiption on the strain data sheet | ||
| 004161 | B6;129-Fgf7tm1Efu/J | Repository-Cryopreserved |
| Mice homozygous for this targeted allele are viable, fertile and normal in size. No Fgf7 transcript is detected. By 2 months of age, the hair coat takes on a matted/greasy appearance that becomes more prominent with age. Homozygote kidneys are markedly smaller and posses structural anomalies. Morphometric analyses indicate a reduction (~30% of wildtype) in the total number of nephrons present. Kidney development appears to be effected as early as embryonic day 16.5. This mutant mouse strain represents a model that may be useful in studies related to kidney disease. | ||
| 007208 | B6;129S4-Axud1Gt(ROSA)80Sor/J | Repository-Cryopreserved |
| Mice homozygous for this Axud1-mutant allele are viable and fertile, with some incidence of perinatal lethality before two weeks of age (the Donating Investigator reports 18% of homozygotes die by two weeks of age). Homozygotes have abnormalities in palate bone fusion. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects. These Axud1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 007207 | B6;129S4-Zfp640Gt(ROSA)81Sor/J | Repository-Cryopreserved |
| Mice homozygous for this Zfp640-mutant allele are viable and fertile, with abnormalities in palate bone fusion and increased weight gain observed only in males after adolescence. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects. Additionally, homozygotes are reported to have low β-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These Zfp640-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 001378 | B6;D2-In(3)55Rk Uoxin/J | Repository-Cryopreserved |
| The Uoxin homozygous phenotype has incomplete penetrance. While 63% of Uoxin homozygotes die by 12-14 days of age, those that live to adulthood generally live a normal breeding life span. Homozygous adults display chronic polyuria, increased serum BUN and creatinine levels, and hydronephrosis with a concomitant inflammatory response that is followed by glomerular and tubular dilation. (Cook et al., 2001.) | ||
| 000248 | B6C3Fe a/a-Xpl/J | Repository-Cryopreserved |
| 006010 | B6Ei.129-Wnt4tm1Amc/Ei | Repository-Cryopreserved |
| 004317 | BALB/cBy-Gulosfx/J | Repository-Cryopreserved |
| The sfx phenotype is not apparent until shortly after weaning age. By 26-30 days of age, homozygotes display decreased mobility, diminished weight gain, and more scruffy appearance than their heterozygous or wildtype siblings. Dissection reveals smaller spleen and thymus and increased kidney and brain weights. A reduction in bone mass is accompanied by a paucity of mature osteoblasts on bone surfaces, a subtle reduction of chrondrocytes in epiphyseal-plate columns, growth plate arrest in long bones, and other architectural abnormalities. Bone analysis shows sponteneous fractures both in large bones and smaller ones such as metacarpals. Serum analysis shows a decrease in calcium, inorganic phosphate, alkaline phosphatase, osteocalcin, and insulin-like growth factor 1. These homozygotes also have a reduction in the number of both the red and white blood cells. Homozygotes are fragile and must be handled with great care. (Beamer et al., 2000.) | ||
| 002588 | C3HeB/FeJ-Eya1bor/J | Repository-Cryopreserved |
| The human Branchio-Oto-Renal Syndrome is generally a dominant disorder with incomplete penetrance and variable expressivity resulting from null mutations in the EYA1 gene. The mouse Eya1bor allele is primarily a recessive hypomorphic mutation. Nevertheless, homozygous mice with this hypomorphic allele offer a good model for Branchio-Oto-Renal Syndrome. The phenotype of Eya1bor/Eya1bor mice parallels that of the human Branchio-Oto-Renal Syndrome and both are thought to result from reduced gene dosage. During mapping crosses using CAST/Ei and C3H/HeJ, it was found that genetic background impacts both the kidney and inner ear phenotypes, and modifier genes in humans also may impact the severity of Branchio-Oto-Renal-Syndrome. | ||
| 005921 | C57BL/6J-Aqp2F204V/J | Repository-Cryopreserved |
| Mice homozygous for this mutation are viable with normal body size and lifespan. Homozygotes are fertile, but females usually die during labor. The predicted valine for phenylalanine substitution at amino acid 204 of the mutant protein (F204V) leads to an enrichment in kidney cells of a normally short-lived, intermediately glycosylated 31 kDa isoform and to a reduction in the mature, glycosylated protein level. The mutant AQP2F204V protein is mis-localized in kidney collecting duct cells, and fails to translocate to the apical cell surface in response to desmopressin. Homozygous mice exhibit excessive water consumption and urination, normal plasma glucose levels, and no glucose in the urine. Mutant mice are unable to concentrate urine and exhibit severe hydronephrosis. The presence of some mature, glycosylated protein and a defective, but not completely absent, desmopressin response in homozygous mutant mice likely permits their survival. Heterozygous mice are viable and fer
..... For more information please see the full descriiption on the strain data sheet | ||
| 002854 | C57BL/6J-Nek1kat-2J/J | Repository-Cryopreserved |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J
..... For more information please see the full descriiption on the strain data sheet | ||
| 003779 | C57BL/6J-Nek1kat-3J/J | Repository-Cryopreserved |
| 002561 | C57BL/6J-Nek8jck/J | Repository-Cryopreserved |
| Mice homozygous for the Nek8jck mutation develop polycystic kidney disease. Histology revealed that the kidneys of some 3 day old pups from heterozygous parents had small isolated cysts lined by cuboidal epithelial cells, and 15 day old pups had cysts lined by flattened epithelia. Disease is progressive but not evident by kidney palpation until at least 4 to 5 weeks of age. Homozygotes generally remain active until shortly before death and usually die between 20 and 25 weeks of age. Homozygous females are fertile but do not consistently care for their litters; homozygous males are fertile but decreased fertility is reported after 15 weeks of age. No histologic abnormalities were found in the liver, spleen, or pancreas. (Atala et al., 1993) | ||
| 001595 | DW/J-Acdacd/J | Repository-Cryopreserved |
| acd/acd homozygotes can be distinguished from their wildtype (?/+) littermates by darkened pigmentation, short, curly vibrissae, smaller overall size, and abnormal pelage. Hair growth is retarded and lacks zigzag and guard hairs producing a sparse coat. There is heavy pigmentation in the nose, ears, body, feet and tail, and foci of melanin are also found in the skin and lymph nodes. Tail kinks or polydactyly of the hind feet are sometimes found and external genitalia are underdeveloped. It is rare for homozygotes to breed. Hydronephrosis is sometimes found in post-wean aged homozygotes resulting from focal hypertrophy of ureteral epithelium which causes ureteral blockage. The adrenals are abnormal in both males and females. Although the size of the medullary cells is normal, the cortical cells and nuclei are much larger than normal with nuclear inclusions and many mitochondria in the cytoplasm. These mitochondria have tubular cristae and cholesterol ester droplets, whic
..... For more information please see the full descriiption on the strain data sheet | ||
| 000265 | MY/HuLeJ | Repository-Cryopreserved |
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