Search Criteria: Research Area is "Internal/Organ Research: Adrenal Cortex Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000648 | AKR/J | Level 2 |
| Originally inbred at the Rockefeller Institute, AKR mice are widely used in cancer research for their high leukemia incidence (60-90%) and in immunology as a source of the Thy1.1 (theta AKR) antigen. AKR/J mice are viremic from birth, and express the ecotropic retrovirus AKV in all tissues. The hair interior defect (hid) mutation, a strain characteristic of AKR mice, causes alterations in hair development that is only evident microscopically. Adrenocortical lipid depletion (ald) in AKR mice is caused by a mutation in sterol O-acyltransferase 1 (Soat1), and leads to a truncated SOAT1 protein. AKR/J mice are relatively resistant to aortic lesion formation on a semi-synthetic high fat diet and are hyporesponsive to diets containing high levels of fat and cholesterol. | ||
| 002468 | KK.Cg-Ay/J | Level 2 |
| Ay and other mutations at the a locus conferring a completely yellow coat color are dominant to all a alleles that produce a darker coat. Hair pigment of Ay heterozygotes is yellow, but eyes are black. Heterozygotes usually become obese and infertile within a few months after birth. Increased adipose tissue mass is due to fat cell hypertrophy, and it has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine. Heterozygotes are more susceptible to several kinds of tumors than are normal mice, possibly due, at least in part, to a general increase in cell proliferation that also manifests as a slight increase in lean body mass and skeletal length. Further spleen cells from heterozygotes cause a significantly lower graft vs. host reaction. Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation, or shortly thereafter. The time of death and
..... For more information please see the full descriiption on the strain data sheet | ||
| 007005 | 129S-Scg5tm1Led/J | Repository- Live |
| The following text reflects the phenotype reported by the donating investigator on a "129Sv" genetic background (probably "Taconic Sv129" (129S6/SvEvJ)). While heterozygotes are viable and fertile, mice homozygous for this mutation (7B2-null) die in prepubertal or pubertal ages (5 weeks) with severe cardio-respiratory failure, convulsions, and hypothermia. No transcripts are detected in brain tissue from the targeted gene. 7B2 null mice are unable to make an active form of prohormone convertase 2 (PC2) and have high circulating corticosterone. Homozygotes on the 129S genetic background exhibit Cushing's-like disease pathologies of liver, pancreas, and pituitary; including pituitary-dependent hyperadrenocorticosteronism, severe hypoglycemia, hyperproinsulinemia, adrenal hypertrophy, pituitary hypotrophy, and altered islet cell morphology. 7B2-null mice develop the disease from intermediate lobe ACTH hypersecretion (rather than from pituitary adenomas). Other abnormalities include thinni
..... For more information please see the full descriiption on the strain data sheet | ||
| 000021 | B6.Cg-Ay/J | Repository- Live |
| Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation or shortly thereafter. The time of death and type of abnormality is, in part, determined by the genetic background on which the mutation is placed. Hair pigment in heterozygous mice is yellow, but eyes are black. Heterozygotes usually become obese and infertile after the first few months. Increased adipose tissue mass is due to fat-cell hypertrophy. It has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine levels. Insulin resistance and hyperglycemia follow development of hyperinsulinemia in early adulthood, although the degree is less severe than on the KK/UpJ genetic background (Stock No. 002468). Heterozygotes are also more susceptible to several kinds of tumors than normal mice, and their spleen cells cause a significantly lower graft vs. host reaction. The level of
..... For more information please see the full descriiption on the strain data sheet | ||
| 003322 | B6.129S4-Soat1tm1Far/J | Repository-Cryopreserved |
| Mice homozygous for the Soat1tm1 targeted mutation display tissue specific decreases in cholesterol esterification. Fibroblasts and adrenal membranes of homozygous mutant mice show diminished cholesterol esterification and markedly reduced cholesterol ester levels in adrenal glands and peritoneal macrophages. However, the livers of SOAT1-deficient mice contained substantial amounts of cholesterol esters and exhibited no reduction in cholesterol esterification activity. These findings support the presence of more than one form of esterification enzyme in mammals. A second sterol O-acyltransferase gene (Soat2), expressed in the liver and intestine, has subsequently been identified in mice and humans. | ||
| 007147 | B6.129S4-Soat1tm1Far/Pgn | Repository-Cryopreserved |
| Phenotypically similar to B6.129S4-Soat1tm1Far/J (003322), B6.129S4-Soat1tm1Far/Pgn has a reduced congenic interval making the closely linked Apoa2 gene of C57BL/6 rather than 129S4 origin. The donating investigator indicates that HDL levels exhibit a 24% increase on high fat diet in this strain in contrast to the 73% increase observed in the original strain. Triglyceride levels are unchanged. This strain may be useful in atherosclerosis research. | ||
| 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. | ||
| 000017 | B6.C3Fe-Avy/J | Repository-Cryopreserved |
| Homozygous (Avy/Avy) and heterozygotes (Avy/A and Avy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. Avy resembles Ay in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in Avy/a mice of mottled phenotype but not in those of agouti phenotype. | ||
| 002896 | B6;129S4-Soat1tm1Far/J | Repository-Cryopreserved |
| Mice homozygous for the Soat1tm1 targeted mutation display tissue specific decreases in cholesterol esterification. Fibroblasts and adrenal membranes of homozygous mutant mice show diminished cholesterol esterification and markedly reduced cholesterol ester levels in adrenal glands and peritoneal macrophages. However, the livers of SOAT1-deficient mice contained substantial amounts of cholesterol esters and exhibited no reduction in cholesterol esterification activity. These findings support the presence of more than one form of esterification enzyme in mammals. A second sterol O-acyltransferase gene (Soat2), expressed in the liver and intestine, has subsequently been identified in mice and humans. | ||
| 000504 | B6EiC3Sn a/A-Cacnb4lh/J | Repository-Cryopreserved |
| Mice homozygous for the lethargic spontaneous mutation (Cacnb4lh) are first recognizable at 15 days by their lethargic behavior with gait instability and occasional seizures. The seizures resemble human petit mal seizures. No pathological changes were found in the CNS or in skeletal muscles, but peripheral motor nerves show reduced conduction velocity and prolonged distal latency. There is early thymic involution at 3 to 4 weeks in Cacnb4lh homozygotes, accompanied by decreased lymphocyte count, decreased cell-mediated immunity, and increased levels of serum IgG1. The defects in the immune system tend to disappear by 2 months of age in mice that survive. In addition to neurological and immunological defects, homozygous lethargic mice show pituitary-adrenal hypercorticism. Homozygotes are smaller and weaker than their normal littermates and often die before 2 months old. Survivors of both sexes may breed, but their reproductivity is low. | ||
| 000099 | C3HeB/FeJ-Avy/J | Repository-Cryopreserved |
| Homozygotes (Avy/Avy) and heterozygotes (Avy/A and Avy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. Avy resembles APy in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in Avy/a mice of mottled phenotype but not in those of agout
..... For more information please see the full descriiption on the strain data sheet | ||
| 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 | ||
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