Search Criteria: Research Area is "Endocrine Deficiency Research: Adrenal Medulla Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 008115 | B6.129X1-Pomctm2Ute/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. 60 to 75% of homozygotes die perinatally. Surviving homozygotes have decreased fertility and homozygous females produce milk that does not allow pups to survive past 14 days of age. No serum adrenocorticotropic hormone (ACTH) or corticosterone was detected by radioimmunoassay (RIA) of homozygotes. Serum epinephrine and aldosterone levels are reduced. Although homozygotes are born with adrenal glands or normal size, adrenal glands fail to grow postnatally and become almost undetectable with age. By 3 months of age, mice homozygous for the mutation are twice the weight of wildtype controls and increased serum leptin levels. Heterozygotes exhibit elevated serum leptin levels, but not increased weight and reduced levels of serum adrenocorticotropic hormone (ACTH), corticosterone, and aldosterone levels. Both heterozygotes and homozygote
..... For more information please see the full descriiption on the strain data sheet | ||
| 007005 | 129S-Scg5tm1Led/J | Repository-Cryopreserved |
| 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 | ||
| 000253 | DLS/LeJ | Repository-Cryopreserved |
| Mice homozygous for the dilute-lethal spontaneous mutation (Myo5ad-l) display a severe neuromuscular disorder characterized by convulsions and opisthotonus. Homozygous mutant mice usually die by approximately 3 weeks of age. Dilute lethal homozygotes lack smooth endoplasmic reticulum in the dendritic spine of Purkinje cells causing an absence of intracellular calcium. Loss of this intracellular calcium may be the cause of dilute-lethal neurological symptoms. Homozygous dilute-neurological mutant mice (Myo5ad-n, Stock No. 001013) display a neuromuscular disorder, but the condition is less severe than in dilute-lethal homozygotes. In this DLS/Le inbred strain the dilute-lethal mutation is maintained in repulsion with short ear (Bmpse), closely linked mutations on Chromosome 9. | ||
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