Search Criteria: Research Area is "Developmental Biology Research: Internal/Organ Defects (spleen: GI)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 004425 | B6;129-Gdf1tm1Sjl/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have an embryonic and perinatal lethal phenotype, most develop past embryonic day 14.5 with two thirds dying at birth and almost all not surviving beyond 48 hours after birth. Homozygous mutant newborn mice display a range of left-right axis defects such as visceral situs inversus, right pulmonary isomerism and cardiac anomalies including abnormal positioning of the aorta and pulmonary artery, and septal defects. Spleen and lungs were malformed in some homozygotes. This mutant mouse strain represents a model that may be useful in studies of situs inversus. | ||
| 000209 | B6C3Fe a/a-Dh/J | Repository-Cryopreserved |
| A spontaneous mutation on chromosome 1 of the dominant hemimelia gene, Dh, causes a defect in the embryonic splanchnic mesoderm and induces congenital absence of the spleen and widespread visceral and skeletal abnormalities. Mice homozygous for the Dh mutation die shortly after birth. Heterozygotes may exhibit tibial hemimelia, polydactyly, and extra fused toes. Rear leg(s) may be held at an odd angle with bent rear ankles. Heterozygotes have enlarged lymph nodes and elevated numbers of circulating lymphocytes, granulocytes and thrombocytes. They show reduced serum IgM and IgG2 and impaired humoral antibody response as well as decreased numbers of lymph node mast cells. The Pde6brd1 allele contributed to this strain by C3FeLe.B6-a causes blindness and is segregating in this strain. | ||
(2 stocks) Back to Top
Send questions to our Technical Support team using the Express Technical Support Form.
(3.2)