Search Criteria: Research Area is "Mouse/Human Gene Homologs: amyotrophic lateral sclerosis (ALS)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002726 | B6SJL-Tg(SOD1*G93A)1Gur/J | Level 3 |
| Mice hemizygous for this SOD1-G93A (also called G93A-SOD1) transgene are viable and fertile, with transgenic expression of a G93A mutant form of human SOD1. This founder line (often referred to as G1H) is reported to have high transgene copy number. Hemizygotes exhibit a phenotype similar to amyotrophic lateral sclerosis (ALS) in humans; becoming paralyzed in one or more limbs with paralysis due to loss of motor neurons from the spinal cord. Transgenic mice have a life span of approximately 19-23 weeks. These SOD1-G93A (also called G93A-SOD1) transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease). | ||
| 008342 | B6.Cg-Tg(SOD1*G37R)42Dpr/J | Repository- Live |
| Mice hemizygous for this G37R-SOD1 transgene are viable and fertile. The expressed G37R mutant form of human SOD1 is characterized as an enzymatically active, "gain of adverse function" mutation. Hemizygotes develop symptoms and pathology resembling human Amyotrophic Lateral Sclerosis (ALS), with paralyzation in one or more limbs attributable to the loss of motor neurons from the spinal cord. Transgenic mice from the highest expressing founder line (G37R(42) or line 42) express a 14-fold increase in SOD1 activity in spinal cord with death occurring around 3.5-4 months of age. High expression of G37R-SOD1 is associated with ALS pathology in motor neurons of the spinal cord and brainstem, widespread degenerative changes in other neuronal populations, and mild-to-moderate vacuolar changes in kidney. These high-expressing G37R(42) (or G37R-SOD1 line 42) transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Dis
..... For more information please see the full descriiption on the strain data sheet | ||
| 004435 | B6.Cg-Tg(SOD1*G93A)1Gur/J | Repository- Live |
| Mice hemizygous for this SOD1-G93A (also called G93A-SOD1) transgene are viable and fertile, with transgenic expression of a G93A mutant form of human SOD1. This founder line (often referred to as G1H) is reported to have high transgene copy number. Hemizygotes exhibit a phenotype similar to amyotrophic lateral sclerosis (ALS) in humans; becoming paralyzed in one or more limbs with paralysis due to loss of motor neurons from the spinal cord. Transgenic mice have a life span of approximately 19-23 weeks. Female hemizygotes are poor breeders, and rarely produce more than one litter before the onset of disease. These SOD1-G93A (also called G93A-SOD1) transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease).
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first cha
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| 002297 | B6SJL-Tg(SOD1)2Gur/J | Repository- Live |
| This transgenic strain carries the normal allele of the human SOD1 gene. Originally published as N1029, it has been reported that the SOD1 protein level is the same as in the transgenic strain carrying the SOD1*G93A transgene (002726), even though the copy number in the SOD1*G93A transgenic is higher. This strain serves as a control for the B6SJL-Tg(SOD1*G93A)1Gur/J (002726) and the B6SJL-Tg(SOD1*G93A)dl1Gur/J (002300) strains. | ||
| 002298 | B6.Cg-Tg(SOD1)2Gur/J | Repository-Cryopreserved |
| This transgenic strain carries the normal allele of the human SOD1 gene. Originally published as N1029, it expresses the same SOD1 protein level as the transgenic strain carrying the SOD1*G93A transgene (002726), even though the copy number in the SOD1*G93A transgenic is higher. This strain serves as a control for the B6.Cg-Tg(SOD1*G93A)dl1Gur/J mutant strain (Stock No. 002299). | ||
| 002299 | B6.Cg-Tg(SOD1*G93A)dl1Gur/J | Repository-Cryopreserved |
| Mice carrying the transgene exhibit paralysis resulting in a reduced life expectancy. They serve as a model for human amyotrophic lateral sclerosis (ALS). The transgene carries a variant of the human Superoxide dismutase-1 gene (glycine to alanine at position 93). Paralysis is due to loss of motor neurons from the spinal cord. The onset of the ALS phenotype is delayed compared to the original high copy number strain (SOD1*G93A)1Gur, Stock No. 002726) because of a reduction in transgenic copy number. This reduction most likely occurred during the importation and establishment of the original high copy number mutant transgenic strain. Mice on the B6SJL background (Stock No. 002300) become paralyzed in one or more limbs beginning around six to seven months of age. Life expectancy is normally four to six weeks beyond onset of symptoms. The transgene was backcrossed to C57BL/6J 5
..... For more information please see the full descriiption on the strain data sheet | ||
| 002300 | B6SJL-Tg(SOD1*G93A)dl1Gur/J | Repository-Cryopreserved |
| Mice carrying the transgene exhibit paralysis resulting in a reduced life expectancy. They serve as a model for human amyotrophic lateral sclerosis (ALS). The transgene carries a variant of the human Superoxide dismutase-1 gene (glycine to alanine at position 93). Paralysis is due to loss of motor neurons from the spinal cord. The onset of the ALS phenotype is delayed compared to the original high copy number strain (SOD1*G93A)1Gur, Stock No. 002726) because of a reduction in transgenic copy number. This reduction most likely occurred during the importation and establishment of the original high copy number mutant transgenic strain. Mice become paralyzed in one or more limbs beginning around six to seven months of age. Life expectancy is normally four to six weeks beyond onset of symptoms. | ||
| 002628 | C57BL/6-Tg(SOD1)10Cje/J | Repository-Cryopreserved |
| Transgenic mice are viable and express human SOD1. Transgenic mice express three times the normal level of SOD1 in the blood, brain, and fibroblasts. Homozygote males for the Tg(SOD1)10Cje transgene are sterile; homozygote females for the Tg(SOD1)10Cje transgene are fertile. Described in the literature as 218/10 denoting that the transgene insertion site maps to Chr 10. | ||
| 002629 | C57BL/6-Tg(SOD1)3Cje/J | Repository-Cryopreserved |
| Transgenic mice are viable and express human SOD1. Transgenic mice express three times the normal level of SOD1 in the blood, brain, and fibroblasts. Homozygotes for the Tg(SOD1)3Cje transgene are fertile. Described in the literature as 218/3 denoting that the transgene insertion site is maps to Chr 3 (Shi, et al., 1994). Of the two lines (the other being C57BL/6-Tg(SOD1)10Cje/J, Stock No. 002628), this is the most widely used. | ||
| 005706 | C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J | Repository-Cryopreserved |
| Hemizygous transgenic mice are viable, fertile, normal in size and do not display any behavioral abnormalities. Mice homozygous for this transgene may not be viable. When these transgenic mice are bred with mice expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, expression of the CDK5R1/GFP fusion protein in the appropriate tissue of the bitransgenic offspring can be regulated by doxycycline administration. These mice may be useful in studies of Alzheimer's disease and other neurodegenerative tauopathies, amyotrophic lateral sclerosis (ALS), Niemann Pick Type C (NPC) disease, and Parkinson's disease.
Note: this transgenic strain was designed to breed with Tg(Camk2a-tTA) transgenic mice, (Stock No. 003010), a transgenic strain that expresses tTA in forebrain neurons. The resulting bitransgenic offspring exhibit the hallmark phenotype of Alzheimer's disease;
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