Search Criteria: Research Area is "Mouse/Human Gene Homologs: amyotrophic lateral sclerosis (ALS)"

New Strains Under Development

JAX® Mice Strains

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 .....
For more information please see the full descriiption on the strain data sheet

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; .....
For more information please see the full descriiption on the strain data sheet

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New Strains Under Development

(See informational text following listing of strains)
How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.

View a Data sheet for New Strains Under Development
Select the strain name to link to the strain data sheet.

Stock
Number
Strain Name
 
Strain Description
Standard Supply
008248B6.Cg-Tg(SOD1*G85R)148Dwc/J
Under Development for Production
Mice hemizygous for this G85R-SOD1 transgene are viable and fertile, with transgenic expression of a G85R mutant form of human SOD1 associated with human familial Amyotrophic Lateral Sclerosis (ALS). Mice from this founder line (line 148) exhibit unaltered endogenous SOD1 activity; the G85R mutation is characterized as an "enzymatically inactive" mutation. Hemizygotes develop symptoms and pathology resembling human ALS; becoming paralyzed in one or more limbs due to loss of motor neurons from the spinal cord, with disease onset and rapid progression to death between 7-8 months of age. Like wildtype SOD1, the G85R mutant SOD1 protein also forms monomer-misfolded oligomers associated with degenerating motor neurons. These G85R-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 frequen .....
For more information please see the full description on the strain data sheet

008230FVB(Cg)-Tg(Thy1-SOD1*G93A)T3Hgrd/J
Under Development for Production
These Thy1.2-G93A transgenic mice have a human SOD1 cDNA harboring the G93A mutation driven by the murine Thy1.2 expression cassette. Expression of the G93A mutant SOD1 (G93A-SOD1) is directed to neurons throughout the brain and spinal cord (including spinal motor neurons). In addition, mutant SOD1 immunoreactivity is selectively distributed in axons and nerve endings at the neuromuscular junctions. While Thy1.2-G93A hemizygous mice from founder line T3 are viable and fertile with no clinical or pathological signs of motor abnormalities up to two years of age, neuronal expression of mutant SOD1 in homozygous Thy1.2-G93A mice from founder line T3 (also called T3T3 mice) develop an Amyotrophic Lateral Sclerosis (ALS)-like motor neuron disease between one to two years of age, characterized by motor neuron degeneration, muscle denervation, paralysis, and muscle weakness with cytosolic dendritic ubiquitinated SOD1 aggregates as the dominant pathological feature. Additionally, when these T3 .....
For more information please see the full description on the strain data sheet

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New Strains Under Development The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
  1. Strains that will be made available from a live distribution colony at The Jackson Laboratory.
    These strains are designated as: "Under Development for Distribution Colony"
  2. Strains that will be made available through the Cryopreservation Repository.
    These strains are designated as: "Under Development for Cryopreservation Repository"
It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.

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