B6 cg tg sod1 g93a 1gur j line

Name: B6 cg tg sod1 g93a 1gur j line
Brand: Jackson ImmunoResearch
SKU: JzDiCZIBPBHhf-iFnC9q
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The B6.Cg-Tg(SOD1*G93A)1Gur/J line is a transgenic mouse model that expresses a mutant form of the superoxide dismutase 1 (SOD1) gene. This model is commonly used in research related to amyotrophic lateral sclerosis (ALS).

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7 protocols using «b6 cg tg sod1 g93a 1gur j line»

Preclinical Model of ALS in Mice

2023

Male mice of the congenic B6.Cg-Tg(SOD1*G93A)1Gur/J line were purchased from JAX (Strain #: 004435, The Jackson Laboratory, Bar Harbor, ME, USA) and bred in-house with C57BL/6J females obtained from CRIVER (Strain Code 632, Charles River Laboratories, Sulzfeld, Germany). Each mouse was genotyped using RT-PCR with DNA extracted from ear tissue collected at P21. The SOD1 copy number was checked prior to the study start to ensure a stable phenotype progression as previously described [17 (link)].
The mice were housed at the animal facility of the Forschungszentrum Jülich under a controlled specific-pathogen-free (SPF) environment (12/12 h light/dark cycle, humidity maintained around 50%, and a room temperature between 20 and 23 °C). Food, water, and cages were autoclaved prior to entering the SPF area. A maximum of five SOD1*G93A mice and non-transgenic littermates were housed in individually ventilated cages on standardized rodent bedding (Rettenmaier, Rosenberg, Germany). Dried, pelleted standard rodent chow (Altromin, Lage, Germany) as well as tap water were available for the animals ad libitum. After disease onset, nutrition of the animals was ensured using gel pads (Solid Drink® SDST-75, Triple A trading, Tiel, The Netherlands).

Wintz K., Post J., Langen K.J., Willbold D., Willuweit A, & Kutzsche J. (2023). Oral Treatment with d-RD2RD2 Impedes Early Disease Mechanisms in SOD1*G93A Transgenic Mice but Does Not Prolong Survival. Biomedicines, 11(4), 995.

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Corresponding organizations : Forschungszentrum Jülich, RWTH Aachen University, Heinrich Heine University Düsseldorf

Transgenic Mouse Model for ALS

2022

All animal procedures were performed in accordance with the guidelines of the Australian National Health and Medical Research Council’s published Code of Practice for the use of animals in research and were approved by the Florey Institute of Neuroscience and Mental Health Animal Ethics Committee (permit number: 16-026). Transgenic HB9:GFP mice [B6.Cg-Tg(Hlxb9-GFP)1Tmj/J, stock no. 005029]^{19 (link)} and SOD1^G93A mice [B6.Cg-Tg(SOD1*G93A)1Gur/J line; stock no. 004435; RRID:IMSR_JAX:004435] were obtained from the Jackson Laboratory (Bar Harbor, ME, USA) and maintained on C57BL/6J backgrounds. SOD1^G93A male and HB9:GFP female mice were crossed to generate SOD1^G93A; HB9:GFP^+/− and HB9:GFP^+/− mice, which were subsequently crossed to generate experimental animals: SOD1^G93A; HB9:GFP^+/+ and HB9:GFP^+/+ mice. HB9:GFP^+/+ mice were henceforth called WT for this study. Mice were maintained under standard conditions of 12 h light/dark cycles with access to food and water ad libitum. Mice were time-mated overnight, and embryonic (E) Day 0.5 was designated following visualization of a vaginal plug the next morning.

Zanganeh P.F., Barton S.K., Lim K., Qian E.L., Crombie D.E., Bye C.R, & Turner B.J. (2022). α-Amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor and RNA processing gene dysregulation are early determinants of selective motor neuron vulnerability in a mouse model of amyotrophic lateral sclerosis. Brain Communications, 4(2), fcac081.

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Corresponding organizations : Florey Institute of Neuroscience and Mental Health, University of Melbourne, Perron Institute for Neurological and Translational Science

Transgenic Mouse Model for ALS

2021

Male mice of the congenic B6.Cg-Tg(SOD1^*G93A)1Gur/J line, which was backcrossed for at least 10 generations to C57Bl/6J, were purchased from JAX (Stock No. 004435, The Jackson Laboratory, Bar Harbor, ME, USA). Male mice were bred in-house with C57Bl/6J females obtained from CRIVER (Charles River Laboratories, Sulzfeld, Germany). Mating generated hemizygous SOD1^G93A transgenic mice and non-transgenic littermate (ntg) controls. Progenies were genotyped for presence of the human SOD1 gene by a quantitative PCR assay of DNA obtained from ear markings, as previously described [71 (link)]. Copy numbers of the transgene were checked by calculation of the delta cycle threshold (∆CT) = CT_{internal control} − CT_{gene of interest}. Female SOD1^G93A mice with a high copy number of the transgene were selected for stratified randomisation into equal groups. As control, the genotype of each animal was confirmed by a second quantitative PCR at the end of the study. Housing of the animals was under the same terms at the animal facility of the Forschungszentrum Jülich as described previously [72 (link)]. Mice were housed in mixed-genotype in a controlled environment (12/12 h light/dark cycle, humidity maintained around 50% and a room temperature between 20 °C and 23 °C). Food and water were available ad libitum.

Post J., Schaffrath A., Gering I., Hartwig S., Lehr S., Shah N.J., Langen K.J., Willbold D., Kutzsche J, & Willuweit A. (2021). Oral Treatment with RD2RD2 Impedes Development of Motoric Phenotype and Delays Symptom Onset in SOD1G93A Transgenic Mice. International Journal of Molecular Sciences, 22(13), 7066.

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Corresponding organizations : Forschungszentrum Jülich, Deutsches Diabetes-Zentrum e.V., Heinrich Heine University Düsseldorf, German Center for Diabetes Research, Jülich Aachen Research Alliance, RWTH Aachen University

Transgenic SOD1(G93A) Mouse Model for ALS

2018

The study was conducted in accordance with the ARRIVE guidelines (Kilkenny et al., 2010 (link)). All experiments and procedures were approved by the Italian Ministry of Health (authorization n. 78/2017-PR) in accordance with the ethical guidelines on use of animals from the EC Council Directive 2010/63/EU and from the Italian D.Leg 26/2014. All possible efforts were made to minimize animal suffering, and to reduce the number of animals used per condition by calculating the necessary sample size before performing the experiments. hSOD1(G93A) transgenic mice, which express about 20 copies of mutant human SOD1^G93A [B6.Cg-Tg(SOD1-G93A)1Gur/J line] were obtained from Jackson Laboratory (Bar Harbor, ME, USA) (RRID:IMSR_JAX:004435) (Charles River, Calco, Italy). B6.Cg-Tg(SOD1-G93A)1Gur/J were also maintained as hemizygotes by breeding transgenic males with wild-type C57BL/6J females from Charles River Laboratories, both maintained on C57BL/6J genetic background. Age-matched non-transgenic C57BL/6J mice were always used as control mice. Only male mice were used for the experiments to minimize gender-induced differences in motor impairment and survival (Choi et al. 2008 (link)). Transgenic mice were identified by PCR on DNA obtained from tail biopsies. Briefly, tail tips were digested (overnight, 58 °C) in a buffer containing 100mM Tris–HCl pH 8, 0.1 % SDS 20, 5mM EDTA pH8, 200mM NaCl and 20 mg/ml proteinase K (Ambion-Thermo Fisher, Germany, #2548) and the genomic DNA was amplified with SsoFast Eva Green Supermix (Bio-Rad, California, #172-5201) using the following primers: SOD1 forward 5′-CATCAGCCCTAATCCATCTGA-3′; SOD1 reverse 5′-CGCGACTAACAATCAAAGTGA-3′. Animals were housed in regular polycarbonate cages (30 × 16 × 11 cm), 2–3 per cage, at constant temperature (22 ± 1 °C) and humidity (50%), and were kept on a 12-h light cycle (light 7 a.m.to 7 p.m.). Housing comprised nesting objects, with bedding (sawdust) materials. Food (regular chow, containing 14% protein, 5% fat, 3041 kcal ME/kg) and water were freely available. Microbiological analyses were routinely (each 3–4 months) performed and defined endemic Norovirus and Helicobacter in our conventional animal facility. Transgenic animals were weighed two times a week, beginning at 7 weeks of age. Starting at 6 weeks of age mice were evaluated for motor deficits with a behavioral score system: 0 = Full extension of hind legs away from the lateral midline when the mouse is suspended by tail; the mouse must hold this position for 2 s, and is suspended 2–3 times; 1 = Collapse or partial collapse of leg extension towards lateral midline (weakness) or trembling of hind legs during tail suspension; 2 = Curling of the toes and dragging of at least one limb during walking; 3 = Rigid paralysis or minimal joint movement; foot not used for forward motion; 4 = Mouse cannot stand up in 20 s from either side, euthanasia.
Mice were always treated in blinded fashion.

Cocozza G., di Castro M.A., Carbonari L., Grimaldi A., Antonangeli F., Garofalo S., Porzia A., Madonna M., Mainiero F., Santoni A., Grassi F., Wulff H., D’Alessandro G, & Limatola C. (2018). Ca2+-activated K+ channels modulate microglia affecting motor neuron survival in hSOD1G93A mice. Brain, behavior, and immunity, 73, 584-595.

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Corresponding organizations : Italian Institute of Technology, Sapienza University of Rome, Istituto Pasteur, Istituto Neurologico Mediterraneo, University of California, Davis

Transgenic Mouse Protocols for Neurological Research

2013

The animal experiments described in this article were performed in accordance with protocols approved by the Animal Care and Use Committee of Nagoya University Graduate School of Medicine. All animals were treated and cared for in accordance with the Nagoya University School of Medicine Guidelines pertaining to the treatment of experimental animals. SOD1^G93A transgenic mice, which carry the G93A mutant form of the human SOD1 (B6.Cg-Tg [SOD1-G93A] 1Gur/J line), were purchased from the Jackson Laboratory. Maintenance of these mice and their genotyping were done as described previously [24] . GlcNAc6ST-1^−/− mice were produced using D3 embryonic stem cells and ordinary gene-targeting as described previously [14] (link). GlcNAc6ST-1^+/− mice obtained after backcrossing with C57BL/6J for more than 11 generations were interbred and these mice were used for mating. The sequences of the primers used for genotyping are listed in Table 1.

Hirano K., Ohgomori T., Kobayashi K., Tanaka F., Matsumoto T., Natori T., Matsuyama Y., Uchimura K., Sakamoto K., Takeuchi H., Hirakawa A., Suzumura A., Sobue G., Ishiguro N., Imagama S, & Kadomatsu K. (2013). Ablation of Keratan Sulfate Accelerates Early Phase Pathogenesis of ALS. PLoS ONE, 8(6), e66969.

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Corresponding organizations : Nagoya University, Yamanashi Gakuin University, Hamamatsu University School of Medicine

Top 2 most cited protocols using «b6 cg tg sod1 g93a 1gur j line»

Minocycline Treatment in SOD1G93A Mice

Cited 1 time

The animal experiments described in this article were performed in accordance with protocols approved by the institutional animal committee. All animals were treated and cared for in accordance with the Nagoya University School of Medicine Guidelines pertaining to the treatment of experimental animals. SOD1^G93A transgenic mice, which carry the G93A mutant form of the human SOD1 (B6.Cg-Tg [SOD1-G93A] 1Gur/J line), were purchased from the Jackson Laboratory (Bar Harbor, ME, USA). The protocols for the maintenance and genotyping of these mice were described previously.^{29 (link)} **The transgenic mice were randomly divided into minocycline hydrochloride (Nichi-iko Pharmacceutical Co. Ltd., Toyama, Japan)-treated and untreated groups. Minocycline (33 mg/kg) was administered intraperitoneally five times a week from 8 weeks after birth to end stage.

Kobayashi K., Imagama S., Ohgomori T., Hirano K., Uchimura K., Sakamoto K., Hirakawa A., Takeuchi H., Suzumura A., Ishiguro N, & Kadomatsu K. (2013). Minocycline selectively inhibits M1 polarization of microglia. Cell Death & Disease, 4(3), e525-.

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Corresponding organizations : Nagoya University

Transgenic Mouse Model for ALS

SOD1(G93A) transgenic mice, which express the human SOD1 gene containing a G93A mutation [B6SJL-TgN(SOD1-G93A)1Gur/J line and B6.Cg-Tg(SOD1-G93A)1Gur/J line] were obtained from Jackson Laboratory. B6SJL-TgN(SOD1-G93A)1Gur/J mice were maintained as hemizygotes by breeding transgenic males with wild-type B6SJL females. The littermates were used in most experiments. B6.Cg-Tg(SOD1-G93A)1Gur/J were also maintained as hemizygotes by breeding transgenic males with wild-type C57BL/6J females. B6.Cg-Tg(SOD1-G93A)1Gur/J and C57BL/6J-IFNAR1^−/− (Muller et al. 1994 (link)) mice served as founders for the cross-breeding experiment. The mice were housed in a virus-free barrier facility under a 12-h light/dark cycle, with ad libitum access to food and water. All procedures were performed in accordance with the NIH Guide for the Care and Use of Laboratory Animals and the Society for Neuroscience “Guidelines for the Use of Animals in Neuroscience Research,” using protocols approved by Sanford-Burnham Medical Research Institute Animal Research Committee.

WANG R., YANG B, & ZHANG D. (2011). Activation of Interferon Signaling Pathways in Spinal Cord Astrocytes from an ALS Mouse Model. Glia, 59(6), 946-958.

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Corresponding organizations : Sanford Burnham Prebys Medical Discovery Institute

Spelling variants (same manufacturer)

B6.Cg-Tg(SOD1*G93A)1Gur/J - 89 citations B6.Cg-Tg(SOD1-G93A)1Gur - 3 citations Tg(SOD1*G93A)1Gur - 2 citations Cg-Tg ( - 2 citations SOD1G93A mice (B6.Cg-Tg(SOD1*G93A)1Gur/J line, - 2 citations

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SOD1) G93A (by Taconic Biosciences) - 2 citations

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