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- Description
- Disease & phenotype
- Genes & alleles
- Genotyping
- Health & care
- References
- Pricing & purchasing
- Terms of use
Description
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Strain Information
Type Congenic; Mutant Strain; Transgenic; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Generation N5+N2pN1
Generation DefinitionsDonating Investigator IMR Colony, The Jackson Laboratory Description
Mice hemizygous for this HSA-Cre79 transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These HSA-Cre79 transgenic mice have the cre recombinase gene driven by the human alpha-skeletal actin (HSA or ACTA1) promoter. Cre activity is restricted to adult striated muscle fibers and embryonic striated muscle cells of the somites and heart. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in striated muscle-specific deletion of the flanked genome. Specifically, these HSA-Cre79 (or ACTA1-Cre) transgenic mice were originally used to breed with mice heterozygous for a deletion of exon 7 and a loxP-flanked exon 7 mutation on homologous chromosomes of the Smn1 gene (see Stock No. 006138 or Stock No. 006146). The resulting offspring (heterozygous for the deletion in all cells and homozygous for the deletion in striated muscle cells) have extremely reduced lifespan characterized by progressive muscle necrosis and paralysis, and represent a model of spinal muscular atrophy (SMA). Additional SMA strains expressing cre in neurons are available as well (see Stock No. 005938, Stock No. 006297, and Stock No. 006663).HSA-Cre79 transgenic mice are available on different genetic backgrounds (see Stock No. 005936, Stock No. 006139, and Stock No. 006149). 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 characterized. It should be noted that the HSA-Cre79 phenotype could vary from that originally described on a mixed genetic background. We will modify the strain description if necessary as published results become available.
Importation of this model was supported by the Spinal Muscular Atrophy Foundation. Creation and development was supported by the National Institute of Health and Medical Research of France (Inserm) and the Association Française contre les Myopathies (AFM). An additional help was provided by Families of SMA (U.S.A.) and Andrew’s Buddies (U.S.A.).
Development
A targeting vector was designed to place a cre recombinase gene (preceded by the rabbit beta-globin intron and followed by the SV40 polyadenylation signal) under control of the human alpha-skeletal actin (HSA, ACTA1) promoter. This construct was microinjected into (C57BL6 x SJL)F1 embryos and implanted into pseudopregnant CD1 foster mothers. Founder 79 was bred to C57BL/6 to generate transgenic mice. At different points while maintaining this strain, transgenic mice were bred with C57BL/6 wild-type mice and/or mice harboring a loxP-flanked exon 7 mutation (Smn1tm1Jme or SMNF7) on a C57BL/6 and "129Sv" mixed background. Because expression of this transgene is confined to muscle tissue, Cre-mediated deletion of the ?floxed? exon does not occur in the germline. Thus, offspring contained either the wild-type Smn1 locus or the ?floxed? locus; never the Smn1 deletion. Transgenic offspring bearing the wild-type Smn1 locus on this mixed (but predominantly B6;129) background were sent to The Jackson Laboratory by Dr. Judith Melki in April 2006. After arriving, mutant mice were backcrossed to FVB/NJ (Stock No. 001800) for 5-10 generations.
Control Information
| Control | ||
|---|---|---|
| Noncarrier | ||
| 001800 FVB/NJ | ||
| Considerations for Choosing Controls | ||
Related Strains
Spinal Muscular Atrophy (SMA) Models
View Spinal Muscular Atrophy (SMA) Models (49 strains)
006149 B6.Cg-Tg(ACTA1-cre)79Jme/J
Additional Web Information
Reference Guide to Mouse Models of Spinal Muscular Atrophy manual [.pdf]
Introduction to Cre-lox technology
Visit the Spinal Muscular Atrophy (SMA) Mouse Model Resource site for helpful information on SMA Disease and research resources.
Phenotype
Phenotype Information
This mouse can be used to support research in many areas including:
cre relatedNeurobiology Research
Neurodegeneration
Spinal Muscular Atrophy (SMA)
Research Tools
Cre-lox System
Cre Recombinase Expression
Cre Recombinase Expression: Germline/Embryonic Expression
Genetics Research
Mutagenesis and Transgenesis
Mutagenesis and Transgenesis: Cre-lox System
Neurobiology Research
Research Tools
Cre-lox System
Genetics Research
Mutagenesis and Transgenesis
Mutagenesis and Transgenesis: Cre-lox System
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Tg(ACTA1-cre)79Jme | ||
|---|---|---|---|
| Allele Name | transgene insertion 79, Judith Melki | ||
| Allele Type | Transgenic (Cre/Flp) | ||
| Common Name(s) | HSA-Cre; HSA-Cre79; HSA::cre; | ||
| Mutation Made By | Judith Melki, Genopole, Inserm U798 | ||
| Strain of Origin | (C57BL/6J x SJL)F1 | ||
| Site of Expression | adult striated muscle fibers and embryonic striated muscle cells of the somites and heart | ||
| Expressed Gene | cre, cre recombinase, bacteriophage P1 | ||
| Cre recombinase is an enzyme derived from the bacteriophage P1 that specifically recognizes loxP sites. Cre has been shown to effectively mediate the excision of DNA located between loxP sites. After the excision event, the DNA ends recombine leaving a single loxP site in place of the intervening sequence. | |||
| Promoter | ACTA1, actin, alpha 1, skeletal muscle, human | ||
| Driver Note | ACTA1 | ||
| Molecular Note | This transgene expresses Cre recombinase under the control of a human alpha-skeletal actin promoter, active in striated muscle, heart, and skeletal muscle. [MGI Ref ID J:67906] | ||
| Gene Symbol and Name | Tg(ACTA1-cre)79Jme, transgene insertion 79, Judith Melki | ||
| Chromosome | UN | ||
| Gene Common Name(s) | HSA-Cre; HSA-Cre79; HSA::cre; | ||
Genotyping
Genotyping Information
Genotyping Protocols
Generic Cre Melt Curve Analysis, Melt Curve Analysis
Generic Cre, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Miniou P; Tiziano D; Frugier T; Roblot N; Le Meur M; Melki J. 1999. Gene targeting restricted to mouse striated muscle lineage. Nucleic Acids Res 27(19):e27. [PubMed: 10481039] [MGI Ref ID J:67906]
Additional References
Tg(ACTA1-cre)79Jme relatedAgrawal PB; Joshi M; Savic T; Chen Z; Beggs AH. 2012. Normal myofibrillar development followed by progressive sarcomeric disruption with actin accumulations in a mouse Cfl2 knockout demonstrates requirement of cofilin-2 for muscle maintenance. Hum Mol Genet :. [PubMed: 22343409] [MGI Ref ID J:182571]
Buj-Bello A; Laugel V; Messaddeq N; Zahreddine H; Laporte J; Pellissier JF; Mandel JL. 2002. The lipid phosphatase myotubularin is essential for skeletal muscle maintenance but not for myogenesis in mice. Proc Natl Acad Sci U S A 99(23):15060-5. [PubMed: 12391329] [MGI Ref ID J:81791]
Chambon C; Duteil D; Vignaud A; Ferry A; Messaddeq N; Malivindi R; Kato S; Chambon P; Metzger D. 2010. Myocytic androgen receptor controls the strength but not the mass of limb muscles. Proc Natl Acad Sci U S A 107(32):14327-32. [PubMed: 20660752] [MGI Ref ID J:163603]
Charvet C; Houbron C; Parlakian A; Giordani J; Lahoute C; Bertrand A; Sotiropoulos A; Renou L; Schmitt A; Melki J; Li Z; Daegelen D; Tuil D. 2006. New role for serum response factor in postnatal skeletal muscle growth and regeneration via the interleukin 4 and insulin-like growth factor 1 pathways. Mol Cell Biol 26(17):6664-74. [PubMed: 16914747] [MGI Ref ID J:112113]
Chen W; Huang FW; de Renshaw TB; Andrews NC. 2011. Skeletal muscle hemojuvelin is dispensable for systemic iron homeostasis. Blood 117(23):6319-25. [PubMed: 21493799] [MGI Ref ID J:174702]
Cheusova T; Khan MA; Schubert SW; Gavin AC; Buchou T; Jacob G; Sticht H; Allende J; Boldyreff B; Brenner HR; Hashemolhosseini S. 2006. Casein kinase 2-dependent serine phosphorylation of MuSK regulates acetylcholine receptor aggregation at the neuromuscular junction. Genes Dev 20(13):1800-16. [PubMed: 16818610] [MGI Ref ID J:110237]
Chipman PH; Franz CK; Nelson A; Schachner M; Rafuse VF. 2010. Neural cell adhesion molecule is required for stability of reinnervated neuromuscular junctions. Eur J Neurosci 31(2):238-49. [PubMed: 20074227] [MGI Ref ID J:158382]
Church C; Moir L; McMurray F; Girard C; Banks GT; Teboul L; Wells S; Bruning JC; Nolan PM; Ashcroft FM; Cox RD. 2010. Overexpression of Fto leads to increased food intake and results in obesity. Nat Genet 42(12):1086-92. [PubMed: 21076408] [MGI Ref ID J:166829]
Cifuentes-Diaz C; Frugier T; Tiziano FD; Lacene E; Roblot N; Joshi V; Moreau MH; Melki J. 2001. Deletion of murine smn exon 7 directed to skeletal muscle leads to severe muscular dystrophy. J Cell Biol 152(5):1107-14. [PubMed: 11238465] [MGI Ref ID J:67884]
Escher P; Lacazette E; Courtet M; Blindenbacher A; Landmann L; Bezakova G; Lloyd KC; Mueller U; Brenner HR. 2005. Synapses form in skeletal muscles lacking neuregulin receptors. Science 308(5730):1920-3. [PubMed: 15976301] [MGI Ref ID J:99246]
Gaudel C; Schwartz C; Giordano C; Abumrad NA; Grimaldi PA. 2008. Pharmacological activation of PPARbeta promotes rapid and calcineurin-dependent fiber remodeling and angiogenesis in mouse skeletal muscle. Am J Physiol Endocrinol Metab 295(2):E297-304. [PubMed: 18492772] [MGI Ref ID J:140074]
Gheyara AL; Vallejo-Illarramendi A; Zang K; Mei L; St-Arnaud R; Dedhar S; Reichardt LF. 2007. Deletion of integrin-linked kinase from skeletal muscles of mice resembles muscular dystrophy due to alpha 7 beta 1-integrin deficiency. Am J Pathol 171(6):1966-77. [PubMed: 18055553] [MGI Ref ID J:128949]
Huang Z; Rivas B; Agoulnik AI. 2012. Insulin-like 3 signaling is important for testicular descent but dispensable for spermatogenesis and germ cell survival in adult mice. Biol Reprod 87(6):143. [PubMed: 23100620] [MGI Ref ID J:194006]
Jaworski A; Burden SJ. 2006. Neuromuscular synapse formation in mice lacking motor neuron- and skeletal muscle-derived Neuregulin-1. J Neurosci 26(2):655-61. [PubMed: 16407563] [MGI Ref ID J:104252]
Jaworski A; Smith CL; Burden SJ. 2007. GA-Binding Protein Is Dispensable for Neuromuscular Synapse Formation and Synapse-Specific Gene Expression. Mol Cell Biol 27(13):5040-6. [PubMed: 17485447] [MGI Ref ID J:121823]
Kuwahara H; Horie T; Ishikawa S; Tsuda C; Kawakami S; Noda Y; Kaneko T; Tahara S; Tachibana T; Okabe M; Melki J; Takano R; Toda T; Morikawa D; Nojiri H; Kurosawa H; Shirasawa T; Shimizu T. 2010. Oxidative stress in skeletal muscle causes severe disturbance of exercise activity without muscle atrophy. Free Radic Biol Med 48(9):1252-62. [PubMed: 20156551] [MGI Ref ID J:158821]
Lantier L; Mounier R; Leclerc J; Pende M; Foretz M; Viollet B. 2010. Coordinated maintenance of muscle cell size control by AMP-activated protein kinase. FASEB J 24(9):3555-61. [PubMed: 20460585] [MGI Ref ID J:163878]
Lawlor MW; Read BP; Edelstein R; Yang N; Pierson CR; Stein MJ; Wermer-Colan A; Buj-Bello A; Lachey JL; Seehra JS; Beggs AH. 2011. Inhibition of activin receptor type IIB increases strength and lifespan in myotubularin-deficient mice. Am J Pathol 178(2):784-93. [PubMed: 21281811] [MGI Ref ID J:169075]
Li XM; Dong XP; Luo SW; Zhang B; Lee DH; Ting AK; Neiswender H; Kim CH; Carpenter-Hyland E; Gao TM; Xiong WC; Mei L. 2008. Retrograde regulation of motoneuron differentiation by muscle beta-catenin. Nat Neurosci 11(3):262-8. [PubMed: 18278041] [MGI Ref ID J:135587]
Luquet S; Lopez-Soriano J; Holst D; Fredenrich A; Melki J; Rassoulzadegan M; Grimaldi PA. 2003. Peroxisome proliferator-activated receptor delta controls muscle development and oxidative capability. FASEB J 17(15):2299-301. [PubMed: 14525942] [MGI Ref ID J:127917]
Nicole S; Desforges B; Millet G; Lesbordes J; Cifuentes-Diaz C; Vertes D; Cao ML; De Backer F; Languille L; Roblot N; Joshi V; Gillis JM; Melki J. 2003. Intact satellite cells lead to remarkable protection against Smn gene defect in differentiated skeletal muscle. J Cell Biol 161(3):571-82. [PubMed: 12743106] [MGI Ref ID J:83343]
O'Leary DA; Noakes PG; Lavidis NA; Kola I; Hertzog PJ; Ristevski S. 2007. Targeting of the ETS factor GABPalpha disrupts neuromuscular junction synaptic function. Mol Cell Biol 27(9):3470-80. [PubMed: 17325042] [MGI Ref ID J:121356]
Piccoli M; Franzin C; Bertin E; Urbani L; Blaauw B; Repele A; Taschin E; Cenedese A; Zanon GF; Andre-Schmutz I; Rosato A; Melki J; Cavazzana-Calvo M; Pozzobon M; De Coppi P. 2012. Amniotic fluid stem cells restore the muscle cell niche in a HSA-Cre, Smn(F7/F7) mouse model. Stem Cells 30(8):1675-84. [PubMed: 22644669] [MGI Ref ID J:194656]
Prins KW; Call JA; Lowe DA; Ervasti JM. 2011. Quadriceps myopathy caused by skeletal muscle-specific ablation of beta(cyto)-actin. J Cell Sci 124(Pt 6):951-7. [PubMed: 21325027] [MGI Ref ID J:182996]
Prins KW; Lowe DA; Ervasti JM. 2008. Skeletal muscle-specific ablation of gamma(cyto)-actin does not exacerbate the mdx phenotype. PLoS ONE 3(6):e2419. [PubMed: 18545671] [MGI Ref ID J:137146]
Raben N; Hill V; Shea L; Takikita S; Baum R; Mizushima N; Ralston E; Plotz P. 2008. Suppression of autophagy in skeletal muscle uncovers the accumulation of ubiquitinated proteins and their potential role in muscle damage in Pompe disease. Hum Mol Genet 17(24):3897-908. [PubMed: 18782848] [MGI Ref ID J:142536]
Risson V; Mazelin L; Roceri M; Sanchez H; Moncollin V; Corneloup C; Richard-Bulteau H; Vignaud A; Baas D; Defour A; Freyssenet D; Tanti JF; Le-Marchand-Brustel Y; Ferrier B; Conjard-Duplany A; Romanino K; Bauche S; Hantai D; Mueller M; Kozma SC; Thomas G; Ruegg MA; Ferry A; Pende M; Bigard X; Koulmann N; Schaeffer L; Gangloff YG. 2009. Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy. J Cell Biol 187(6):859-74. [PubMed: 20008564] [MGI Ref ID J:162918]
Romanino K; Mazelin L; Albert V; Conjard-Duplany A; Lin S; Bentzinger CF; Handschin C; Puigserver P; Zorzato F; Schaeffer L; Gangloff YG; Ruegg MA. 2011. Myopathy caused by mammalian target of rapamycin complex 1 (mTORC1) inactivation is not reversed by restoring mitochondrial function. Proc Natl Acad Sci U S A 108(51):20808-13. [PubMed: 22143799] [MGI Ref ID J:180519]
Schmidt N; Akaaboune M; Gajendran N; Martinez-Pena y Valenzuela I; Wakefield S; Thurnheer R; Brenner HR. 2011. Neuregulin/ErbB regulate neuromuscular junction development by phosphorylation of alpha-dystrobrevin. J Cell Biol 195(7):1171-84. [PubMed: 22184199] [MGI Ref ID J:180660]
Schuler M; Ali F; Chambon C; Duteil D; Bornert JM; Tardivel A; Desvergne B; Wahli W; Chambon P; Metzger D. 2006. PGC1alpha expression is controlled in skeletal muscles by PPARbeta, whose ablation results in fiber-type switching, obesity, and type 2 diabetes. Cell Metab 4(5):407-14. [PubMed: 17084713] [MGI Ref ID J:129759]
Sonnemann KJ; Fitzsimons DP; Patel JR; Liu Y; Schneider MF; Moss RL; Ervasti JM. 2006. Cytoplasmic gamma-actin is not required for skeletal muscle development but its absence leads to a progressive myopathy. Dev Cell 11(3):387-97. [PubMed: 16950128] [MGI Ref ID J:112808]
Takikita S; Myerowitz R; Zaal K; Raben N; Plotz PH. 2009. Murine muscle cell models for Pompe disease and their use in studying therapeutic approaches. Mol Genet Metab 96(4):208-17. [PubMed: 19167256] [MGI Ref ID J:146894]
Viscomi C; Bottani E; Civiletto G; Cerutti R; Moggio M; Fagiolari G; Schon EA; Lamperti C; Zeviani M. 2011. In vivo correction of COX deficiency by activation of the AMPK/PGC-1alpha axis. Cell Metab 14(1):80-90. [PubMed: 21723506] [MGI Ref ID J:176080]
Wang J; Fu XQ; Lei WL; Wang T; Sheng AL; Luo ZG. 2010. Nuclear factor kappaB controls acetylcholine receptor clustering at the neuromuscular junction. J Neurosci 30(33):11104-13. [PubMed: 20720118] [MGI Ref ID J:163304]
Wu H; Lu Y; Barik A; Joseph A; Taketo MM; Xiong WC; Mei L. 2012. beta-Catenin gain of function in muscles impairs neuromuscular junction formation. Development 139(13):2392-404. [PubMed: 22627288] [MGI Ref ID J:185531]
Wu H; Lu Y; Shen C; Patel N; Gan L; Xiong WC; Mei L. 2012. Distinct roles of muscle and motoneuron LRP4 in neuromuscular junction formation. Neuron 75(1):94-107. [PubMed: 22794264] [MGI Ref ID J:188352]
Yamamoto H; Williams EG; Mouchiroud L; Canto C; Fan W; Downes M; Heligon C; Barish GD; Desvergne B; Evans RM; Schoonjans K; Auwerx J. 2011. NCoR1 is a conserved physiological modulator of muscle mass and oxidative function. Cell 147(4):827-39. [PubMed: 22078881] [MGI Ref ID J:178827]
Health & husbandry
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Health & Colony Maintenance Information
Animal Health Reports
Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.Colony Maintenance
Breeding & Husbandry After arriving at The Jackson Laboratory on a mixed background, mutant mice were bred to wildtype FVB/NJ (Stock No. 001800) for 5-10 generations. The resulting backcrossed hemizygotes were maintained thereafter by breeding transgenic mice to either wildtype siblings from the colony or FVB/NJ.
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $1980.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Supply Notes
- Cryorecovery - Standard.
Progeny testing is not required.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
| Pricing for International shipping destinations |
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2574.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Supply Notes
- Cryorecovery - Standard.
Progeny testing is not required.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
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Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
General Supply Notes
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| Noncarrier | ||
| 001800 FVB/NJ | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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The Jackson Laboratory's Genotype Promise
The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.Ordering Information
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JAX® Mice, Products & Services Conditions of Use
"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.No Warranty
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