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; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Generation N8+N1F1pN1 Generation Definitions   Donating Investigator Morris J. Birnbaum,   Un of Pennsylvania Schl of Medicine

Description
Mice homozygous for this Akt2 (thymoma viral proto-oncogene 2) mutant allele are viable and fertile. Homozygotes develop insulin resistance, hyperglycemia, impaired glucose tolerance, abnormal glucose uptake in muscle tissue, increased pancreatic beta-cell mass, and diabetes.

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 phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
This mutation was created by Dr. Morris Birnbaum (University of Pennsylvania) by flanking exons 4-5 of the targeted gene with loxP sites. The targeting vector was electroporated into 129P2/OlaHsd-derived E14 embryonic stem (ES) cells, and the chimeric males were bred with C57BL/6 females. Mutant mice were then bred to cre transgenic mice to remove exons 4-5 and bred for an unknown number of generations. These mutant mice on a mixed (approximately 80% C57BL/6J) background were then shipped to Dr. Jan Breslow at The Rockefeller University. Dr. Breslow's lab crossed these mice to another mutant strain and further backcrossed to C57BL/6J for approximately 7 generations prior to arrival at The Jackson Laboratory (as Stock No. 006952). The donating investigators report that 102/104 microsatellite markers indicate C57BL/6J background; the only exceptions are D7Mit21 and D7Mit294. The Y chromosome may not have been fixed to the C57BL/6J genetic background. Upon arrival, some Stock No. 006952 mice were bred to C57BL/6J to isolate the Akt2 mutant allele; generating this single mutant congenic strain (Stock No. 006966).

Control Information

	Control
	Wild-type from the colony
	000664 C57BL/6J
Considerations for Choosing Controls

Related Strains

Strains carrying   Akt2^tm1.1Mbb allele

006952

B6.129-Akt2tm1.1Mbb Ldlrtm1Her/J

View Strains carrying   Akt2^tm1.1Mbb     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI

- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Diabetes Mellitus, Noninsulin-Dependent; NIDDM

- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Hypoinsulinemic Hypoglycemia with Hemihypertrophy; HIHGHH   (AKT2)

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

Akt2^tm1.1Mbb/Akt2^tm1.1Mbb

        B6.129P2-Akt2^tm1.1Mbb

• homeostasis/metabolism phenotype
• decreased circulating glucose level
  • in fasted mice Surwit fed a high-fat diet   (MGI Ref ID J:155432)
• decreased liver triglyceride level
  • at 4 months when Surwit fed a high-fat diet   (MGI Ref ID J:155432)
• decreased susceptibility to diet-induced obesity
  • at 4 months when Surwit fed a high-fat diet   (MGI Ref ID J:155432)
• increased circulating insulin level
  • in fasted mice Surwit fed a high-fat diet   (MGI Ref ID J:155432)
• growth/size phenotype
• decreased susceptibility to diet-induced obesity
  • at 4 months when Surwit fed a high-fat diet   (MGI Ref ID J:155432)
• liver/biliary system phenotype
• decreased liver triglyceride level
  • at 4 months when Surwit fed a high-fat diet   (MGI Ref ID J:155432)

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Akt2^tm1.1Mbb/Akt2^tm1.1Mbb

        involves: 129P2/OlaHsd * C57BL/6

• homeostasis/metabolism phenotype
• hyperglycemia
  • homozygotes develop into adulthood without apparent growth defects but exhibit a mild but significant fasting hyperglycemia, which is more pronounced during fed states   (MGI Ref ID J:71491)
• impaired glucose tolerance
  • in response to oral glucose load, 2-mo-old homozygotes display a mild glucose intolerance, with increased blood glucose levels at all time points measured   (MGI Ref ID J:71491)
• increased circulating insulin level
  • homozygotes develop inadequate compensatory hyperinsulinemia   (MGI Ref ID J:71491)
• insulin resistance
  • in response to i.p. administration of insulin, homozygotes display significantly elevated blood glucose levels relative to wild-type mice at all time points measured (at 60 min; 70.8 ± 7.9 mg/dl vs 22.3 ± 1.1 mg/dl, respectively)   (MGI Ref ID J:71491)
  • in euglycemic-hyperinsulinemic clamp expts, homozygotes exhibit peripheral insulin resistance along with complete failure of insulin to suppress hepatic glucose output   (MGI Ref ID J:71491)
  • notably, circulating free fatty acid concentrations remain normal   (MGI Ref ID J:71491)
• muscle phenotype
• abnormal muscle cell glucose uptake
  • in euglycemic-hyperinsulinemic clamp studies, 2-5-mo-old homozygotes show a ~50% reduction in total body insulin-dependent glucose disposal relative to wild-type mice   (MGI Ref ID J:71491)
  • insulin-stimulated hexose uptake into the glycolytic extensor digitorum longus (EDL) muscle is severely blunted in the presence of 0.33 nM insulin; however, no impairment is noted upon exposure of the mutant EDL to a higher insulin concentration (13.3 nM)   (MGI Ref ID J:71491)
  • insulin-stimulated deoxyglucose uptake into the oxidative soleus muscle is not significantly impaired at either an intermediate or maximal concentration of insulin   (MGI Ref ID J:71491)
• endocrine/exocrine gland phenotype
• increased pancreatic beta cell number
  • pancreata from 2- to 3-month-old male homozygotes respond to insulin resistance with an increase in islet mass (~4-fold) and number (~2-fold) relative to wild-type mice   (MGI Ref ID J:71491)
• adipose tissue phenotype
• abnormal adipocyte glucose uptake
  • in euglycemic-hyperinsulinemic clamp studies, insulin-stimulated hexose uptake is mildly impaired in mutant adipocytes   (MGI Ref ID J:71491)

Akt2^tm1.1Mbb/Akt2^tm1.1Mbb

        involves: 129P2/OlaHsd

• immune system phenotype
• *normal* immune system phenotype
  • no abnormalities in T cell development are observed   (MGI Ref ID J:135903)
• homeostasis/metabolism phenotype
• decreased liver triglyceride level
  • 2-fold decrease in liver triglyceride levels   (MGI Ref ID J:160759)
• hyperglycemia
  • about 25-30% increase in fasting glucose levels at 1 month of age   (MGI Ref ID J:160759)
• impaired glucose tolerance
  • glucose intolerance   (MGI Ref ID J:160759)
• liver/biliary system phenotype
• decreased liver triglyceride level
  • 2-fold decrease in liver triglyceride levels   (MGI Ref ID J:160759)

View Research Applications

Research Applications

This mouse can be used to support research in many areas including:

Diabetes and Obesity Research
Hyperglycemia
Insulin Resistance
Type 2 Diabetes (NIDDM)

Research Tools
Diabetes and Obesity Research
Metabolism Research

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Akt2tm1.1Mbb
Allele Name		targeted mutation 1.1, Morris J Birnbaum
Allele Type		Targeted (knock-out)
Common Name(s)		Akt2 KO; Akt2-; PKBbeta-;
Mutation Made By		Morris Birnbaum,   Un of Pennsylvania Schl of Medicine
Strain of Origin		129P2/OlaHsd
ES Cell Line Name		E14
ES Cell Line Strain		129P2/OlaHsd
Gene Symbol and Name		Akt2, thymoma viral proto-oncogene 2
Chromosome		7
Gene Common Name(s)		2410016A19Rik; AW554154; HIHGHH; PKB; PKBB; PKBBETA; PRKBB; RAC-BETA; RIKEN cDNA 2410016A19 gene; expressed sequence AW554154;
Molecular Note		This allele is a derivative of Akt2tm1Mbb. Cre-mediated recombination in vivo under the control of a 6 kb 5'-flanking sequence from the Pou3f4 gene excised the floxed exons 4 and 5 in the germline. The excision of exons 4 and 5 results in a frameshift mutation that would lead to a premature termination even if the remaining exon 3 were to splice to exon 6. Exon 5 encodes the lysine residue necessary for catalytic activity. Western blot analyses using a polyclonal antibody did not detect protein in liver, muscle, and isolated adipocytes from homozygous mice. [MGI Ref ID J:71491]

Genotyping

Genotyping Information

Genotyping Protocols

Akt2^tm1.1Mbb, Fast MCA
Akt2^tm1.1Mbb, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Cho H; Mu J; Kim JK; Thorvaldsen JL; Chu Q; Crenshaw EB 3rd; Kaestner KH; Bartolomei MS; Shulman GI; Birnbaum MJ. 2001. Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKB beta). Science 292(5522):1728-31. [PubMed: 11387480]  [MGI Ref ID J:71491]

Leavens KF; Easton RM; Shulman GI; Previs SF; Birnbaum MJ. 2009. Akt2 is required for hepatic lipid accumulation in models of insulin resistance. Cell Metab 10(5):405-18. [PubMed: 19883618]  [MGI Ref ID J:155432]

Additional References

Akt2^tm1.1Mbb related

Ackah E; Yu J; Zoellner S; Iwakiri Y; Skurk C; Shibata R; Ouchi N; Easton RM; Galasso G; Birnbaum MJ; Walsh K; Sessa WC. 2005. Akt1/protein kinase Balpha is critical for ischemic and VEGF-mediated angiogenesis. J Clin Invest 115(8):2119-2127. [PubMed: 16075056]  [MGI Ref ID J:100143]

Arranz A; Doxaki C; Vergadi E; Martinez de la Torre Y; Vaporidi K; Lagoudaki ED; Ieronymaki E; Androulidaki A; Venihaki M; Margioris AN; Stathopoulos EN; Tsichlis PN; Tsatsanis C. 2012. Akt1 and Akt2 protein kinases differentially contribute to macrophage polarization. Proc Natl Acad Sci U S A 109(24):9517-22. [PubMed: 22647600]  [MGI Ref ID J:185519]

Bauerfeld CP; Rastogi R; Pirockinaite G; Lee I; Huttemann M; Monks B; Birnbaum MJ; Franchi L; Nunez G; Samavati L. 2012. TLR4-Mediated AKT Activation Is MyD88/TRIF Dependent and Critical for Induction of Oxidative Phosphorylation and Mitochondrial Transcription Factor A in Murine Macrophages. J Immunol 188(6):2847-57. [PubMed: 22312125]  [MGI Ref ID J:181864]

Boxer RB; Stairs DB; Dugan KD; Notarfrancesco KL; Portocarrero CP; Keister BA; Belka GK; Cho H; Rathmell JC; Thompson CB; Birnbaum MJ; Chodosh LA. 2006. Isoform-specific requirement for Akt1 in the developmental regulation of cellular metabolism during lactation. Cell Metab 4(6):475-90. [PubMed: 17141631]  [MGI Ref ID J:129773]

Calamito M; Juntilla MM; Thomas M; Northrup DL; Rathmell J; Birnbaum MJ; Koretzky G; Allman D. 2010. Akt1 and Akt2 promote peripheral B-cell maturation and survival. Blood 115(20):4043-50. [PubMed: 20042722]  [MGI Ref ID J:160279]

Chang X; Lazorchak AS; Liu D; Su B. 2012. Sin1 regulates Treg-cell development but is not required for T-cell growth and proliferation. Eur J Immunol 42(6):1639-47. [PubMed: 22678916]  [MGI Ref ID J:187755]

Chatterjee S; Browning EA; Hong N; DeBolt K; Sorokina EM; Liu W; Birnbaum MJ; Fisher AB. 2012. Membrane depolarization is the trigger for PI3K/Akt activation and leads to the generation of ROS. Am J Physiol Heart Circ Physiol 302(1):H105-14. [PubMed: 22003059]  [MGI Ref ID J:181582]

Chen CC; Stairs DB; Boxer RB; Belka GK; Horseman ND; Alvarez JV; Chodosh LA. 2012. Autocrine prolactin induced by the Pten-Akt pathway is required for lactation initiation and provides a direct link between the Akt and Stat5 pathways. Genes Dev 26(19):2154-68. [PubMed: 23028142]  [MGI Ref ID J:188260]

DeBosch B; Sambandam N; Weinheimer C; Courtois M; Muslin AJ. 2006. Akt2 regulates cardiac metabolism and cardiomyocyte survival. J Biol Chem 281(43):32841-51. [PubMed: 16950770]  [MGI Ref ID J:117383]

Di Lorenzo A; Fernandez-Hernando C; Cirino G; Sessa WC. 2009. Akt1 is critical for acute inflammation and histamine-mediated vascular leakage. Proc Natl Acad Sci U S A 106(34):14552-7. [PubMed: 19622728]  [MGI Ref ID J:152016]

Easton RM; Cho H; Roovers K; Shineman DW; Mizrahi M; Forman MS; Lee VM; Szabolcs M; de Jong R; Oltersdorf T; Ludwig T; Efstratiadis A; Birnbaum MJ. 2005. Role for Akt3/protein kinase Bgamma in attainment of normal brain size. Mol Cell Biol 25(5):1869-78. [PubMed: 15713641]  [MGI Ref ID J:96823]

Espeillac C; Mitchell C; Celton-Morizur S; Chauvin C; Koka V; Gillet C; Albrecht JH; Desdouets C; Pende M. 2011. S6 kinase 1 is required for rapamycin-sensitive liver proliferation after mouse hepatectomy. J Clin Invest 121(7):2821-32. [PubMed: 21633171]  [MGI Ref ID J:175661]

Goncalves MD; Pistilli EE; Balduzzi A; Birnbaum MJ; Lachey J; Khurana TS; Ahima RS. 2010. Akt deficiency attenuates muscle size and function but not the response to ActRIIB inhibition. PLoS One 5(9):e12707. [PubMed: 20856813]  [MGI Ref ID J:165125]

He L; Hou X; Kanel G; Zeng N; Galicia V; Wang Y; Yang J; Wu H; Birnbaum MJ; Stiles BL. 2010. The critical role of AKT2 in hepatic steatosis induced by PTEN loss. Am J Pathol 176(5):2302-8. [PubMed: 20348245]  [MGI Ref ID J:160759]

Hollander MC; Maier CR; Hobbs EA; Ashmore AR; Linnoila RI; Dennis PA. 2011. Akt1 deletion prevents lung tumorigenesis by mutant K-ras. Oncogene 30(15):1812-21. [PubMed: 21242979]  [MGI Ref ID J:170765]

Hollander MC; Zhou X; Maier CR; Patterson AD; Ding X; Dennis PA. 2011. A Cyp2a polymorphism predicts susceptibility to NNK-induced lung tumorigenesis in mice. Carcinogenesis 32(8):1279-84. [PubMed: 21625009]  [MGI Ref ID J:174977]

Jiang K; Patel NA; Watson JE; Apostolatos H; Kleiman E; Hanson O; Hagiwara M; Cooper DR. 2009. Akt2 regulation of Cdc2-like kinases (Clk/Sty), serine/arginine-rich (SR) protein phosphorylation, and insulin-induced alternative splicing of PKCbetaII messenger ribonucleic acid. Endocrinology 150(5):2087-97. [PubMed: 19116344]  [MGI Ref ID J:151810]

Juntilla MM; Patil VD; Calamito M; Joshi RP; Birnbaum MJ; Koretzky GA. 2010. AKT1 and AKT2 maintain hematopoietic stem cell function by regulating reactive oxygen species. Blood 115(20):4030-8. [PubMed: 20354168]  [MGI Ref ID J:160459]

Juntilla MM; Wofford JA; Birnbaum MJ; Rathmell JC; Koretzky GA. 2007. Akt1 and Akt2 are required for {alpha}beta thymocyte survival and differentiation. Proc Natl Acad Sci U S A 104(29):12105-10. [PubMed: 17609365]  [MGI Ref ID J:123155]

Kramer HF; Witczak CA; Fujii N; Jessen N; Taylor EB; Arnolds DE; Sakamoto K; Hirshman MF; Goodyear LJ. 2006. Distinct signals regulate AS160 phosphorylation in response to insulin, AICAR, and contraction in mouse skeletal muscle. Diabetes 55(7):2067-76. [PubMed: 16804077]  [MGI Ref ID J:111856]

Lazorchak AS; Liu D; Facchinetti V; Di Lorenzo A; Sessa WC; Schatz DG; Su B. 2010. Sin1-mTORC2 suppresses rag and il7r gene expression through Akt2 in B cells. Mol Cell 39(3):433-43. [PubMed: 20705244]  [MGI Ref ID J:163678]

Li D; August S; Woulfe DS. 2008. GSK3beta is a negative regulator of platelet function and thrombosis. Blood 111(7):3522-30. [PubMed: 18218855]  [MGI Ref ID J:133503]

Li G; Anderson RE; Tomita H; Adler R; Liu X; Zack DJ; Rajala RV. 2007. Nonredundant role of Akt2 for neuroprotection of rod photoreceptor cells from light-induced cell death. J Neurosci 27(1):203-11. [PubMed: 17202487]  [MGI Ref ID J:117208]

Lu M; Wan M; Leavens KF; Chu Q; Monks BR; Fernandez S; Ahima RS; Ueki K; Kahn CR; Birnbaum MJ. 2012. Insulin regulates liver metabolism in vivo in the absence of hepatic Akt and Foxo1. Nat Med 18(3):388-95. [PubMed: 22344295]  [MGI Ref ID J:181642]

Mao C; Tili EG; Dose M; Haks MC; Bear SE; Maroulakou I; Horie K; Gaitanaris GA; Fidanza V; Ludwig T; Wiest DL; Gounari F; Tsichlis PN. 2007. Unequal contribution of Akt isoforms in the double-negative to double-positive thymocyte transition. J Immunol 178(9):5443-53. [PubMed: 17442925]  [MGI Ref ID J:135903]

Maroulakou IG; Oemler W; Naber SP; Tsichlis PN. 2007. Akt1 ablation inhibits, whereas Akt2 ablation accelerates, the development of mammary adenocarcinomas in mouse mammary tumor virus (MMTV)-ErbB2/neu and MMTV-polyoma middle T transgenic mice. Cancer Res 67(1):167-77. [PubMed: 17210696]  [MGI Ref ID J:117336]

McCurdy CE; Cartee GD. 2005. Akt2 is essential for the full effect of calorie restriction on insulin-stimulated glucose uptake in skeletal muscle. Diabetes 54(5):1349-56. [PubMed: 15855319]  [MGI Ref ID J:105199]

Polytarchou C; Iliopoulos D; Hatziapostolou M; Kottakis F; Maroulakou I; Struhl K; Tsichlis PN. 2011. Akt2 Regulates All Akt Isoforms and Promotes Resistance to Hypoxia through Induction of miR-21 upon Oxygen Deprivation. Cancer Res 71(13):4720-31. [PubMed: 21555366]  [MGI Ref ID J:173622]

Sakamoto K; Arnolds DE; Fujii N; Kramer HF; Hirshman MF; Goodyear LJ. 2006. Role of Akt2 in contraction-stimulated cell signaling and glucose uptake in skeletal muscle. Am J Physiol Endocrinol Metab 291(5):E1031-7. [PubMed: 16803855]  [MGI Ref ID J:113860]

Southgate RJ; Bruce CR; Carey AL; Steinberg GR; Walder K; Monks R; Watt MJ; Hawley JA; Birnbaum MJ; Febbraio MA. 2005. PGC-1alpha gene expression is down-regulated by Akt- mediated phosphorylation and nuclear exclusion of FoxO1 in insulin-stimulated skeletal muscle. FASEB J 19(14):2072-4. [PubMed: 16203862]  [MGI Ref ID J:104633]

Treebak JT; Taylor EB; Witczak CA; An D; Toyoda T; Koh HJ; Xie J; Feener EP; Wojtaszewski JF; Hirshman MF; Goodyear LJ. 2010. Identification of a novel phosphorylation site on TBC1D4 regulated by AMP-activated protein kinase in skeletal muscle. Am J Physiol Cell Physiol 298(2):C377-85. [PubMed: 19923418]  [MGI Ref ID J:157508]

Treins C; Alliouachene S; Hassouna R; Xie Y; Birnbaum MJ; Pende M. 2012. The combined deletion of S6K1 and Akt2 deteriorates glycemic control in a high-fat diet. Mol Cell Biol 32(19):4001-11. [PubMed: 22851690]  [MGI Ref ID J:189139]

Vichaiwong K; Purohit S; An D; Toyoda T; Jessen N; Hirshman MF; Goodyear LJ. 2010. Contraction regulates site-specific phosphorylation of TBC1D1 in skeletal muscle. Biochem J 431(2):311-20. [PubMed: 20701589]  [MGI Ref ID J:166169]

Wofford JA; Wieman HL; Jacobs SR; Zhao Y; Rathmell JC. 2008. IL-7 promotes Glut1 trafficking and glucose uptake via STAT5-mediated activation of Akt to support T-cell survival. Blood 111(4):2101-11. [PubMed: 18042802]  [MGI Ref ID J:131334]

Woulfe D; Jiang H; Morgans A; Monks R; Birnbaum M; Brass LF. 2004. Defects in secretion, aggregation, and thrombus formation in platelets from mice lacking Akt2. J Clin Invest 113(3):441-50. [PubMed: 14755341]  [MGI Ref ID J:87588]

Yin H; Stojanovic A; Hay N; Du X. 2008. The role of Akt in the signaling pathway of the glycoprotein Ib-IX induced platelet activation. Blood 111(2):658-65. [PubMed: 17914025]  [MGI Ref ID J:130112]

Yun SJ; Tucker DF; Kim EK; Kim MS; Do KH; Ha JM; Lee SY; Yun J; Kim CD; Birnbaum MJ; Bae SS. 2009. Differential regulation of Akt/protein kinase B isoforms during cell cycle progression. FEBS Lett 583(4):685-90. [PubMed: 19166849]  [MGI Ref ID J:146145]

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	When maintaining a live colony, heterozygous or homozygous mice can be bred. Homozygous mice may have impaired fecundity as a result of diabetic phenotype.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

Control Information

	Control
	Wild-type from the colony
	000664 C57BL/6J
Considerations for Choosing Controls
Control Pricing Information for Genetically Engineered Mutant Strains.

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Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

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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.

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