Strain Name:

B6.Cg-Akt2tm1.1Mbb/J

Stock Number:

006966

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

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.
Specieslaboratory mouse
GenerationN8+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   Akt2tm1.1Mbb allele
006952   B6.129-Akt2tm1.1Mbb Ldlrtm1Her/J
View Strains carrying   Akt2tm1.1Mbb     (1 strain)

Strains carrying other alleles of Akt2
026475   B6.129-Akt2tm1.2Mbb/J
View Strains carrying other alleles of Akt2     (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

Akt2tm1.1Mbb/Akt2tm1.1Mbb

        B6.129P2-Akt2tm1.1Mbb
  • 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/body 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 is associated with a similar, but not exact match to this JAX® Mice strain.

Akt2tm1.1Mbb/Akt2tm1.1Mbb

        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)
  • cellular 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)

Akt2tm1.1Mbb/Akt2tm1.1Mbb

        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 (Null/Knockout)
Common Name(s) Akt2 KO; Akt2-; PKBbeta-;
Mutation Made By Morris Birnbaum,   Un of Pennsylvania Schl of Medicine
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14
ES Cell Line Strain129P2/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

Akt2tm1.1Mbb, Fast MCA
Akt2tm1.1Mbb, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Akt2tm1.1Mbb 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]

Borst O; Munzer P; Gatidis S; Schmidt EM; Schonberger T; Schmid E; Towhid ST; Stellos K; Seizer P; May AE; Lang F; Gawaz M. 2012. The inflammatory chemokine CXC motif ligand 16 triggers platelet activation and adhesion via CXC motif receptor 6-dependent phosphatidylinositide 3-kinase/Akt signaling. Circ Res 111(10):1297-307. [PubMed: 22927331]  [MGI Ref ID J:212626]

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]

Canaud G; Bienaime F; Viau A; Treins C; Baron W; Nguyen C; Burtin M; Berissi S; Giannakakis K; Muda AO; Zschiedrich S; Huber TB; Friedlander G; Legendre C; Pontoglio M; Pende M; Terzi F. 2013. AKT2 is essential to maintain podocyte viability and function during chronic kidney disease. Nat Med 19(10):1288-96. [PubMed: 24056770]  [MGI Ref ID J:202319]

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]

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]

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]

Hu N; Dong M; Ren J. 2014. Hydrogen sulfide alleviates cardiac contractile dysfunction in an Akt2-knockout murine model of insulin resistance: role of mitochondrial injury and apoptosis. Am J Physiol Regul Integr Comp Physiol 306(10):R761-71. [PubMed: 24622975]  [MGI Ref ID J:212975]

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]

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]

Li C; Li Y; He L; Agarwal AR; Zeng N; Cadenas E; Stiles BL. 2013. PI3K/AKT signaling regulates bioenergetics in immortalized hepatocytes. Free Radic Biol Med 60:29-40. [PubMed: 23376468]  [MGI Ref ID J:201239]

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]

Qiao G; Zhao Y; Li Z; Tang PQ; Langdon WY; Yang T; Zhang J. 2013. T cell activation threshold regulated by E3 ubiquitin ligase Cbl-b determines fate of inducible regulatory T cells. J Immunol 191(2):632-9. [PubMed: 23749633]  [MGI Ref ID J:204828]

Rajala A; Dighe R; Agbaga MP; Anderson RE; Rajala RV. 2013. Insulin receptor signaling in cones. J Biol Chem 288(27):19503-15. [PubMed: 23673657]  [MGI Ref ID J:199655]

Rastogi R; Jiang Z; Ahmad N; Rosati R; Liu Y; Beuret L; Monks R; Charron J; Birnbaum MJ; Samavati L. 2013. Rapamycin induces mitogen-activated protein (MAP) kinase phosphatase-1 (MKP-1) expression through activation of protein kinase B and mitogen-activated protein kinase kinase pathways. J Biol Chem 288(47):33966-77. [PubMed: 24126911]  [MGI Ref ID J:204975]

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]

Shen YH; Zhang L; Ren P; Nguyen MT; Zou S; Wu D; Wang XL; Coselli JS; LeMaire SA. 2013. AKT2 confers protection against aortic aneurysms and dissections. Circ Res 112(4):618-32. [PubMed: 23250987]  [MGI Ref ID J:212864]

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]

Sun W; Wang Y; Miao X; Wang Y; Zhang L; Xin Y; Zheng S; Epstein PN; Fu Y; Cai L. 2014. Renal improvement by zinc in diabetic mice is associated with glucose metabolism signaling mediated by metallothionein and Akt, but not Akt2. Free Radic Biol Med 68:22-34. [PubMed: 24296248]  [MGI Ref ID J:211875]

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]

Tsen F; Bhatia A; O'Brien K; Cheng CF; Chen M; Hay N; Stiles B; Woodley DT; Li W. 2013. Extracellular heat shock protein 90 signals through subdomain II and the NPVY motif of LRP-1 receptor to Akt1 and Akt2: a circuit essential for promoting skin cell migration in vitro and wound healing in vivo. Mol Cell Biol 33(24):4947-59. [PubMed: 24126057]  [MGI Ref ID J:206064]

Vergadi E; Vaporidi K; Theodorakis EE; Doxaki C; Lagoudaki E; Ieronymaki E; Alexaki VI; Helms M; Kondili E; Soennichsen B; Stathopoulos EN; Margioris AN; Georgopoulos D; Tsatsanis C. 2014. Akt2 deficiency protects from acute lung injury via alternative macrophage activation and miR-146a induction in mice. J Immunol 192(1):394-406. [PubMed: 24277697]  [MGI Ref ID J:207095]

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]

Wan M; Leavens KF; Hunter RW; Koren S; von Wilamowitz-Moellendorff A; Lu M; Satapati S; Chu Q; Sakamoto K; Burgess SC; Birnbaum MJ. 2013. A Noncanonical, GSK3-Independent Pathway Controls Postprandial Hepatic Glycogen Deposition. Cell Metab 18(1):99-105. [PubMed: 23823480]  [MGI Ref ID J:199233]

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 & HusbandryWhen 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


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2525.00
Animals Provided

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 10 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 View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3283.00
Animals Provided

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 10 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).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

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

Payment Terms and Conditions

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.


See Terms of Use tab for General Terms and Conditions


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
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

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

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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