Strain Name:

STOCK Tsc1tm1Djk/J

Stock Number:

005680

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These floxed mutant mice possess loxP sites flanking exons 17 and 18 of the Tsc1 gene. This mutant strain may be useful in tissue-specific studies including tuberous sclerosis or other hamartoma syndromes, regulation of the actin cytoskeleton and motility, cellular and organismal glucose homeostasis, cell growth responses, apoptosis regulation, and regulation of cell size.

Description

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHomozygote x Homozygote         (Female x Male)   31-MAR-06
Specieslaboratory mouse
GenerationF?+Np1F2 (28-MAR-13)
Generation Definitions
 
Donating Investigator David J. Kwiatkowski,   Brigham and Women's Hospital

Description
Homozygous mice are viable, fertile, normal in size, have normal expression of hamartin (the targeted gene's protein product), have no growth or behavioral defects, and are devoid of tumors through age 18 months. This mutant carries a "floxed" allele of the endogenous gene. When combined with a mutant carrying a Cre recombinase gene under the control of a promoter of interest, exons 17 and 18 of Tsc1 are deleted in the tissue of interest. This mutant may be useful in many tissue-specific studies including tuberous sclerosis or other hamartoma syndromes, regulation of the actin cytoskeleton and motility, cellular and organismal glucose homeostasis, cell growth responses, apoptosis regulation, and regulation of cell size.

When bred to a strain expressing Cre recombinase in neuronal cells (see Stock No. 003966 for example), this mutant mouse strain may be useful in studies of tuberous sclerosis.

When bred to a strain expressing Cre recombinase in oocytes of the primordial follicles (see Stock No. 011062 for example), this mutant mouse strain may be useful in studies of primordial follicle quiescence and activation.

When bred to a strain expressing Cre recombinase in liver (see Stock No. 003574 for example), this mutant mouse strain may be useful in studies of hepatic lipid metabolism.

Importation of this model was supported by the Tuberous Sclerosis Alliance.

Development
A targeting vector containing a loxP-flanked neomycin resistance-thymidine kinase gene cassette preceding exon 17 and a third loxP site downstream of exon 18 was electroporated into 129S4/SvJae derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. Chimeric mice were backcrossed for germ-line transmission to C57BL/6J, BALB/cJ, or 129/SvJae mice. The resulting heterozygotes were intercrossed to produce homozygotes on a mixed background.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls

Additional Web Information

Introduction to Cre-lox technology

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).
Tuberous Sclerosis 1; TSC1
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Focal Cortical Dysplasia of Taylor; FCDT   (TSC1)
Lymphangioleiomyomatosis; LAM   (TSC1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Tsc1tm1Djk/Tsc1tm1Djk

        involves: 129S4/SvJae * C57BL/6   (conditional)
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology
    • increase in hepatocyte size following adenoviral cre retro-orbital injection   (MGI Ref ID J:167208)
  • abnormal liver physiology
    • decrease in liver protein content following adenoviral cre retro-orbital injection   (MGI Ref ID J:167208)
    • in cre injected mice, the liver is largely refractory to fast induced shrinkage   (MGI Ref ID J:167208)
    • cre injected mice are unable to generate ketones when given sodium octanoate   (MGI Ref ID J:167208)
  • enlarged liver
    • about a 40% increase in liver mass following adenoviral cre retro-orbital injection   (MGI Ref ID J:167208)
  • homeostasis/metabolism phenotype
  • decreased body temperature
    • in fasted cre injected mice   (MGI Ref ID J:167208)
  • decreased circulating ketone body level
    • markedly lower serum ketones in young fasted cre injected mice but not in aged fasted cre injected mice   (MGI Ref ID J:167208)
  • behavior/neurological phenotype
  • hypoactivity
    • in fasted cre injected mice   (MGI Ref ID J:167208)

The following phenotype relates to a compound genotype created using this strain.
Contact JAX® Services jaxservices@jax.org for customized breeding options.

Tsc1tm1Djk/Tsc1tm1.1Djk Tg(Syn1-cre)671Jxm/0

        involves: 129S4/SvJae * C57BL/6 * CBA   (conditional)
  • mortality/aging
  • premature death
    • mice treated with rapamycin or RAD001 (mTOR inhibitor) show 90-100% survival to 80 days of age compared to median survival of 33 days for untreated mutants   (MGI Ref ID J:136366)
    • discontinuation of drug treatment at P30 results in clinical symptom improvement for 1-2 weeks followed by clinical deterioration and death at 79 days for rapamycin-treated and 77 days for RAD001-treated mutants   (MGI Ref ID J:136366)
    • median survival of 35 days, with no survivors beyond 65 days   (MGI Ref ID J:121858)
  • growth/size/body phenotype
  • slow postnatal weight gain
    • after P5 until death, mutants fail to gain weight at same rate as controls; average maximum weight is 10 grams   (MGI Ref ID J:121858)
  • nervous system phenotype
  • abnormal brain morphology
    • enlarged cells are seen outside cerebral cortex, in other parts of brain including thalamus, hypothalamus and brainstem   (MGI Ref ID J:121858)
    • no increased cell loss or degeneration is observed in regions containing anomalous enlarged cells   (MGI Ref ID J:121858)
    • abnormal cerebral cortex morphology
      • mutants display subset of enlarged pS6-positive cells at base of cortex and in cortical layer V; drug treatment results in marked reduction in size of enlarged cells   (MGI Ref ID J:136366)
      • mild cortical disorganization is observed in mutants with or without rapamycin treatment   (MGI Ref ID J:136366)
      • laminar organization is less distinct than in the 6 cortical layers of controls   (MGI Ref ID J:121858)
      • unusually large cells are observed in all six layers in mutants, particularly in layer V; layer of enlarged cells is seen at gray-white matter border throughout cerebral cortex at P21   (MGI Ref ID J:121858)
      • abnormal neocortex morphology
        • contains some enlarged cells   (MGI Ref ID J:121858)
    • abnormal dentate gyrus morphology
      • enlarged cells are observed in hilus   (MGI Ref ID J:121858)
    • abnormal hippocampus pyramidal cell layer
      • enlarged cells are seen throughout pyramidal cell layer, particularly in CA3 region   (MGI Ref ID J:121858)
    • abnormal hippocampus region morphology
      • enlarged ectopic cells are seen outside the CA1-CA3 fields in stratum oriens and stratum radiatum   (MGI Ref ID J:121858)
    • increased brain weight
      • brain weight to body weight ratio is significantly greater (2.4-fold) in mutants compared to wild-type; with rapamycin/RAD001 treatment, difference from control is significantly reduced but still observed   (MGI Ref ID J:136366)
  • abnormal brain wave pattern
    • mice aged P21-48 display 3 types of electrographic abnormalities: short spike bursts observed in all mice examined, occasionally spontaneous period of desynchronization with electrodecrement and at low incidence, frequent high-amplitude sharp waves   (MGI Ref ID J:121858)
    • interictal (seizure) 1-2 second bursts of high-amplitude 7-8 hertz spikes are observed with high frequency compared with controls; these are without obvious clinical correlate   (MGI Ref ID J:121858)
  • abnormal myelination
    • myelination particularly in cortex is impaired due to decreased myelin production by oligodendrocytes; rapamycin treatment works to restore myelination throughout brain with greatest improvement in cortex and hippocampus   (MGI Ref ID J:136366)
    • hypomyelination is observed in brains of mutants   (MGI Ref ID J:121858)
    • oligodendrocyte number and distribution appears similar to wild-type   (MGI Ref ID J:121858)
  • abnormal neuron morphology
    • population of neurons in lateral somatosensory cortex are considerably enlarged compared with those in controls; size is significantly reduced after drug treatment (from 1.8-fold to 1.2-fold), but effect reverses when treatment is stopped   (MGI Ref ID J:136366)
    • in somatosensory cortex, layer V neurons often have major dendrites extending tangentially and diagonally to the pia, in contrast to control neurons which mainly have long apical dendrite oriented directly toward pial surface; rapamycin treatment initiated at P7 does not significantly decrease abnormally oriented dendrite percentage   (MGI Ref ID J:136366)
    • Nissl bodies and filamentous aggregates are often detected in enlarged neurons, prominently in brainstem but rarely in enlarged cortical cells   (MGI Ref ID J:121858)
    • some neurons are aberrantly localized outside primary pyramidal cell layers; ectopic neurons are isolated, not organized into clusters or columns   (MGI Ref ID J:121858)
    • some neurons in somatosensory cortex show 60% increase in soma size relative to controls   (MGI Ref ID J:121858)
    • many pyramidal neurons demonstrate dysplastic features including increased size and thicker dendritic arbors compared to control neurons   (MGI Ref ID J:121858)
    • abnormal dendrite morphology
      • in hippocampal neuron cultures, neuronal dendritic spine density is reduced >20% compared to controls   (MGI Ref ID J:136366)
      • with rapamycin treatment, spine density is marginally increased; spine length however is increased 9% compared to treated and untreated controls or untreated mutants   (MGI Ref ID J:136366)
    • abnormal neuron differentiation
      • in mutant brains, neurons appear to be still actively growing after P14-21, whereas wild-type neurons have stopped growing   (MGI Ref ID J:121858)
      • this may result in the hypomyelination, due to secondary myelination failure   (MGI Ref ID J:121858)
  • seizures
    • mice develop clinical seizures, spontaneous and some provoked in most part by physical simulation; both types of seizures are mild or severe   (MGI Ref ID J:121858)
    • severe seizures are characterized by brief behavioral arrest, followed by several seconds of clonic activity, followed by tonic extensor posturing of trunk and limbs for 15-45 seconds   (MGI Ref ID J:121858)
    • after P21, suspension by the tail results in gentle spinning leading severe seizure activity, followed by bradycardia and death   (MGI Ref ID J:121858)
    • sporadic seizures
      • only mild seizures occur spontaneously, characterized by brief myoclonic jerking of head and torso   (MGI Ref ID J:121858)
  • behavior/neurological phenotype
  • abnormal involuntary movement
    • clasping behavior and tremor are significantly ameliorated by rapamycin/RAD001 treatment relative to untreated animals at 30, 60, and 100 days postnatal   (MGI Ref ID J:136366)
    • increased startle reflex
      • apparent by P10   (MGI Ref ID J:121858)
    • limb grasping
      • display posterior limb-clasping behavior when lifted by tail   (MGI Ref ID J:121858)
    • tremors
      • progressive high-frequency trunk and limb tremor apparent by P10   (MGI Ref ID J:121858)
  • abnormal limb posture
    • at death, usually in third to fifth postnatal week, mice are found with extensor posture of fore- and hindlimbs   (MGI Ref ID J:121858)
  • hunched posture
    • develops by by third or fourth postnatal week   (MGI Ref ID J:121858)
  • hyperactivity
    • apparent by P10   (MGI Ref ID J:121858)
  • hypoactivity
    • mice show progressive decline in activity with limited mobility by third or fourth postnatal week   (MGI Ref ID J:121858)
  • seizures
    • mice develop clinical seizures, spontaneous and some provoked in most part by physical simulation; both types of seizures are mild or severe   (MGI Ref ID J:121858)
    • severe seizures are characterized by brief behavioral arrest, followed by several seconds of clonic activity, followed by tonic extensor posturing of trunk and limbs for 15-45 seconds   (MGI Ref ID J:121858)
    • after P21, suspension by the tail results in gentle spinning leading severe seizure activity, followed by bradycardia and death   (MGI Ref ID J:121858)
    • sporadic seizures
      • only mild seizures occur spontaneously, characterized by brief myoclonic jerking of head and torso   (MGI Ref ID J:121858)
  • straub tail
    • tail dorsiflexion is exhibited   (MGI Ref ID J:121858)
  • skeleton phenotype
  • abnormal spine curvature
    • kyphosis is significantly improved in rapamycin/RAD001-treated mice compared with untreated mutants   (MGI Ref ID J:136366)
  • cellular phenotype
  • abnormal neuron differentiation
    • in mutant brains, neurons appear to be still actively growing after P14-21, whereas wild-type neurons have stopped growing   (MGI Ref ID J:121858)
    • this may result in the hypomyelination, due to secondary myelination failure   (MGI Ref ID J:121858)

Tsc1tm1Djk/Tsc1tm1Djk Tg(Alb-cre)21Mgn/0

        involves: 129S4/SvJae * C57BL/6 * DBA   (conditional)
  • homeostasis/metabolism phenotype
  • abnormal homeostasis
    • gene expression analysis indicates that fat utilization and glucose production are promoted in mutants   (MGI Ref ID J:171445)
    • decreased circulating triglyceride level
      • plasma triglyceride levels are lower than in wild-type mice, however adiponectin and leptin levels are no different   (MGI Ref ID J:171445)
      • mutants do not show an increase in plasma triglyceride levels in response to the high-fat diet as is seen in wild-type mice   (MGI Ref ID J:171445)
    • impaired glucose tolerance
      • mutants exhibit mild but significant glucose intolerance   (MGI Ref ID J:171445)
    • insulin resistance
      • mutants exhibit a slight reduction in systemic insulin sensitivity   (MGI Ref ID J:171445)
      • insulin levels at 30 minutes following glucose administration are higher in mutants than controls, indicating insulin resistance   (MGI Ref ID J:171445)
      • however, fasting plasma glucose and insulin levels are normal   (MGI Ref ID J:171445)
  • liver/biliary system phenotype
  • *normal* liver/biliary system phenotype
    • mutants normally do not exhibit hepatic steatosis, however when fed a high-fat diet and treated with rapamycin, they develop steatosis and show increased levels of hepatic triglycerides   (MGI Ref ID J:171445)
    • abnormal hepatocyte morphology
      • increase in hepatocyte cell size   (MGI Ref ID J:171445)
    • abnormal hepatocyte physiology
      • hepatocytes are resistant to steatosis induced by a high-fat diet   (MGI Ref ID J:171445)
    • enlarged liver
      • mutants develop hepatomegaly   (MGI Ref ID J:171445)

Tsc1tm1Djk/Tsc1tm1Djk Tg(Gdf9-cre)5092Coo/?

        involves: 129S4/SvJae * C57BL/6J   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal ovarian follicle morphology
    • mutants exhibit premature activation of the entire primordial follicle pool by P23, leading to follicle depletion and premature ovarian failure in early adulthood (2-3 months of age)   (MGI Ref ID J:155357)
    • injection with rapamycin reverses the overactivation of primordial follicles, indicative that mTORC1 activity is responsible for increased activation of follicles   (MGI Ref ID J:155357)
  • homeostasis/metabolism phenotype
  • increased circulating follicle stimulating hormone level
    • higher levels at 3-4 months of age   (MGI Ref ID J:155357)
  • increased circulating luteinizing hormone level
    • higher levels at 3-4 months of age   (MGI Ref ID J:155357)
  • reproductive system phenotype
  • abnormal ovarian follicle morphology
    • mutants exhibit premature activation of the entire primordial follicle pool by P23, leading to follicle depletion and premature ovarian failure in early adulthood (2-3 months of age)   (MGI Ref ID J:155357)
    • injection with rapamycin reverses the overactivation of primordial follicles, indicative that mTORC1 activity is responsible for increased activation of follicles   (MGI Ref ID J:155357)
  • reduced female fertility
    • from 6-27 weeks of age, females produce at most 2 litters of normal size and then become infertile after around 12-13 weeks   (MGI Ref ID J:155357)

Tsc1tm1Djk/Tsc1tm1Djk Tg(Syn1-cre)671Jxm/0

        involves: 129S4/SvJae * C57BL/6 * CBA   (conditional)
  • mortality/aging
  • premature death
  • growth/size/body phenotype
  • abnormal body size   (MGI Ref ID J:121858)
  • nervous system phenotype
  • abnormal nervous system morphology   (MGI Ref ID J:121858)
  • abnormal nervous system physiology   (MGI Ref ID J:121858)
  • behavior/neurological phenotype
  • abnormal behavior   (MGI Ref ID J:121858)
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Research Applications
This mouse can be used to support research in many areas including:

Research Tools
Cancer Research
      Hamartoma Syndromes
Cre-lox System
      loxP-flanked Sequences

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tsc1tm1Djk
Allele Name targeted mutation 1, David J Kwiatkowski
Allele Type Targeted (Conditional ready (e.g. floxed), No functional change)
Common Name(s) Tsc1L; Tsc1c; Tsc1fl; Tsc1flox; Tsc1lox;
Mutation Made By David Kwiatkowski,   Brigham and Women's Hospital
Strain of Origin129S4/SvJae
ES Cell Line NameJ1
ES Cell Line Strain129S4/SvJae
Gene Symbol and Name Tsc1, tuberous sclerosis 1
Chromosome 2
Gene Common Name(s) LAM; TSC; hamartin;
Molecular Note A floxed neo-TK cassette was inserted into the intron preceding exon 17 and a third loxP site was introduced downstream of exon 18 by homologous recombination. [MGI Ref ID J:75243]

Genotyping

Genotyping Information

Genotyping Protocols

Tsc1tm1Djk, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Kwiatkowski DJ; Zhang H; Bandura JL; Heiberger KM; Glogauer M; el-Hashemite N; Onda H. 2002. A mouse model of TSC1 reveals sex-dependent lethality from liver hemangiomas, and up-regulation of p70S6 kinase activity in Tsc1 null cells. Hum Mol Genet 11(5):525-34. [PubMed: 11875047]  [MGI Ref ID J:75243]

Additional References

Tsc1tm1Djk related

Adhikari D; Zheng W; Shen Y; Gorre N; Hamalainen T; Cooney AJ; Huhtaniemi I; Lan ZJ; Liu K. 2009. Tsc/mTORC1 signaling in oocytes governs the quiescence and activation of primordial follicles. Hum Mol Genet :. [PubMed: 19843540]  [MGI Ref ID J:155357]

Ai D; Baez JM; Jiang H; Conlon DM; Hernandez-Ono A; Frank-Kamenetsky M; Milstein S; Fitzgerald K; Murphy AJ; Woo CW; Strong A; Ginsberg HN; Tabas I; Rader DJ; Tall AR. 2012. Activation of ER stress and mTORC1 suppresses hepatic sortilin-1 levels in obese mice. J Clin Invest 122(5):1677-87. [PubMed: 22466652]  [MGI Ref ID J:184540]

Ai D; Chen C; Han S; Ganda A; Murphy AJ; Haeusler R; Thorp E; Accili D; Horton JD; Tall AR. 2012. Regulation of hepatic LDL receptors by mTORC1 and PCSK9 in mice. J Clin Invest 122(4):1262-70. [PubMed: 22426206]  [MGI Ref ID J:184553]

Armour EA; Carson RP; Ess KC. 2012. Cystogenesis and elongated primary cilia in Tsc1-deficient distal convoluted tubules. Am J Physiol Renal Physiol 303(4):F584-92. [PubMed: 22674026]  [MGI Ref ID J:188431]

Banerjee S; Crouse NR; Emnett RJ; Gianino SM; Gutmann DH. 2011. Neurofibromatosis-1 regulates mTOR-mediated astrocyte growth and glioma formation in a TSC/Rheb-independent manner. Proc Natl Acad Sci U S A 108(38):15996-6001. [PubMed: 21896734]  [MGI Ref ID J:176586]

Bateup HS; Johnson CA; Denefrio CL; Saulnier JL; Kornacker K; Sabatini BL. 2013. Excitatory/inhibitory synaptic imbalance leads to hippocampal hyperexcitability in mouse models of tuberous sclerosis. Neuron 78(3):510-22. [PubMed: 23664616]  [MGI Ref ID J:197979]

Benhamron S; Tirosh B. 2011. Direct activation of mTOR in B lymphocytes confers impairment in B-cell maturation andloss of marginal zone B cells. Eur J Immunol 41(8):2390-6. [PubMed: 21674478]  [MGI Ref ID J:176815]

Byles V; Covarrubias AJ; Ben-Sahra I; Lamming DW; Sabatini DM; Manning BD; Horng T. 2013. The TSC-mTOR pathway regulates macrophage polarization. Nat Commun 4:2834. [PubMed: 24280772]  [MGI Ref ID J:206148]

Carson RP; Van Nielen DL; Winzenburger PA; Ess KC. 2012. Neuronal and glia abnormalities in Tsc1-deficient forebrain and partial rescue by rapamycin. Neurobiol Dis 45(1):369-80. [PubMed: 21907282]  [MGI Ref ID J:179842]

Castets P; Lin S; Rion N; Di Fulvio S; Romanino K; Guridi M; Frank S; Tintignac LA; Sinnreich M; Ruegg MA. 2013. Sustained activation of mTORC1 in skeletal muscle inhibits constitutive and starvation-induced autophagy and causes a severe, late-onset myopathy. Cell Metab 17(5):731-44. [PubMed: 23602450]  [MGI Ref ID J:198962]

Chen C; Liu Y; Liu R; Ikenoue T; Guan KL; Liu Y; Zheng P. 2008. TSC-mTOR maintains quiescence and function of hematopoietic stem cells by repressing mitochondrial biogenesis and reactive oxygen species. J Exp Med 205(10):2397-408. [PubMed: 18809716]  [MGI Ref ID J:140099]

Chen H; Zhang L; Zhang H; Xiao Y; Shao L; Li H; Yin H; Wang R; Liu G; Corley D; Yang Z; Zhao Y. 2013. Disruption of TSC1/2 signaling complex reveals a checkpoint governing thymic CD4+ CD25+ Foxp3+ regulatory T-cell development in mice. FASEB J 27(10):3979-90. [PubMed: 23882125]  [MGI Ref ID J:203700]

Chevere-Torres I; Kaphzan H; Bhattacharya A; Kang A; Maki JM; Gambello MJ; Arbiser JL; Santini E; Klann E. 2012. Metabotropic glutamate receptor-dependent long-term depression is impaired due to elevated ERK signaling in the DeltaRG mouse model of tuberous sclerosis complex. Neurobiol Dis 45(3):1101-10. [PubMed: 22198573]  [MGI Ref ID J:182345]

Daikoku T; Terakawa J; Hossain MM; Yoshie M; Cappelletti M; Yang P; Ellenson LH; Dey SK. 2014. Mammalian target of rapamycin complex 1 and cyclooxygenase 2 pathways cooperatively exacerbate endometrial cancer. Am J Pathol 184(9):2390-402. [PubMed: 25058027]  [MGI Ref ID J:213943]

Daikoku T; Yoshie M; Xie H; Sun X; Cha J; Ellenson LH; Dey SK. 2013. Conditional deletion of Tsc1 in the female reproductive tract impedes normal oviductal and uterine function by enhancing mTORC1 signaling in mice. Mol Hum Reprod 19(7):463-72. [PubMed: 23475984]  [MGI Ref ID J:211231]

Dasgupta B; Yi Y; Hegedus B; Weber JD; Gutmann DH. 2005. Cerebrospinal fluid proteomic analysis reveals dysregulation of methionine aminopeptidase-2 expression in human and mouse neurofibromatosis 1-associated glioma. Cancer Res 65(21):9843-50. [PubMed: 16267007]  [MGI Ref ID J:102692]

Di Nardo A; Kramvis I; Cho N; Sadowski A; Meikle L; Kwiatkowski DJ; Sahin M. 2009. Tuberous sclerosis complex activity is required to control neuronal stress responses in an mTOR-dependent manner. J Neurosci 29(18):5926-37. [PubMed: 19420259]  [MGI Ref ID J:148479]

Di Nardo A; Wertz MH; Kwiatkowski E; Tsai PT; Leech JD; Greene-Colozzi E; Goto J; Dilsiz P; Talos DM; Clish CB; Kwiatkowski DJ; Sahin M. 2014. Neuronal Tsc1/2 complex controls autophagy through AMPK-dependent regulation of ULK1. Hum Mol Genet 23(14):3865-74. [PubMed: 24599401]  [MGI Ref ID J:210659]

Ehninger D; Han S; Shilyansky C; Zhou Y; Li W; Kwiatkowski DJ; Ramesh V; Silva AJ. 2008. Reversal of learning deficits in a Tsc2+/- mouse model of tuberous sclerosis. Nat Med 14(8):843-8. [PubMed: 18568033]  [MGI Ref ID J:138621]

Erbayat-Altay E; Zeng LH; Xu L; Gutmann DH; Wong M. 2007. The natural history and treatment of epilepsy in a murine model of tuberous sclerosis. Epilepsia 48(8):1470-6. [PubMed: 17484760]  [MGI Ref ID J:147693]

Ess KC; Uhlmann EJ; Li W; Li H; Declue JE; Crino PB; Gutmann DH. 2004. Expression profiling in tuberous sclerosis complex (TSC) knockout mouse astrocytes to characterize human TSC brain pathology. Glia 46(1):28-40. [PubMed: 14999811]  [MGI Ref ID J:156064]

Feliciano DM; Quon JL; Su T; Taylor MM; Bordey A. 2012. Postnatal neurogenesis generates heterotopias, olfactory micronodules and cortical infiltration following single-cell Tsc1 deletion. Hum Mol Genet 21(4):799-810. [PubMed: 22068588]  [MGI Ref ID J:179742]

Feliciano DM; Su T; Lopez J; Platel JC; Bordey A. 2011. Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in mice. J Clin Invest 121(4):1596-607. [PubMed: 21403402]  [MGI Ref ID J:172004]

Fu C; Cawthon B; Clinkscales W; Bruce A; Winzenburger P; Ess KC. 2012. GABAergic interneuron development and function is modulated by the Tsc1 gene. Cereb Cortex 22(9):2111-9. [PubMed: 22021912]  [MGI Ref ID J:199987]

Gan B; Lim C; Chu G; Hua S; Ding Z; Collins M; Hu J; Jiang S; Fletcher-Sananikone E; Zhuang L; Chang M; Zheng H; Wang YA; Kwiatkowski DJ; Kaelin WG Jr; Signoretti S; DePinho RA. 2010. FoxOs enforce a progression checkpoint to constrain mTORC1-activated renal tumorigenesis. Cancer Cell 18(5):472-84. [PubMed: 21075312]  [MGI Ref ID J:166830]

Goldfinger M; Shmuel M; Benhamron S; Tirosh B. 2011. Protein synthesis in plasma cells is regulated by crosstalk between endoplasmic reticulum stress and mTOR signaling. Eur J Immunol 41(2):491-502. [PubMed: 21268018]  [MGI Ref ID J:175427]

Goto J; Talos DM; Klein P; Qin W; Chekaluk YI; Anderl S; Malinowska IA; Di Nardo A; Bronson RT; Chan JA; Vinters HV; Kernie SG; Jensen FE; Sahin M; Kwiatkowski DJ. 2011. Regulable neural progenitor-specific Tsc1 loss yields giant cells with organellar dysfunction in a model of tuberous sclerosis complex. Proc Natl Acad Sci U S A 108(45):E1070-9. [PubMed: 22025691]  [MGI Ref ID J:180260]

Gui YS; Wang L; Tian X; Feng R; Ma A; Cai B; Zhang H; Xu KF. 2012. SPC-Cre-ERT2 transgenic mouse for temporal gene deletion in alveolar epithelial cells. PLoS One 7(9):e46076. [PubMed: 23049940]  [MGI Ref ID J:192111]

Herrema H; Lee J; Zhou Y; Copps KD; White MF; Ozcan U. 2014. IRS1Ser(3)(0)(7) phosphorylation does not mediate mTORC1-induced insulin resistance. Biochem Biophys Res Commun 443(2):689-93. [PubMed: 24333417]  [MGI Ref ID J:211864]

Inoki K; Mori H; Wang J; Suzuki T; Hong S; Yoshida S; Blattner SM; Ikenoue T; Ruegg MA; Hall MN; Kwiatkowski DJ; Rastaldi MP; Huber TB; Kretzler M; Holzman LB; Wiggins RC; Guan KL. 2011. mTORC1 activation in podocytes is a critical step in the development of diabetic nephropathy in mice. J Clin Invest 121(6):2181-96. [PubMed: 21606597]  [MGI Ref ID J:174017]

Jansen LA; Uhlmann EJ; Crino PB; Gutmann DH; Wong M. 2005. Epileptogenesis and reduced inward rectifier potassium current in tuberous sclerosis complex-1-deficient astrocytes. Epilepsia 46(12):1871-80. [PubMed: 16393152]  [MGI Ref ID J:116872]

Jiang X; Kenerson H; Aicher L; Miyaoka R; Eary J; Bissler J; Yeung RS. 2008. The tuberous sclerosis complex regulates trafficking of glucose transporters and glucose uptake. Am J Pathol 172(6):1748-56. [PubMed: 18511518]  [MGI Ref ID J:136406]

Kaul A; Chen YH; Emnett RJ; Dahiya S; Gutmann DH. 2012. Pediatric glioma-associated KIAA1549:BRAF expression regulates neuroglial cell growth in a cell type-specific and mTOR-dependent manner. Genes Dev 26(23):2561-6. [PubMed: 23152448]  [MGI Ref ID J:191207]

Kenerson HL; Yeh MM; Yeung RS. 2011. Tuberous sclerosis complex-1 deficiency attenuates diet-induced hepatic lipid accumulation. PLoS One 6(3):e18075. [PubMed: 21479224]  [MGI Ref ID J:171445]

Kladney RD; Cardiff RD; Kwiatkowski DJ; Chiang GG; Weber JD; Arbeit JM; Lu ZH. 2010. Tuberous sclerosis complex 1: an epithelial tumor suppressor essential to prevent spontaneous prostate cancer in aged mice. Cancer Res 70(21):8937-47. [PubMed: 20940396]  [MGI Ref ID J:165796]

Knight ZA; Tan K; Birsoy K; Schmidt S; Garrison JL; Wysocki RW; Emiliano A; Ekstrand MI; Friedman JM. 2012. Molecular profiling of activated neurons by phosphorylated ribosome capture. Cell 151(5):1126-37. [PubMed: 23178128]  [MGI Ref ID J:193338]

Lebrun-Julien F; Bachmann L; Norrmen C; Trotzmuller M; Kofeler H; Ruegg MA; Hall MN; Suter U. 2014. Balanced mTORC1 activity in oligodendrocytes is required for accurate CNS myelination. J Neurosci 34(25):8432-48. [PubMed: 24948799]  [MGI Ref ID J:212082]

Liang MC; Ma J; Chen L; Kozlowski P; Qin W; Li D; Goto J; Shimamura T; Hayes DN; Meyerson M; Kwiatkowski DJ; Wong KK. 2010. TSC1 loss synergizes with KRAS activation in lung cancer development in the mouse and confers rapamycin sensitivity. Oncogene 29(11):1588-97. [PubMed: 19966866]  [MGI Ref ID J:160400]

Ma A; Wang L; Gao Y; Chang Z; Peng H; Zeng N; Gui YS; Tian X; Li X; Cai B; Zhang H; Xu KF. 2014. Tsc1 deficiency-mediated mTOR hyperactivation in vascular endothelial cells causes angiogenesis defects and embryonic lethality. Hum Mol Genet 23(3):693-705. [PubMed: 24129405]  [MGI Ref ID J:208733]

Magri L; Cambiaghi M; Cominelli M; Alfaro-Cervello C; Cursi M; Pala M; Bulfone A; Garcia-Verdugo JM; Leocani L; Minicucci F; Poliani PL; Galli R. 2011. Sustained Activation of mTOR Pathway in Embryonic Neural Stem Cells Leads to Development of Tuberous Sclerosis Complex-Associated Lesions. Cell Stem Cell 9(5):447-62. [PubMed: 22056141]  [MGI Ref ID J:177840]

Magri L; Cominelli M; Cambiaghi M; Cursi M; Leocani L; Minicucci F; Poliani PL; Galli R. 2013. Timing of mTOR activation affects tuberous sclerosis complex neuropathology in mouse models. Dis Model Mech 6(5):1185-97. [PubMed: 23744272]  [MGI Ref ID J:201333]

Maldonado M; Baybis M; Newman D; Kolson DL; Chen W; McKhann G nd; Gutmann DH; Crino PB. 2003. Expression of ICAM-1, TNF-alpha, NF kappa B, and MAP kinase in tubers of the tuberous sclerosis complex. Neurobiol Dis 14(2):279-90. [PubMed: 14572449]  [MGI Ref ID J:126206]

McMahon J; Huang X; Yang J; Komatsu M; Yue Z; Qian J; Zhu X; Huang Y. 2012. Impaired autophagy in neurons after disinhibition of mammalian target of rapamycin and its contribution to epileptogenesis. J Neurosci 32(45):15704-14. [PubMed: 23136410]  [MGI Ref ID J:192244]

Meikle L; McMullen JR; Sherwood MC; Lader AS; Walker V; Chan JA; Kwiatkowski DJ. 2005. A mouse model of cardiac rhabdomyoma generated by loss of Tsc1 in ventricular myocytes. Hum Mol Genet 14(3):429-35. [PubMed: 15601645]  [MGI Ref ID J:96138]

Meikle L; Pollizzi K; Egnor A; Kramvis I; Lane H; Sahin M; Kwiatkowski DJ. 2008. Response of a neuronal model of tuberous sclerosis to mammalian target of rapamycin (mTOR) inhibitors: effects on mTORC1 and Akt signaling lead to improved survival and function. J Neurosci 28(21):5422-32. [PubMed: 18495876]  [MGI Ref ID J:136366]

Meikle L; Talos DM; Onda H; Pollizzi K; Rotenberg A; Sahin M; Jensen FE; Kwiatkowski DJ. 2007. A mouse model of tuberous sclerosis: neuronal loss of Tsc1 causes dysplastic and ectopic neurons, reduced myelination, seizure activity, and limited survival. J Neurosci 27(21):5546-58. [PubMed: 17522300]  [MGI Ref ID J:121858]

Miceli AP; Saporita AJ; Weber JD. 2012. Hypergrowth mTORC1 signals translationally activate the ARF tumor suppressor checkpoint. Mol Cell Biol 32(2):348-64. [PubMed: 22064482]  [MGI Ref ID J:183671]

Mietzsch U; McKenna J 3rd; Reith RM; Way SW; Gambello MJ. 2013. Comparative analysis of Tsc1 and Tsc2 single and double radial glial cell mutants. J Comp Neurol 521(16):3817-31. [PubMed: 23749404]  [MGI Ref ID J:203971]

Mori H; Inoki K; Munzberg H; Opland D; Faouzi M; Villanueva EC; Ikenoue T; Kwiatkowski D; MacDougald OA; Myers MG Jr; Guan KL. 2009. Critical role for hypothalamic mTOR activity in energy balance. Cell Metab 9(4):362-74. [PubMed: 19356717]  [MGI Ref ID J:148167]

Mori H; Inoki K; Opland D; Muenzberg H; Villanueva EC; Faouzi M; Ikenoue T; Kwiatkowski D; Macdougald OA; Myers Jr MG; Guan KL. 2009. Critical roles for the TSC-mTOR pathway in {beta}-cell function. Am J Physiol Endocrinol Metab :. [PubMed: 19690069]  [MGI Ref ID J:159576]

Normand EA; Crandall SR; Thorn CA; Murphy EM; Voelcker B; Browning C; Machan JT; Moore CI; Connors BW; Zervas M. 2013. Temporal and mosaic Tsc1 deletion in the developing thalamus disrupts thalamocortical circuitry, neural function, and behavior. Neuron 78(5):895-909. [PubMed: 23664552]  [MGI Ref ID J:201553]

O'Brien TF; Gorentla BK; Xie D; Srivatsan S; McLeod IX; He YW; Zhong XP. 2011. Regulation of T-cell survival and mitochondrial homeostasis by TSC1. Eur J Immunol 41(11):3361-70. [PubMed: 21805467]  [MGI Ref ID J:179527]

Pan H; O'Brien TF; Wright G; Yang J; Shin J; Wright KL; Zhong XP. 2013. Critical role of the tumor suppressor tuberous sclerosis complex 1 in dendritic cell activation of CD4 T cells by promoting MHC class II expression via IRF4 and CIITA. J Immunol 191(2):699-707. [PubMed: 23776173]  [MGI Ref ID J:205451]

Pan H; O'Brien TF; Zhang P; Zhong XP. 2012. The role of tuberous sclerosis complex 1 in regulating innate immunity. J Immunol 188(8):3658-66. [PubMed: 22412198]  [MGI Ref ID J:184070]

Park Y; Jin HS; Lopez J; Elly C; Kim G; Murai M; Kronenberg M; Liu YC. 2013. TSC1 regulates the balance between effector and regulatory T cells. J Clin Invest 123(12):5165-78. [PubMed: 24270422]  [MGI Ref ID J:207832]

Parker WE; Orlova KA; Heuer GG; Baybis M; Aronica E; Frost M; Wong M; Crino PB. 2011. Enhanced epidermal growth factor, hepatocyte growth factor, and vascular endothelial growth factor expression in tuberous sclerosis complex. Am J Pathol 178(1):296-305. [PubMed: 21224066]  [MGI Ref ID J:168083]

Pilipow K; Basso V; Migone N; Mondino A. 2014. Monoallelic germline TSC1 mutations are permissive for T lymphocyte development and homeostasis in tuberous sclerosis complex individuals. PLoS One 9(3):e91952. [PubMed: 24633152]  [MGI Ref ID J:215111]

Rodgers JT; King KY; Brett JO; Cromie MJ; Charville GW; Maguire KK; Brunson C; Mastey N; Liu L; Tsai CR; Goodell MA; Rando TA. 2014. mTORC1 controls the adaptive transition of quiescent stem cells from G0 to G(Alert). Nature 510(7505):393-6. [PubMed: 24870234]  [MGI Ref ID J:213273]

Sathaliyawala T; O'Gorman WE; Greter M; Bogunovic M; Konjufca V; Hou ZE; Nolan GP; Miller MJ; Merad M; Reizis B. 2010. Mammalian target of rapamycin controls dendritic cell development downstream of flt3 ligand signaling. Immunity 33(4):597-606. [PubMed: 20933441]  [MGI Ref ID J:165522]

Sengupta S; Peterson TR; Laplante M; Oh S; Sabatini DM. 2010. mTORC1 controls fasting-induced ketogenesis and its modulation by ageing. Nature 468(7327):1100-4. [PubMed: 21179166]  [MGI Ref ID J:167208]

Shin J; Pan H; Zhong XP. 2012. Regulation of mast cell survival and function by tuberous sclerosis complex 1. Blood 119(14):3306-14. [PubMed: 22362037]  [MGI Ref ID J:183777]

Shinoda G; Shyh-Chang N; de Soysa TY; Zhu H; Seligson MT; Shah SP; Abo-Sido N; Yabuuchi A; Hagan JP; Gregory RI; Asara JM; Cantley LC; Moss EG; Daley GQ. 2013. Fetal Deficiency of Lin28 Programs Life-Long Aberrations in Growth and Glucose Metabolism. Stem Cells :. [PubMed: 23666760]  [MGI Ref ID J:199720]

Squarize CH; Castilho RM; Bugge TH; Gutkind JS. 2010. Accelerated wound healing by mTOR activation in genetically defined mouse models. PLoS One 5(5):e10643. [PubMed: 20498714]  [MGI Ref ID J:160830]

Suzuki T; Bridges D; Nakada D; Skiniotis G; Morrison SJ; Lin JD; Saltiel AR; Inoki K. 2013. Inhibition of AMPK catabolic action by GSK3. Mol Cell 50(3):407-19. [PubMed: 23623684]  [MGI Ref ID J:199198]

Tanaka Y; Park JH; Tanwar PS; Kaneko-Tarui T; Mittal S; Lee HJ; Teixeira JM. 2012. Deletion of tuberous sclerosis 1 in somatic cells of the murine reproductive tract causes female infertility. Endocrinology 153(1):404-16. [PubMed: 22128018]  [MGI Ref ID J:181774]

Tanwar PS; Kaneko-Tarui T; Zhang L; Tanaka Y; Crum CP; Teixeira JM. 2012. Stromal liver kinase B1 [STK11] signaling loss induces oviductal adenomas and endometrial cancer by activating mammalian Target of Rapamycin Complex 1. PLoS Genet 8(8):e1002906. [PubMed: 22916036]  [MGI Ref ID J:188124]

Tanwar PS; Kaneko-Tarui T; Zhang L; Teixeira JM. 2012. Altered LKB1/AMPK/TSC1/TSC2/mTOR signaling causes disruption of Sertoli cell polarity and spermatogenesis. Hum Mol Genet 21(20):4394-405. [PubMed: 22791749]  [MGI Ref ID J:187754]

Tanwar PS; Mohapatra G; Chiang S; Engler DA; Zhang L; Kaneko-Tarui T; Ohguchi Y; Birrer MJ; Teixeira JM. 2014. Loss of LKB1 and PTEN tumor suppressor genes in the ovarian surface epithelium induces papillary serous ovarian cancer. Carcinogenesis 35(3):546-53. [PubMed: 24170201]  [MGI Ref ID J:206514]

Tavazoie SF; Alvarez VA; Ridenour DA; Kwiatkowski DJ; Sabatini BL. 2005. Regulation of neuronal morphology and function by the tumor suppressors Tsc1 and Tsc2. Nat Neurosci 8(12):1727-34. [PubMed: 16286931]  [MGI Ref ID J:103933]

Traykova-Brauch M; Schonig K; Greiner O; Miloud T; Jauch A; Bode M; Felsher DW; Glick AB; Kwiatkowski DJ; Bujard H; Horst J; von Knebel Doeberitz M; Niggli FK; Kriz W; Grone HJ; Koesters R. 2008. An efficient and versatile system for acute and chronic modulation of renal tubular function in transgenic mice. Nat Med 14(9):979-84. [PubMed: 18724376]  [MGI Ref ID J:140925]

Tsai PT; Hull C; Chu Y; Greene-Colozzi E; Sadowski AR; Leech JM; Steinberg J; Crawley JN; Regehr WG; Sahin M. 2012. Autistic-like behaviour and cerebellar dysfunction in Purkinje cell Tsc1 mutant mice. Nature 488(7413):647-51. [PubMed: 22763451]  [MGI Ref ID J:186699]

Uhlmann EJ; Li W; Scheidenhelm DK; Gau CL; Tamanoi F; Gutmann DH. 2004. Loss of tuberous sclerosis complex 1 (Tsc1) expression results in increased Rheb/S6K pathway signaling important for astrocyte cell size regulation. Glia 47(2):180-8. [PubMed: 15185396]  [MGI Ref ID J:104911]

Uhlmann EJ; Wong M; Baldwin RL; Bajenaru ML; Onda H; Kwiatkowski DJ; Yamada K; Gutmann DH. 2002. Astrocyte-specific TSC1 conditional knockout mice exhibit abnormal neuronal organization and seizures. Ann Neurol 52(3):285-96. [PubMed: 12205640]  [MGI Ref ID J:82532]

Wang Y; Huang G; Zeng H; Yang K; Lamb RF; Chi H. 2013. Tuberous sclerosis 1 (Tsc1)-dependent metabolic checkpoint controls development of dendritic cells. Proc Natl Acad Sci U S A 110(50):E4894-903. [PubMed: 24282297]  [MGI Ref ID J:205513]

Wolff NC; Vega-Rubin-de-Celis S; Xie XJ; Castrillon DH; Kabbani W; Brugarolas J. 2011. Cell-type-dependent regulation of mTORC1 by REDD1 and the tumor suppressors TSC1/TSC2 and LKB1 in response to hypoxia. Mol Cell Biol 31(9):1870-84. [PubMed: 21383064]  [MGI Ref ID J:172815]

Wu J; Shin J; Xie D; Wang H; Gao J; Zhong XP. 2014. Tuberous sclerosis 1 promotes invariant NKT cell anergy and inhibits invariant NKT cell-mediated antitumor immunity. J Immunol 192(6):2643-50. [PubMed: 24532578]  [MGI Ref ID J:209909]

Wu J; Yang J; Yang K; Wang H; Gorentla B; Shin J; Qiu Y; Que LG; Foster WM; Xia Z; Chi H; Zhong XP. 2014. iNKT cells require TSC1 for terminal maturation and effector lineage fate decisions. J Clin Invest 124(4):1685-98. [PubMed: 24614103]  [MGI Ref ID J:209612]

Xie DL; Wu J; Lou YL; Zhong XP. 2012. Tumor suppressor TSC1 is critical for T-cell anergy. Proc Natl Acad Sci U S A 109(35):14152-7. [PubMed: 22891340]  [MGI Ref ID J:188573]

Xie X; Brown MS; Shelton JM; Richardson JA; Goldstein JL; Liang G. 2011. Amino acid substitution in NPC1 that abolishes cholesterol binding reproduces phenotype of complete NPC1 deficiency in mice. Proc Natl Acad Sci U S A 108(37):15330-5. [PubMed: 21896731]  [MGI Ref ID J:176587]

Yang K; Neale G; Green DR; He W; Chi H. 2011. The tumor suppressor Tsc1 enforces quiescence of naive T cells to promote immune homeostasis and function. Nat Immunol 12(9):888-97. [PubMed: 21765414]  [MGI Ref ID J:176473]

Yecies JL; Zhang HH; Menon S; Liu S; Yecies D; Lipovsky AI; Gorgun C; Kwiatkowski DJ; Hotamisligil GS; Lee CH; Manning BD. 2011. Akt stimulates hepatic SREBP1c and lipogenesis through parallel mTORC1-dependent and independent pathways. Cell Metab 14(1):21-32. [PubMed: 21723501]  [MGI Ref ID J:176082]

Zeng LH; Bero AW; Zhang B; Holtzman DM; Wong M. 2010. Modulation of astrocyte glutamate transporters decreases seizures in a mouse model of Tuberous Sclerosis Complex. Neurobiol Dis 37(3):764-71. [PubMed: 20045054]  [MGI Ref ID J:158397]

Zeng LH; Ouyang Y; Gazit V; Cirrito JR; Jansen LA; Ess KC; Yamada KA; Wozniak DF; Holtzman DM; Gutmann DH; Wong M. 2007. Abnormal glutamate homeostasis and impaired synaptic plasticity and learning in a mouse model of tuberous sclerosis complex. Neurobiol Dis 28(2):184-96. [PubMed: 17714952]  [MGI Ref ID J:134889]

Zeng LH; Rensing NR; Zhang B; Gutmann DH; Gambello MJ; Wong M. 2011. Tsc2 gene inactivation causes a more severe epilepsy phenotype than Tsc1 inactivation in a mouse model of Tuberous Sclerosis Complex. Hum Mol Genet 20(3):445-54. [PubMed: 21062901]  [MGI Ref ID J:167241]

Zhang B; McDaniel SS; Rensing NR; Wong M. 2013. Vigabatrin inhibits seizures and mTOR pathway activation in a mouse model of tuberous sclerosis complex. PLoS One 8(2):e57445. [PubMed: 23437388]  [MGI Ref ID J:197188]

Zhou J ; Blundell J ; Ogawa S ; Kwon CH ; Zhang W ; Sinton C ; Powell CM ; Parada LF. 2009. Pharmacological inhibition of mTORC1 suppresses anatomical, cellular, and behavioral abnormalities in neural-specific Pten knock-out mice. J Neurosci 29(6):1773-83. [PubMed: 19211884]  [MGI Ref ID J:146632]

Zhou J; Brugarolas J; Parada LF. 2009. Loss of Tsc1, but not Pten, in renal tubular cells causes polycystic kidney disease by activating mTORC1. Hum Mol Genet 18(22):4428-41. [PubMed: 19692352]  [MGI Ref ID J:153717]

Zhou J; Shrikhande G; Xu J; McKay RM; Burns DK; Johnson JE; Parada LF. 2011. Tsc1 mutant neural stem/progenitor cells exhibit migration deficits and give rise to subependymal lesions in the lateral ventricle. Genes Dev 25(15):1595-600. [PubMed: 21828270]  [MGI Ref ID J:174417]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are maintained as homozygotes.
Mating SystemHomozygote x Homozygote         (Female x Male)   31-MAR-06
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $239.00Female or MaleHomozygous for Tsc1tm1Djk  
Price per Pair (US dollars $)Pair Genotype
$478.00Homozygous for Tsc1tm1Djk x Homozygous for Tsc1tm1Djk  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Cryopreserved

Frozen Products

Price (US dollars $)
Frozen Embryo $1650.00

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $310.70Female or MaleHomozygous for Tsc1tm1Djk  
Price per Pair (US dollars $)Pair Genotype
$621.40Homozygous for Tsc1tm1Djk x Homozygous for Tsc1tm1Djk  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Cryopreserved

Frozen Products

Price (US dollars $)
Frozen Embryo $2145.00

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   None Available
 
  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.
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JAX® Mice
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JAX® Services
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Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
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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

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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

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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.

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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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