Description

Strain Information

Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse   Donating Investigator Michael Grusby,   Harvard Medical School

Description
Mice homozygous for the targeted allele are viable yet sterile and exhibit a progressive development of a type 2 diabetic phenotype. At birth, mice are slightly (10%) smaller than wildtype littermates. This weight difference is maintained from birth through adulthood. Elevated blood sugar levels can be detected by 3 days of age. By 3-6 weeks of age mice develop fasting hyperglycemia and become diabetic by 10 weeks. A reduced beta-cell mass can be detected by 4 weeks and a profound insulin resistance is observed in skeletal muscle and liver tissue by 6-8 weeks. Levels of fasting sugars continue to rise until male mice eventually succumb to dehydration and hyperosomolar coma. Female mice, while exhibiting a similar progression, tend not to die. This mutant mouse represents a model useful in studies related to type 2 diabetes.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to delete the entire insulin receptor 2 gene. The construct was electroporated into 129X1/SvJ x 129S1/Sv-derived R1 embryonic stem (ES) cells in the laboratory of Dr. Morris White, Joslin Diabetes Center/HHMI, Boston. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6 mice.

Control Information

	Control
	Wild-type from the colony
Considerations for Choosing Controls

Additional Web Information

Genetic Quality Control Annual Report

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms

Diabetes Mellitus, Noninsulin-Dependent; NIDDM - Models with phenotypic similarity to human disease where etiologies involve orthologs.1

1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

Irs2^tm1Mfw/Irs2^tm1Mfw

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6

• life span-post-weaning/aging
• premature death (MGI Ref ID J:46134)
  • male mutants die prematurely from dehydration and hyperosomolar coma
  • female mutants exhibit a similar disease progression but rarely die
• homeostasis/metabolism phenotype
• hyperglycemia (MGI Ref ID J:46134)
  • homozygotes show increased levels of randomly fed sugars at postnatal day 3, and fasting hyperglycemia between 3 and 6 weeks of age
  • at 10 weeks, homozygotes exhibit overt diabetes with fasting glucose levels of 323 35 mg dl^-1; if left untreated, the fasting sugar levels rise progressively to >400 mg dl^-1 at 12-16 weeks of age
• impaired glucose tolerance (MGI Ref ID J:46134)
  • at 6-8 weeks, homozygotes display significant glucose intolerance (>95% penetrance) during an intraperitoneal glucose-tolerance test
• increased circulating insulin level (MGI Ref ID J:46134)
  • at >6 weeks, homozygotes display a 3-fold increase in fasting insulin levels relative to wild-type mice
  • despite fasting hyperinsulinemia, homozygotes respond with a nearly 2-fold increase in insulin levels 60 minutes after glucose loading
• insulin resistance (MGI Ref ID J:46134)
  • homozygotes exhibit profound insulin resistance in both skeletal muscle and liver
• behavior/neurological phenotype
• polydipsia (MGI Ref ID J:46134)
• renal/urinary system phenotype
• polyuria (MGI Ref ID J:46134)
  • homozygotes display polyuria without ketosis
• endocrine/exocrine gland phenotype
• abnormal pancreatic beta cell morphology (MGI Ref ID J:46134)
  • at 4 weeks, homozygotes show a significant reduction in pancreatic beta-cell mass indicating failure of compensatory islet hyperplasia
  • no significant difference in non-beta endocrine-cell mass is observed
• digestive/alimentary phenotype
• abnormal pancreatic beta cell morphology (MGI Ref ID J:46134)
  • at 4 weeks, homozygotes show a significant reduction in pancreatic beta-cell mass indicating failure of compensatory islet hyperplasia
  • no significant difference in non-beta endocrine-cell mass is observed
• growth/size phenotype
• decreased body size (MGI Ref ID J:46134)
  • homozygous neonates are 10% smaller than heterozygous or wild-type littermates
• decreased body weight (MGI Ref ID J:46134)
  • homozygotes exhibit a small reduction in body weight that persists during weaning and into adulthood

Irs2^tm1Mfw/Irs2^tm1Mfw

        involves: 129/Sv * C57BL/6

• reproductive system phenotype
• abnormal oogenesis (MGI Ref ID J:64791)
• abnormal ovarian follicle morphology (MGI Ref ID J:64791)
  • at 6 weeks, mutant ovaries contain very few surface follicles and show thickening of the cortex relative to wild-type
• impaired ovarian folliculogenesis (MGI Ref ID J:64791)
  • adult mutant ovaries contain reduced numbers of primary follicles with few growing follicles reaching an antral phase of development
• abnormal ovulation (MGI Ref ID J:64791)
  • female homozygotes are resistant to exogenous gonadotropin stimulation
  • however, uterine tissues of mutant females respond normally to exogenous sex steroids
• anovulation (MGI Ref ID J:64791)
  • female homozygotes show features of anovulation, such as thickening of the ovarian stroma and absence of corpora lutea
• absent corpus luteum (MGI Ref ID J:64791)
  • mutant ovaries show an almost complete absence of corpora lutea
• absent estrous cycle (MGI Ref ID J:64791)
  • 61% of female homozygotes fail to cycle and remain in an inactive or dioestrous state
• decreased oocyte cell number (MGI Ref ID J:64791)
  • at E18.5, mutant ovaries contain decreased numbers of primary oocytes relative to wild-type ovaries
• female infertility (MGI Ref ID J:64791)
  • when bred with homozygous mutant males, 0% of homozygous virgin females become pregnant during an 8-week period
  • at <10 weeks, female homozygotes are relatively euglycemic and mildly insulin resistant, suggesting that female infertility is not a direct result of impaired glucose metabolism
• reduced female fertility (MGI Ref ID J:64791)
  • when bred with wild-type males, only 9% of homozygous virgin females (4?6-week-old) become pregnant during an 8-week period
• reduced male fertility (MGI Ref ID J:64791)
  • male homozygotes exhibit reduced fertility; males are adequate breeders only if mated prior to the onset of severe diabetes
• small ovary (MGI Ref ID J:64791)
  • at 6 weeks, female homozygotes show normal development of the external genitalia and reproductive tract; however, mutant ovaries are small relative to wild-type
• homeostasis/metabolism phenotype
• abnormal energy balance (MGI Ref ID J:64791)
  • females homozygotes show hypothalamic resistance to leptin, suggesting defects in homeostatic mechanisms involved in leptin sensing and/or signaling
• abnormal glucose homeostasis (MGI Ref ID J:64791)
  • homozygous males are more severely affected than age-matched females with respect to abnormal glucose homeostasis
  • immediately after treadmill exercise, male homozygotes show an attenuated increase in insulin-stimulated, phosphotyrosine-associated PI 3-kinase activity relative to wild-type males
  • however, insulin-stimulated, phosphotyrosine-associated PI 3-kinase response after exercise is slightly higher than the insulin-stimulated response alone
• abnormal circulating glucose level (MGI Ref ID J:74303)
  • treadmill exercise reduces blood glucose by ~20% in fasted wild-type mice but has no effect on blood glucose in fasted homozygotes
  • plasma insulin concentrations are similar between wild-type and mutant mice at rest and remain unchanged after exercise
• decreased glycogen level (MGI Ref ID J:74303)
  • at rest, fasted homozygotes tend to have reduced muscle glycogen levels relative to wild-type mice
  • after treadmill exercise, homozygotes display significantly lower muscle glycogen levels than wild-type mice
• impaired glucose tolerance (MGI Ref ID J:64791)
  • by 6 weeks, male homozygotes are severely glucose intolerant
  • in contrast, age-matched female homozygotes show only slightly increased blood glucose levels and mildly impaired glucose tolerance, suggesting sexual dimorphism in the diabetic phenotype
• decreased circulating estradiol level (MGI Ref ID J:64791)
  • female homozygotes display reduced plasma estradiol levels relative to wild-type females in both dioestrous and oestrous states
• decreased circulating luteinizing hormone level (MGI Ref ID J:64791)
  • surprisingly, female homozygotes display low plasma luteinizing hormone levels relative to wild-type females in both dioestrous and oestrous states
• decreased circulating progesterone level (MGI Ref ID J:64791)
  • female homozygotes display reduced plasma progesterone levels relative to wild-type females in both dioestrous and oestrous states
• decreased circulating prolactin level (MGI Ref ID J:64791)
  • female homozygotes display low plasma prolactin levels relative to wild-type females
• decreased circulating testosterone level (MGI Ref ID J:64791)
  • female homozygotes display reduced plasma testosterone levels relative to wild-type females in both dioestrous and oestrous states
• increased circulating leptin level (MGI Ref ID J:64791)
  • as early as 4 weeks (i.e. prior to the onset of abnormal glucose tolerance) female homozygotes show a 2.5-fold increase in circulating leptin levels
  • at 8 weeks, circulating leptin levels are increased by >5-fold relative to wild-type levels
• endocrine/exocrine gland phenotype
• abnormal ovarian follicle morphology (MGI Ref ID J:64791)
  • at 6 weeks, mutant ovaries contain very few surface follicles and show thickening of the cortex relative to wild-type
• impaired ovarian folliculogenesis (MGI Ref ID J:64791)
  • adult mutant ovaries contain reduced numbers of primary follicles with few growing follicles reaching an antral phase of development
• absent corpus luteum (MGI Ref ID J:64791)
  • mutant ovaries show an almost complete absence of corpora lutea
• decreased gonadotroph cell number (MGI Ref ID J:64791)
  • mutant pituitaries contain ~40% less gonadotrophs than wild-type pituitaries
• small ovary (MGI Ref ID J:64791)
  • at 6 weeks, female homozygotes show normal development of the external genitalia and reproductive tract; however, mutant ovaries are small relative to wild-type
• small pituitary gland (MGI Ref ID J:64791)
  • mutant pituitaries are ~30% smaller
• small pituitary intermediate lobe (MGI Ref ID J:74303)
  • the size of the intermediate lobe is reduced more than that of other lobes
• behavior/neurological phenotype
• abnormal copulation (MGI Ref ID J:64791)
  • only 18.2% of female homozygotes vs 100% of wild-type display copulation plugs, suggesting abnormal oestrous cycle and sexual behavior
• polyphagia (MGI Ref ID J:64791)
  • female homozygotes consume 30% more chow relative to wild-type females
• growth/size phenotype
• decreased body weight (MGI Ref ID J:74303)
  • at 5 weeks, male homozygotes weigh ~18% less than wild-type males
• obese (MGI Ref ID J:64791)
  • female homozygotes weigh 20% more than wild-type females and are obese despite elevated leptin levels
• adipose tissue phenotype
• increased adipose tissue amount (MGI Ref ID J:64791)
  • female homozygotes store twice as much body fat as age-matched wild-type females
• nervous system phenotype
• decreased gonadotroph cell number (MGI Ref ID J:64791)
  • mutant pituitaries contain ~40% less gonadotrophs than wild-type pituitaries
• small pituitary gland (MGI Ref ID J:64791)
  • mutant pituitaries are ~30% smaller
• small pituitary intermediate lobe (MGI Ref ID J:74303)
  • the size of the intermediate lobe is reduced more than that of other lobes

Irs2^tm1Mfw/Irs2^tm1Mfw

        involves: 129 * C57BL/6J

• homeostasis/metabolism phenotype
• hyperglycemia (MGI Ref ID J:135659)
  • developed a progressive increase with severe hyperglycemia
  • fasting glucose levels were higher than in wild-type mice
• increased circulating insulin level (MGI Ref ID J:135659)
  • both fasting and fed insulin levels were higher than in wild-type mice
• insulin resistance (MGI Ref ID J:135659)
  • insulin resistant compared to wild-type
• digestive/alimentary phenotype
• abnormal pancreatic beta cell morphology (MGI Ref ID J:135659)
  • reduced beta cell mass compared to wild-type
  • decreased beta cell proliferation and increased beta cell accounts for reduction in beta cell mass
• endocrine/exocrine gland phenotype
• abnormal pancreatic beta cell morphology (MGI Ref ID J:135659)
  • reduced beta cell mass compared to wild-type
  • decreased beta cell proliferation and increased beta cell accounts for reduction in beta cell mass
• growth/size phenotype
• weight loss (MGI Ref ID J:135659)
  • mice gained weight until about 9 weeks, and began to decline

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

Irs2^tm1Mfw/Irs2^tm1Mfw

        Background Not Specified

• life span-post-weaning/aging
• premature death (MGI Ref ID J:94000)
  • death due to diabetes
• digestive/alimentary phenotype
• decreased pancreatic beta cell number (MGI Ref ID J:94000)
  • at 8 weeks, islet area reduced by threefold due to 50% fewer beta cells
• endocrine/exocrine gland phenotype
• decreased pancreatic beta cell number (MGI Ref ID J:94000)
  • at 8 weeks, islet area reduced by threefold due to 50% fewer beta cells
• homeostasis/metabolism phenotype
• abnormal circulating insulin level (MGI Ref ID J:94000)
  • elevated serum insulin levels at 6 weeks (before diabetes developed) and decreased insulin levels at 8 weeks with the onset of diabetes
• hyperglycemia (MGI Ref ID J:94000)
  • developed in males between 4 and 6 weeks of age, which progressed to overt diabetes during the next 5-6 weeks until they died

Irs2^tm1Mfw/Irs2^tm1Mfw

        involves: 129/Sv * C57BL/6J

• digestive/alimentary phenotype
• abnormal islet of Langerhans morphology (MGI Ref ID J:96047)
  • islet mass and density are significantly decreased compared to wild-type mice
• abnormal pancreatic beta cell morphology (MGI Ref ID J:96047)
  • individual beta cell size is decreased
• endocrine/exocrine gland phenotype
• abnormal islet of Langerhans morphology (MGI Ref ID J:96047)
  • islet mass and density are significantly decreased compared to wild-type mice
• abnormal pancreatic beta cell morphology (MGI Ref ID J:96047)
  • individual beta cell size is decreased
• homeostasis/metabolism phenotype
• abnormal lipid homeostasis (MGI Ref ID J:96047)
  • dyslipidemia
• hyperglycemia (MGI Ref ID J:96047)
  • seen at about 10 weeks of age

View Research Applications

Research Applications

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

Irs2^tm1Mfw related

Diabetes and Obesity Research
Insulin Receptors and Growth Factors
Type 2 Diabetes (NIDDM)

Genes & Alleles

Gene & Allele Information

Allele Symbol		Irs2tm1Mfw
Allele Name		targeted mutation 1, Morris F White
Allele Type		Targeted (knock-out)
Common Name(s)		Irs2-;
Mutation Made By		Morris White,   Joslin Diabetes Center/HHMI
Strain of Origin		(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
ES Cell Line Name		R1
ES Cell Line Strain		(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name		Irs2, insulin receptor substrate 2
Chromosome		8
Gene Common Name(s)		4PS; IRS-2;
Molecular Note		A targeting vector containing a PGK-neomycin cassette replaced the entire gene. Lack of protein was demonstrated in liver and muscle extracts by Western analysis in homozygous mutant animals. [MGI Ref ID J:46134]

Genotyping

Genotyping Information

Genotyping Protocols

Irs2^tm1Mfw, STD PCR, vers. 1

Helpful Links

Optimizing PCR Protocols

References

References

Selected Reference(s)

Withers DJ; Gutierrez JS; Towery H; Burks DJ; Ren JM; Previs S; Zhang Y; Bernal D; Pons S; Shulman GI; Bonner-Weir S; White MF. 1998. Disruption of IRS-2 causes type 2 diabetes in mice. Nature 391(6670):900-4. [PubMed: 9495343]  [MGI Ref ID J:46134]

Additional References

Irs2^tm1Mfw related

Burks DJ; de Mora JF; Schubert M; Withers DJ; Myers MG; Towery HH; Altamuro SL; Flint CL; White MF. 2000. IRS-2 pathways integrate female reproduction and energy homeostasis. Nature 407(6802):377-82. [PubMed: 11014193]  [MGI Ref ID J:64791]

Hennige AM; Burks DJ; Ozcan U; Kulkarni RN; Ye J; Park S; Schubert M; Fisher TL; Dow MA; Leshan R; Zakaria M; Mossa-Basha M; White MF. 2003. Upregulation of insulin receptor substrate-2 in pancreatic beta cells prevents diabetes. J Clin Invest 112(10):1521-32. [PubMed: 14617753]  [MGI Ref ID J:94000]

Howlett KF; Sakamoto K; Hirshman MF; Aschenbach WG; Dow M; White MF; Goodyear LJ. 2002. Insulin signaling after exercise in insulin receptor substrate-2-deficient mice. Diabetes 51(2):479-83. [PubMed: 11812758]  [MGI Ref ID J:74303]

Kido Y; Burks DJ; Withers D; Bruning JC; Kahn CR; White MF; Accili D. 2000. Tissue-specific insulin resistance in mice with mutations in the insulin receptor, IRS-1, and IRS-2. J Clin Invest 105(2):199-205. [PubMed: 10642598]  [MGI Ref ID J:59431]

Kim JJ; Kido Y; Scherer PE; White MF; Accili D. 2007. Analysis of compensatory beta-cell response in mice with combined mutations of Insr and Irs2. Am J Physiol Endocrinol Metab 292(6):E1694-701. [PubMed: 17299086]  [MGI Ref ID J:121915]

Kitamura T; Nakae J; Kitamura Y; Kido Y; Biggs WH rd; Wright CV; White MF; Arden KC; Accili D. 2002. The forkhead transcription factor Foxo1 links insulin signaling to Pdx1 regulation of pancreatic beta cell growth. J Clin Invest 110(12):1839-47. [PubMed: 12488434]  [MGI Ref ID J:80826]

Kitamura YI; Kitamura T; Kruse JP; Raum JC; Stein R; Gu W; Accili D. 2005. FoxO1 protects against pancreatic beta cell failure through NeuroD and MafA induction. Cell Metab 2(3):153-63. [PubMed: 16154098]  [MGI Ref ID J:129682]

Kushner JA; Haj FG; Klaman LD; Dow MA; Kahn BB; Neel BG; White MF. 2004. Islet-Sparing Effects of Protein Tyrosine Phosphatase-1b Deficiency Delays Onset of Diabetes in IRS2 Knockout Mice. Diabetes 53(1):61-66. [PubMed: 14693698]  [MGI Ref ID J:87249]

Kushner JA; Simpson L; Wartschow LM; Guo S; Rankin MM; Parsons R; White MF. 2005. Phosphatase and tensin homolog regulation of islet growth and glucose homeostasis. J Biol Chem 280(47):39388-93. [PubMed: 16170201]  [MGI Ref ID J:104109]

Kushner JA; Ye J; Schubert M; Burks DJ; Dow MA; Flint CL; Dutta S; Wright CV; Montminy MR; White MF. 2002. Pdx1 restores beta cell function in Irs2 knockout mice. J Clin Invest 109(9):1193-201. [PubMed: 11994408]  [MGI Ref ID J:76408]

Nakae J; Biggs WH; Kitamura T; Cavenee WK; Wright CV; Arden KC; Accili D. 2002. Regulation of insulin action and pancreatic beta-cell function by mutated alleles of the gene encoding forkhead transcription factor Foxo1. Nat Genet 32(2):245-53. [PubMed: 12219087]  [MGI Ref ID J:79560]

Sadagurski M; Weingarten G; Rhodes CJ; White MF; Wertheimer E. 2005. Insulin receptor substrate 2 plays diverse cell-specific roles in the regulation of glucose transport. J Biol Chem 280(15):14536-44. [PubMed: 15705592]  [MGI Ref ID J:107134]

Schubert M; Brazil DP; Burks DJ; Kushner JA; Ye J; Flint CL; Farhang-Fallah J; Dikkes P; Warot XM; Rio C; Corfas G; White MF. 2003. Insulin receptor substrate-2 deficiency impairs brain growth and promotes tau phosphorylation. J Neurosci 23(18):7084-92. [PubMed: 12904469]  [MGI Ref ID J:84857]

Selman C; Lingard S; Choudhury AI; Batterham RL; Claret M; Clements M; Ramadani F; Okkenhaug K; Schuster E; Blanc E; Piper MD; Al-Qassab H; Speakman JR; Carmignac D; Robinson IC; Thornton JM; Gems D; Partridge L; Withers DJ. 2008. Evidence for lifespan extension and delayed age-related biomarkers in insulin receptor substrate 1 null mice. FASEB J 22(3):807-18. [PubMed: 17928362]  [MGI Ref ID J:134916]

Sobel BE; Schneider DJ; Lee YH; Pratley RE. 2006. Insulin resistance increases PAI-1 in the heart. Biochem Biophys Res Commun 346(1):102-7. [PubMed: 16750510]  [MGI Ref ID J:110785]

Tanabe K; Liu Z; Patel S; Doble BW; Li L; Cras-Meneur C; Martinez SC; Welling CM; White MF; Bernal-Mizrachi E; Woodgett JR; Permutt MA. 2008. Genetic deficiency of glycogen synthase kinase-3beta corrects diabetes in mouse models of insulin resistance. PLoS Biol 6(2):e37. [PubMed: 18288891]  [MGI Ref ID J:135659]

Uchida T; Nakamura T; Hashimoto N; Matsuda T; Kotani K; Sakaue H; Kido Y; Hayashi Y; Nakayama KI; White MF; Kasuga M. 2005. Deletion of Cdkn1b ameliorates hyperglycemia by maintaining compensatory hyperinsulinemia in diabetic mice. Nat Med 11(2):175-82. [PubMed: 15685168]  [MGI Ref ID J:96047]

Withers DJ; Burks DJ; Towery HH; Altamuro SL; Flint CL; White MF. 1999. Irs-2 coordinates Igf-1 receptor-mediated beta-cell development and peripheral insulin signalling. Nat Genet 23(1):32-40. [PubMed: 10471495]  [MGI Ref ID J:57319]

Yi X; Schubert M; Peachey NS; Suzuma K; Burks DJ; Kushner JA; Suzuma I; Cahill C; Flint CL; Dow MA; Leshan RL; King GL; White MF. 2005. Insulin receptor substrate 2 is essential for maturation and survival of photoreceptor cells. J Neurosci 25(5):1240-8. [PubMed: 15689562]  [MGI Ref ID J:98107]

Health & husbandry

Health & Colony Maintenance Information

Colony Maintenance

Breeding & Husbandry	Mice bearing the Irs2tm1Mfw allele were crossed to B6;129-Stat6tm1Gru targeted mutant mice in the laboratory of Dr. Michael Grusby, Harvard School of Public Health, Boston. The double mutant mice were kindly donated to The Jackson Laboratory. The Stat6tm1Gru allele was bred out of the stock which is currently maintained by breeding heterozygotes. Note that homozygotes are sterile.

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Supply Details

Standard Supply

Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information.

Supply Notes

Cryorecovery - Standard. The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery. Cryorecovery to establish a Dedicated Supply for greater quantities of mice. One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 or 1-207-288-5845. This strain is included in the Induced Mutant Resource Colony collection.

Control Information

	Control
	Wild-type from the colony
Considerations for Choosing Controls
USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
International - Control Pricing Information for Genetically Engineered Mutant Strains.

General Terms and Conditions

See Terms of Use

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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Ordering and Purchasing Information

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Contact Information
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Fax: 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:
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Contact information

General inquiries

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phone:	207-288-6470
fax:	207-288-6655

JAX^® Mice & Services Conditions of Use

“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (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 with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”

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