Strain Name:

BKSChpLt.HRS-Cpefat/J

Stock Number:

002391

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Availability:

Cryopreserved - Ready for recovery

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

Former Names BKS.HRS-Cpefat/J    (Changed: 08-AUG-06 )
Type Congenic; Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain C57BLKS/J
Donor Strain HRS/J
H2 Haplotyped

Appearance
black, fat
Related Genotype: a/a Cpefat/Cpefat

black, lean
Related Genotype: a/a Cpefat/+ or a/a +/+

Description
Mice homozygous for the fat spontaneous mutation (Cpefat) on a C57BLKS/J genetic background (N10) have a diabetes phenotype that is primarily restricted to males and is more severe than what is seen on the original HRS/J or C57BLKS/J (N5) genetic backgrounds. At weaning both males and female homozygous mutant mice were significantly lighter than wildtype or heterozygous littermates. Obesity develops between 6 and 8 weeks of age and mutant mice can be distinguished from wildtype littermates between 8 and 12 weeks of age. By 18 weeks fat mutant mice will reach 45-55 g and may reach 60-70 g by 6 months of age. Thus, the obesity is thus slower to develop than in the obese (Lepob) and diabetes (Leprdb) mutant mice. The excess adiposity is distributed throughout the body's fat stores, in contrast to the largely axial and inguinal fat deposition of the obese and diabetes mutant mice. Hyperinsulinemia is severe by 4 weeks of age and continues throughout life; it is associated with hypertrophy and hyperplasia of the islets of Langerhans. Male homozygotes backcrossed 10 generations to C57BLKS/J develop severe hyperglycemia after the development of gross obesity compared to a milder diabetic syndrome seen in males on a HRS/J or 5th generation backcross to C57BLKS. In contrast to obese and diabetes mutant mice on a C57BLKS background, glucose levels do not continue to rise but plateau around 400 - 600 mg/dL After 30 weeks of age plasma glucose levels of most male mutant mice are below 300 mg/dL despite continued weight gain and obesity. Most female mutant mice are resistant to development of hyperglycemia. Hyperglycemia is not associated with significant beta-cell necrosis or islet atrophy, occurs primarily in males. Homozygous fat mutant mice do not exhibit the hypercorticism characteristic of both obese and diabetes mutant mice. Proopiomelanocortin (POMC), the precursor of several neuroendocrine peptides that are ordinarily secreted in a regulated fashion, is misassorted to the constitutive secretory pathway in the pituitary intermediate lobe of fat mutant mice. Naggert et al. (1995) proposed that the obesity of fat homozygous mutant mice may reflect "defects in processing of prohormone forms of a variety of neuropeptides associated with the control of energy balance, nutrient partitioning and satiety."

Development
The fat spontaneous mutation arose spontaneously on the HRS/J strain and was backcrossed 5 generations (N5) to C57BLKS/J by Drs. Coleman and Eicher. Backcrossing was later continued to N10 by Dr. Edward Leiter.

Control Information

  Control
   Untyped from the colony
   Wild-type from the colony
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Cpefat allele
003923   B6.HRS(BKS)-Cpefat/J
View Strains carrying   Cpefat     (1 strain)

Strains carrying other alleles of Cpe
003713   B6.CAST-Cpe+/J
View Strains carrying other alleles of Cpe     (1 strain)

Phenotype

Phenotype Information

View Phenotypic Data

Phenotypic Data
Mouse Phenome Database
View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Obesity
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Cpefat/Cpefat

        BKSChpLt.HRS-Cpefat/J
  • adipose tissue phenotype
  • abnormal adipose tissue amount
    • noted in all adipose tissue of the body   (MGI Ref ID J:10872)
  • digestive/alimentary phenotype
  • decreased digestive secretion
    • reduced gastric acid secretion and challenged gastrin release   (MGI Ref ID J:52393)
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic beta cell morphology
    • the presence of immature secretory granules was noted   (MGI Ref ID J:24436)
    • degranulated pancreatic beta cells
      • some degranulation of beta cells was noted   (MGI Ref ID J:10872)
  • pancreatic islet hyperplasia
    • hypertrophy and hyperplasia of islets noted   (MGI Ref ID J:10872)
  • growth/size/body phenotype
  • obese
    • abnormal amounts of fat by 4-5 weeks of age; progressive with age; homozygotes weigh up to 60-70 grams by 6-8 months of age   (MGI Ref ID J:10872)
  • homeostasis/metabolism phenotype
  • abnormal hormone level
    • thyrotropin-releasing hormone (TRH) is reduced in the hypothalamus by at least 75% compared to wild-type   (MGI Ref ID J:80698)
    • pro-thyrotropin-releasing hormone forms are increased due to impaired processing in the hypothalamus   (MGI Ref ID J:80698)
    • cold exposure depresses hypothalamic TRH levels even further, by about 38% compared to 13% in wild-type   (MGI Ref ID J:80698)
    • decreased circulating adrenocorticotropin level
      • due to poor processing of pro-opiomalanocortin   (MGI Ref ID J:40372)
    • decreased circulating gastrin level
      • serum gastrin levels are lower than in wild-type after famotidine treatment to inhibit gastric acid secretion   (MGI Ref ID J:52393)
    • increased circulating insulin level
      • severe at weaning age   (MGI Ref ID J:10872)
      • hyperproinsulinemia was noted; a defect in hormone processing was demonstrated in vitro   (MGI Ref ID J:24436)
    • increased circulating triiodothyronine level
      • circulating T3 levels are significantly higher   (MGI Ref ID J:80698)
      • thyroid-stimulating hormone (TSH) concentrations are normal   (MGI Ref ID J:80698)
    • increased pituitary hormone level
      • 24-fold increase in unprocessed pro-opiomelanocortin levels in the pituitary; poor processing to adrenocorticotropin and unregulated secretion of the unprocessed hormone   (MGI Ref ID J:40372)
      • increased circulating pituitary hormone level
        • unregulated secretion of unprocessed pro-opiomelanocortin   (MGI Ref ID J:38227)
        • pro-opiomalanocortin is constitutively secreted from the anterior pituitary resulting in elevated levels in the circulation   (MGI Ref ID J:40372)
        • increased circulating growth hormone level
          • growth hormone is constitutively secreted from the anterior pituitary   (MGI Ref ID J:40372)
      • increased growth hormone level
        • growth hormone is elevated in the anterior pituitary   (MGI Ref ID J:40372)
        • increased circulating growth hormone level
          • growth hormone is constitutively secreted from the anterior pituitary   (MGI Ref ID J:40372)
  • hyperglycemia
    • transient hyperglycemia noted in males at 7-8 weeks of age   (MGI Ref ID J:10872)
    • does not progress to severe diabetes   (MGI Ref ID J:10872)
  • impaired adaptive thermogenesis
    • homozygous mice cannot maintain the core body temperature upon exposure to cold temperature   (MGI Ref ID J:80698)
  • increased circulating cholesterol level
    • increased by 50% over controls   (MGI Ref ID J:18161)
    • noted on a high fat diet compared to controls   (MGI Ref ID J:19043)
    • increased circulating HDL cholesterol level
      • increased 2 fold over controls   (MGI Ref ID J:18161)
      • noted on a high fat diet compared to controls   (MGI Ref ID J:19043)
    • increased circulating LDL cholesterol level
      • noted on a high fat diet compared to controls   (MGI Ref ID J:19043)
    • increased circulating VLDL cholesterol level
      • noted on a high fat diet compared to controls   (MGI Ref ID J:19043)
  • increased circulating triglyceride level
    • noted on a high fat diet compared to controls   (MGI Ref ID J:19043)
  • reproductive system phenotype
  • infertility
    • noted in older obese mice; homozygous mice can produce litters if mated before the onset of obesity   (MGI Ref ID J:10872)
  • nervous system phenotype
  • abnormal hypothalamus secretion
    • deficient processing and unregulated secretion of pro-thyrotrophin releasing hormone   (MGI Ref ID J:80698)

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

Cpefat/Cpefat

        HRS/J
  • adipose tissue phenotype
  • increased total body fat amount
    • noted in all adipose tissue of the body   (MGI Ref ID J:10872)
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic beta cell morphology   (MGI Ref ID J:10872)
    • degranulated pancreatic beta cells
      • some degranulation of beta cells was noted   (MGI Ref ID J:13651)
  • increased pancreatic islet number
    • increased numbers of islets noted   (MGI Ref ID J:13651)
  • pancreatic islet hyperplasia
    • hypertrophy and hyperplasia of islets noted   (MGI Ref ID J:10872)
  • growth/size/body phenotype
  • increased total body fat amount
    • noted in all adipose tissue of the body   (MGI Ref ID J:10872)
  • obese   (MGI Ref ID J:10872)
    • abnormal amounts of fat by 4-5 weeks of age; progressive with age; homozygotes weigh up to 60-70 grams by 6-8 months of age   (MGI Ref ID J:13651)
  • homeostasis/metabolism phenotype
  • hyperglycemia
    • transient hyperglycemia noted in males at 7-8 weeks of age   (MGI Ref ID J:10872)
  • hypoglycemia
    • fluctuations in blood sugar concentrations occur; concentrations of less than 100mg/100ml are common in animals older than 6 months   (MGI Ref ID J:13651)
  • increased circulating insulin level   (MGI Ref ID J:13651)
    • severe at weaning age   (MGI Ref ID J:10872)
  • reproductive system phenotype
  • infertility
    • noted in older mice; mice are not sterile; homozygous mice can produce litters if mated before the onset of obesity   (MGI Ref ID J:10872)
View Research Applications

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

Cpefat related

Diabetes and Obesity Research
Hyperglycemia
      males
Hyperinsulinemia
Impaired Insulin Processing
Insulin Resistance
Obesity With Diabetes
      adult onset
Type 2 Diabetes (NIDDM)
      males

Endocrine Deficiency Research
Adipose Defects
Hypothalamus/Pituitary Defects
Pancreas Defects

Internal/Organ Research
Adipose Defects

Metabolism Research

Reproductive Biology Research
Fertility Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Cpefat
Allele Name fat
Allele Type Spontaneous
Common Name(s) fat;
Strain of OriginHRS/J
Gene Symbol and Name Cpe, carboxypeptidase E
Chromosome 8
Gene Common Name(s) CARBE; CPH; Cph-1; Cph1; R74677; carboxypeptidase H; expressed sequence R74677; fat;
Molecular Note The molecular mutation responsible for the phenotype in the fat mouse is a T to C transition at nucleotide 729 of the mRNA. The codon of this nucleotide corresponds to amino acid 244 of the unprocessed preproenzyme or amino acid 202 of the mature peptidase. The mutation is predicted to alter a conserved serine to a proline residue in the encoded protein. Enzymatic activity of the mutant protein was shown to be abolished in fluorometric assays in vitro. [MGI Ref ID J:24436]

Genotyping

Genotyping Information

Genotyping Protocols

CpefatEnd Point, End Point Analysis
Cpefat, Restriction Enzyme Digest


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Berman Y; Mzhavia N; Polonskaia A; Devi LA. 2001. Impaired prohormone convertases in Cpe(fat)/Cpe(fat) mice. J Biol Chem 276(2):1466-73. [PubMed: 11038363]  [MGI Ref ID J:66910]

Cain BM; Wang W; Beinfeld MC. 1997. Cholecystokinin (CCK) levels are greatly reduced in the brains but not the duodenums of Cpe(fat)/Cpe(fat) mice: a regional difference in the involvement of carboxypeptidase E (Cpe) in pro-CCK processing. Endocrinology 138(9):4034-7. [PubMed: 9275097]  [MGI Ref ID J:42848]

Che FY; Yan L; Li H; Mzhavia N; Devi LA; Fricker LD. 2001. Identification of peptides from brain and pituitary of Cpe(fat)/Cpe(fat) mice. Proc Natl Acad Sci U S A 98(17):9971-6. [PubMed: 11481435]  [MGI Ref ID J:71090]

Coleman DL; Eicher EM. 1990. Fat (fat) and tubby (tub): two autosomal recessive mutations causing obesity syndromes in the mouse. J Hered 81(6):424-7. [PubMed: 2250094]  [MGI Ref ID J:10872]

Cool DR; Normant E; Shen F; Chen HC; Pannell L; Zhang Y; Loh YP. 1997. Carboxypeptidase E is a regulated secretory pathway sorting receptor: genetic obliteration leads to endocrine disorders in Cpe(fat) mice. Cell 88(1):73-83. [PubMed: 9019408]  [MGI Ref ID J:38227]

Friis-Hansen L; Lacourse KA; Samuelson LC; Holst JJ. 2001. Attenuated processing of proglucagon and glucagon-like peptide-1 in carboxypeptidase E-deficient mice. J Endocrinol 169(3):595-602. [PubMed: 11375130]  [MGI Ref ID J:88426]

Leiter EH; Kintner J; Flurkey K; Beamer WG; Naggert JK. 1999. Physiologic and endocrinologic characterization of male sex-biased diabetes in C57BLKS/J mice congenic for the fat mutation at the carboxypeptidease E locus. Endocrine 10(1):57-66. [PubMed: 10403572]  [MGI Ref ID J:54845]

Maddatu T; Naggert JK. 1997. Allele-specific PCR assays for the tub and cpefat mutations. Mamm Genome 8(11):857-8. [PubMed: 9337402]  [MGI Ref ID J:44056]

Naggert JK; Fricker LD; Varlamov O; Nishina PM; Rouille Y; Steiner DF; Carroll RJ; Paigen BJ; Leiter EH. 1995. Hyperproinsulinaemia in obese fat/fat mice associated with a carboxypeptidase E mutation which reduces enzyme activity. Nat Genet 10(2):135-42. [PubMed: 7663508]  [MGI Ref ID J:24436]

Additional References

Bouchard G; Johnson D; Carver T; Paigen B; Carey MC. 2002. Cholesterol gallstone formation in overweight mice establishes that obesity per se is not linked directly to cholelithiasis risk. J Lipid Res 43(7):1105-13. [PubMed: 12091495]  [MGI Ref ID J:88773]

Chiu CH; Lin WD; Huang SY; Lee YH. 2004. Effect of a C/EBP gene replacement on mitochondrial biogenesis in fat cells. Genes Dev 18(16):1970-5. [PubMed: 15289464]  [MGI Ref ID J:91840]

Nillni EA; Xie W; Mulcahy L; Sanchez VC; Wetsel WC. 2002. Deficiencies in pro-thyrotropin-releasing hormone processing and abnormalities in thermoregulation in Cpefat/fat mice. J Biol Chem 277(50):48587-95. [PubMed: 12270926]  [MGI Ref ID J:80698]

Cpefat related

Berk PD; Zhou S; Kiang C; Stump DD; Fan X; Bradbury MW. 1999. Selective up-regulation of fatty acid uptake by adipocytes characterizes both genetic and diet-induced obesity in rodents. J Biol Chem 274(40):28626-31. [PubMed: 10497230]  [MGI Ref ID J:57965]

Bouchard G; Johnson D; Carver T; Paigen B; Carey MC. 2002. Cholesterol gallstone formation in overweight mice establishes that obesity per se is not linked directly to cholelithiasis risk. J Lipid Res 43(7):1105-13. [PubMed: 12091495]  [MGI Ref ID J:88773]

Chiellini C; Costa M; Novelli SE; Amri EZ; Benzi L; Bertacca A; Cohen P; Del Prato S; Friedman JM; Maffei M. 2003. Identification of cathepsin K as a novel marker of adiposity in white adipose tissue. J Cell Physiol 195(2):309-21. [PubMed: 12652657]  [MGI Ref ID J:106181]

Chiu CH; Lin WD; Huang SY; Lee YH. 2004. Effect of a C/EBP gene replacement on mitochondrial biogenesis in fat cells. Genes Dev 18(16):1970-5. [PubMed: 15289464]  [MGI Ref ID J:91840]

Collin GB; Maddatu TP; Sen S; Naggert JK. 2005. Genetic modifiers interact with Cpefat to affect body weight, adiposity, and hyperglycemia. Physiol Genomics 22(2):182-90. [PubMed: 15870393]  [MGI Ref ID J:100832]

Collins S; Surwit RS. 1996. Pharmacologic manipulation of ob expression in a dietary model of obesity. J Biol Chem 271(16):9437-40. [PubMed: 8621612]  [MGI Ref ID J:33332]

Fricker LD; Berman YL; Leiter EH; Devi LA. 1996. Carboxypeptidase E activity is deficient in mice with the fat mutation. Effect on peptide processing. J Biol Chem 271(48):30619-24. [PubMed: 8940036]  [MGI Ref ID J:36810]

Friis-Hansen L; Rehfeld JF. 2000. Impaired feedback of gastric functions in carboxypeptidase E-deficient mice. Biochem Biophys Res Commun 267(2):638-42. [PubMed: 10631115]  [MGI Ref ID J:60206]

Gomez P; Hallberg L; Greeley GHJr. 1999. Carboxypeptidase E (CPE) deficiency in mice with the fat mutation have reduced stomach function. Proc Soc Exp Biol Med 220(1):52-3. [PubMed: 9893169]  [MGI Ref ID J:52393]

Hosaka M; Watanabe T; Sakai Y; Kato T; Takeuchi T. 2005. Interaction between secretogranin III and carboxypeptidase E facilitates prohormone sorting within secretory granules. J Cell Sci 118(Pt 20):4785-95. [PubMed: 16219686]  [MGI Ref ID J:102191]

Hummel KP; Coleman DL. 1974. fat = fat, Chr UN. Mouse News Lett 50:43.  [MGI Ref ID J:13651]

Irminger JC; Verchere CB; Meyer K; Halban PA. 1997. Proinsulin targeting to the regulated pathway is not impaired in carboxypeptidase E-deficient Cpefat/Cpefat mice. J Biol Chem 272(44):27532-4. [PubMed: 9346885]  [MGI Ref ID J:43715]

Johnston RA; Theman TA; Shore SA. 2006. Augmented responses to ozone in obese carboxypeptidase E-deficient mice. Am J Physiol Regul Integr Comp Physiol 290(1):R126-33. [PubMed: 16002559]  [MGI Ref ID J:104048]

Johnston RA; Zhu M; Hernandez CB; Williams ES; Shore SA. 2010. Onset of obesity in carboxypeptidase E-deficient mice and effect on airway responsiveness and pulmonary responses to ozone. J Appl Physiol 108(6):1812-9. [PubMed: 20299617]  [MGI Ref ID J:185840]

Keightley PD. 1995. Chewing the fat [news] Nat Genet 10(2):125-6. [PubMed: 7663503]  [MGI Ref ID J:24138]

Lacourse KA; Friis-Hansen L; Rehfeld JF; Samuelson LC. 1997. Disturbed progastrin processing in carboxypeptidase E-deficient fat mice. FEBS Lett 416(1):45-50. [PubMed: 9369230]  [MGI Ref ID J:43612]

Lacourse KA; Friis-Hansen L; Samuelson LC; Rehfeld JF. 1998. Altered processing of procholecystokinin in carboxypeptidase E-deficient fat mice: differential synthesis in neurons and endocrine cells. FEBS Lett 436(1):61-6. [PubMed: 9771894]  [MGI Ref ID J:50155]

Leiter EH; Fricker L; Young J; Naggert J. 2009. Rescue of the Cpe<fat> hyper pro-insulinemia phenotype by transgene expression of wild-type CPE MGI Direct Data Submission :.  [MGI Ref ID J:148983]

Lim J; Berezniuk I; Che FY; Parikh R; Biswas R; Pan H; Fricker LD. 2006. Altered neuropeptide processing in prefrontal cortex of Cpe (fat/fat) mice: implications for neuropeptide discovery. J Neurochem 96(4):1169-81. [PubMed: 16417576]  [MGI Ref ID J:105999]

Nakahara K; Bannai M; Maruyama K; Suzuki Y; Okame R; Murakami N. 2013. Characterization of a novel genetically obese mouse model demonstrating early onset hyperphagia and hyperleptinemia. Am J Physiol Endocrinol Metab 305(3):E451-63. [PubMed: 23736543]  [MGI Ref ID J:203210]

Nillni EA; Xie W; Mulcahy L; Sanchez VC; Wetsel WC. 2002. Deficiencies in pro-thyrotropin-releasing hormone processing and abnormalities in thermoregulation in Cpefat/fat mice. J Biol Chem 277(50):48587-95. [PubMed: 12270926]  [MGI Ref ID J:80698]

Nishina PM; Lowe S; Wang J; Paigen B. 1994. Characterization of plasma lipids in genetically obese mice: the mutants obese, diabetes, fat, tubby, and lethal yellow. Metabolism 43(5):549-53. [PubMed: 8177042]  [MGI Ref ID J:18161]

Nishina PM; Naggert JK; Verstuyft J; Paigen B. 1994. Atherosclerosis in genetically obese mice: the mutants obese, diabetes, fat, tubby, and lethal yellow. Metabolism 43(5):554-8. [PubMed: 8177043]  [MGI Ref ID J:19043]

Rovere C; Viale A; Nahon J; Kitabgi P. 1996. Impaired processing of brain proneurotensin and promelanin-concentrating hormone in obese fat/fat mice. Endocrinology 137(7):2954-8. [PubMed: 8770919]  [MGI Ref ID J:34268]

Shen FS; Aguilera G; Loh YP. 1999. Altered biosynthesis and secretion of pro-opiomelanocortin in the intermediate and anterior pituitary of carboxypeptidase E-deficient, Cpe(fat)/ Cpe(fat)mice. Neuropeptides 33(4):276-80. [PubMed: 10657504]  [MGI Ref ID J:60515]

Shen FS; Loh YP. 1997. Intracellular misrouting and abnormal secretion of adrenocorticotropin and growth hormone in cpefat mice associated with a carboxypeptidase E mutation. Proc Natl Acad Sci U S A 94(10):5314-9. [PubMed: 9144234]  [MGI Ref ID J:40372]

Shore SA; Lang JE; Kasahara DI; Lu FL; Verbout NG; Si H; Williams ES; Terry RD; Lee A; Johnston RA. 2009. Pulmonary responses to subacute ozone exposure in obese vs. lean mice. J Appl Physiol 107(5):1445-52. [PubMed: 19745193]  [MGI Ref ID J:177975]

Singh U; Yu Y; Kalinina E; Konno T; Sun T; Ohta H; Wakayama T; Soares MJ; Hemberger M; Fundele RH. 2006. Carboxypeptidase E in the mouse placenta. Differentiation 74(9-10):648-60. [PubMed: 17177860]  [MGI Ref ID J:116679]

Stratigopoulos G; Padilla SL; Leduc CA; Watson E; Hattersley AT; McCarthy MI; Zeltser LM; Chung WK; Leibel RL. 2008. Regulation of Fto/Ftm gene expression in mice and humans. Am J Physiol Regul Integr Comp Physiol 294(4):R1185-96. [PubMed: 18256137]  [MGI Ref ID J:133509]

Udupi V; Gomez P; Song L; Varlamov O; Reed JT; Leiter EH; Fricker LD ; Greeley GH Jr. 1997. Effect of carboxypeptidase E deficiency on progastrin processing and gastrin messenger ribonucleic acid expression in mice with the fat mutation. Endocrinology 138(5):1959-63. [PubMed: 9112393]  [MGI Ref ID J:39758]

Wang F; Tong Q. 2008. Transcription factor PU.1 is expressed in white adipose and inhibits adipocyte differentiation. Am J Physiol Cell Physiol 295(1):C213-20. [PubMed: 18463231]  [MGI Ref ID J:138523]

Wang W; Cain BM; Beinfeld MC. 1998. Adult carboxypeptidase E-deficient fat/fat mice have a near-total depletion of brain CCK 8 accompanied by a massive accumulation of glycine and arginine extended CCK: identification of CCK 8 Gly as the immediate precursor of CCK 8 in rodent brain. Endocrine 9(3):329-32. [PubMed: 10221600]  [MGI Ref ID J:53742]

Wei S; Feng Y; Che FY; Pan H; Mzhavia N; Devi LA; McKinzie AA; Levin N; Richards WG; Fricker LD. 2004. Obesity and diabetes in transgenic mice expressing proSAAS. J Endocrinol 180(3):357-68. [PubMed: 15012590]  [MGI Ref ID J:88683]

Zhang X; Che FY; Berezniuk I; Sonmez K; Toll L; Fricker LD. 2008. Peptidomics of Cpe(fat/fat) mouse brain regions: implications for neuropeptide processing. J Neurochem 107(6):1596-613. [PubMed: 19014391]  [MGI Ref ID J:144752]

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 & HusbandryThis strain is maintained by mating heterozygous siblings as fat homozygous mutant mice are generally infertile. The genotype of progeny are determine by an allele specific PCR protocol (see Genetic Typing). Mice are maintained on a NIH-31 6% fat diet.

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 willfulfill 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 willfulfill 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.

General Supply Notes

  • View the complete collection of spontaneous mutants in the Mouse Mutant Resource.

Control Information

  Control
   Untyped from the colony
   Wild-type from the colony
 
  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.
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JAX® Mice
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Tel: 1-800-422-6423 or 1-207-288-5845
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Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

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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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