Strain Name:

B6.129S4-Viptm1Clw/J

Stock Number:

009640

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Mice that are homozygous for this targeted mutation of Vip (vasoactive intestinal polypeptide) exhibit impaired circadian rhythm generation, muscle weakness, increased induced airway hyperresponsiveness/inflammation, gastrointestinal tract abnormalities. Male homozygotes exhibit moderate right ventricular hypertension and hypertrophy, reduced serum testosterone and follicle-stimulating hormone levels. All offspring of heterozygous females exhibit developmental delays such as reduced body weight and impaired social behavior. This mutant mouse strain may be useful in studies of embryonic and neonatal development, circadian rhythm, airway hyperresponsiveness and inflammation(asthma), gastrointestinal innervation and motility and idiopathic pulmonary arterial hypertension.

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
 
Donating Investigator James Waschek,   UCLA

Description
Mice that are heterozygous for the targeted mutation are viable and fertile. No gene product (protein) is detected by immunohistochemical analysis of homozygotes. Homozygous females are subfertile, 15-20% of homozygous females can have litters. Homozygotes exhibit impaired circadian rhythm generation, muscle weakness, increased motor activity and increased induced airway hyperresponsiveness and inflammation. In constant darkness, homozygotes initially display shortened circadian period. Some homozygotes develop arrhythmic circadian periods after extended darkness. Heterozygotes also display abnormal circadian rhythm. Homozygotes have both gross and microscopic anatomical abnormalities of the gastrointestinal tract. 10-15% of homozygotes die of stenosis of the gut before one year of age. Male homozygotes exhibit moderate right ventricular (RV) hypertension, RV hypertrophy, thickened and remodeled pulmonary arteries, perivascular inflammation of smaller pulmonary vessels and airways, reduced serum testosterone levels, and reduced serum follicle-stimulating hormone (FSH) levels. Although male homozygotes had early testicular degeneration, age-dependent degeneration is slowed. All offspring of heterozygous females exhibit developmental delays such as reduced body weight and impaired social behavior. This mutant mouse strain may be useful in studies of embryonic and neonatal development, circadian rhythm, airway hyperresponsiveness and inflammation (asthma), gastrointestinal innervation and motility and idiopathic pulmonary arterial hypertension.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exon 4. The construct was electroporated into 129S4/SvJae derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting male chimeric animals were crossed to C57BL/6 female mice, and then backcrossed to C57BL/6J (see SNP notes) for 12 generations.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, all 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a C57BL/6N genetic background.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Vip
010908   STOCK Viptm1(cre)Zjh/J
View Strains carrying other alleles of Vip     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Pulmonary Hypertension, Primary, 1; PPH1
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Viptm1Clw/Viptm1Clw

        B6.129S-Viptm1Clw
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • male homozygotes are fertile, despite significantly reduced serum testosterone levels   (MGI Ref ID J:122403)
    • abnormal testes secretion
      • at both 4 and 15 months of age, reduced serum testosterone levels are associated with a significant decrease in mRNA expression of two key components of testosterone biosynthesis, i.e. StAR and 3beta-HSD relative to wild-type controls; in contrast, only StAR (but not 3beta-HSD) expression is significantly reduced in wild-type males at 15 months of age   (MGI Ref ID J:122403)
    • decreased seminal vesicle weight
      • at 4 months of age, young adult male homozygotes exhibit significantly reduced seminal vesicle weights relative to age-matched wild-type controls (0.25 +/- 0.01 g vs 0.39 +/- 0.05 g, respectively)   (MGI Ref ID J:122403)
    • seminiferous tubule degeneration
      • at 4 months of age, male homozygotes display a significantly higher % of degenerated seminiferous tubules than wild-type males (15.23 +/- 3.22% vs 4.14 +/- 0.85%, respectively)   (MGI Ref ID J:122403)
      • however, unlike aging wild-type males where 77% of all seminiferous tubules display signs of degeneration associated with reduced testis weight at 15 months, mutant males exhibit a less severe testicular aging phenotype (46.5% of degenerating tubules) with no significant loss in testis weight observed from 4 to 15 months of age   (MGI Ref ID J:122403)
  • endocrine/exocrine gland phenotype
  • abnormal testes secretion
    • at both 4 and 15 months of age, reduced serum testosterone levels are associated with a significant decrease in mRNA expression of two key components of testosterone biosynthesis, i.e. StAR and 3beta-HSD relative to wild-type controls; in contrast, only StAR (but not 3beta-HSD) expression is significantly reduced in wild-type males at 15 months of age   (MGI Ref ID J:122403)
  • decreased seminal vesicle weight
    • at 4 months of age, young adult male homozygotes exhibit significantly reduced seminal vesicle weights relative to age-matched wild-type controls (0.25 +/- 0.01 g vs 0.39 +/- 0.05 g, respectively)   (MGI Ref ID J:122403)
  • seminiferous tubule degeneration
    • at 4 months of age, male homozygotes display a significantly higher % of degenerated seminiferous tubules than wild-type males (15.23 +/- 3.22% vs 4.14 +/- 0.85%, respectively)   (MGI Ref ID J:122403)
    • however, unlike aging wild-type males where 77% of all seminiferous tubules display signs of degeneration associated with reduced testis weight at 15 months, mutant males exhibit a less severe testicular aging phenotype (46.5% of degenerating tubules) with no significant loss in testis weight observed from 4 to 15 months of age   (MGI Ref ID J:122403)
  • homeostasis/metabolism phenotype
  • decreased circulating follicle stimulating hormone level
    • at 4 months of age, male homozygotes exhibit significantly reduced serum FSH levels relative to age-matched wild-type controls (58 +/- 4.94 ng/ml vs 83.44 +/- 3.08 ng/ml, respectively)   (MGI Ref ID J:122403)
    • in contrast, no significant differences in serum LH levels are observed at 4 or 15 months of age   (MGI Ref ID J:122403)
  • decreased circulating testosterone level
    • at 4 months of age, male homozygotes exhibit significantly reduced serum testosterone levels relative to age-matched wild-type controls (0.16 +/- 0.05 ng/ml vs 12.65 +/- 3.8 ng/ml, respectively)   (MGI Ref ID J:122403)
    • unlike wild-type males which show a severe (26-fold) decrease in serum testosterone levels between 4 and 15 months of age, aging mutant males maintain significantly low but constant testosterone levels that match the levels seen in aging wild-type males   (MGI Ref ID J:122403)

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

Viptm1Clw/Vip+

        involves: 129S/Sv * C57BL/6
  • behavior/neurological phenotype
  • abnormal circadian phase
    • at the onset of constant darkness heterozygous mutants begin activity slightly earlier (about 30 min) than predicted from the previous light dark cycle but not as early as homozygous mutants   (MGI Ref ID J:86544)
    • heterozygotes display a 50% reduction in the magnitude of light induced phase shifts compared to wild-type controls   (MGI Ref ID J:86544)

Viptm1Clw/Viptm1Clw

        involves: 129S/Sv * C57BL/6
  • behavior/neurological phenotype
  • abnormal circadian phase
    • at the onset of constant darkness mutants begin activity earlier than predicted from the previous light dark cycle and this onset is too early to be explained by the shorter circadian period   (MGI Ref ID J:86544)
    • mutants display 2 discrete bouts of activity when exposed to two 1 hour light pulses in a 24 hour period unlike controls which display a single bout of activity   (MGI Ref ID J:86544)
  • arrhythmic circadian persistence
    • a few (3/23) mutants become arrhythmic immediately after the onset of constant darkness and 3 of the 20 that initially display short periods become arrhythmic over time   (MGI Ref ID J:86544)
  • shortened circadian period
    • in constant darkness most (20/23) mutants have a significantly shorter period   (MGI Ref ID J:86544)
  • cardiovascular system phenotype
  • abnormal lung vasculature morphology
    • males exhibit pulmonary vascular remodeling   (MGI Ref ID J:132313)
    • males treated with vasoactive intestinal peptide for 4 weeks show attenuation of vascular remodeling and right ventricle hypertrophy   (MGI Ref ID J:132313)
    • however, renal arteries do not show any evidence of vascular thickening   (MGI Ref ID J:132313)
  • abnormal pulmonary artery morphology
    • males show an enlarged, thickened pulmonary artery and smaller branches with increased muscularization and narrowed lumen   (MGI Ref ID J:132313)
    • medial wall of pulmonary arteries is thicker and lumen is narrower resulting in numerous severely narrowed vessels that appear almost totally occluded   (MGI Ref ID J:132313)
    • increase in proliferation of pulmonary medial smooth muscle cells   (MGI Ref ID J:132313)
  • heart right ventricle hypertrophy
    • males, but not females, exhibit moderate right ventricular hypertrophy as indicated by an increased ratio of right ventricle to left ventricle plus septum weight   (MGI Ref ID J:132313)
    • males treated with vasoactive intestinal peptide for 4 weeks show attenuation of vascular remodeling and right ventricle hypertrophy   (MGI Ref ID J:132313)
  • increased right ventricle systolic pressure
    • mean right ventricle systolic pressure is elevated in males at 40 and 48 weeks of age indicating development of moderate right ventricular hypertension   (MGI Ref ID J:132313)
  • pulmonary hypertension
    • right ventricular systolic pressure and right ventricle to left ventricle and septum weight ratio is increased in males indicating presence of moderately severe pulmonary arterial hypertension   (MGI Ref ID J:132313)
  • immune system phenotype
  • lung inflammation
    • perivascular inflammatory cell infiltrates, predominantly mononuclear infiltrates, are seen around smaller pulmonary vessels and airways of males   (MGI Ref ID J:132313)
  • mortality/aging
  • premature death
    • increased mortality is seen in males, with mice starting to die at 6 months   (MGI Ref ID J:132313)
  • respiratory system phenotype
  • abnormal lung vasculature morphology
    • males exhibit pulmonary vascular remodeling   (MGI Ref ID J:132313)
    • males treated with vasoactive intestinal peptide for 4 weeks show attenuation of vascular remodeling and right ventricle hypertrophy   (MGI Ref ID J:132313)
    • however, renal arteries do not show any evidence of vascular thickening   (MGI Ref ID J:132313)
  • lung inflammation
    • perivascular inflammatory cell infiltrates, predominantly mononuclear infiltrates, are seen around smaller pulmonary vessels and airways of males   (MGI Ref ID J:132313)
View Research Applications

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

Cardiovascular Research
Hypertension

Developmental Biology Research
Growth Defects
Neurodevelopmental Defects

Endocrine Deficiency Research
Gastrointestinal Defects
Gonad Defects

Immunology, Inflammation and Autoimmunity Research
Inflammation
      Asthma

Internal/Organ Research
Gastrointestinal Defects

Neurobiology Research
Behavioral and Learning Defects
Circadian Rhythms
Neurodevelopmental Defects

Reproductive Biology Research
Endocrine Deficiencies Affecting Gonads
Fertility Defects
      females only

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Viptm1Clw
Allele Name targeted mutation 1, Christopher S Colwell
Allele Type Targeted (Null/Knockout)
Common Name(s) VIP KO; VIP/PHI-; VIP-;
Mutation Made By James Waschek,   UCLA
Strain of Origin129/Sv
Gene Symbol and Name Vip, vasoactive intestinal polypeptide
Chromosome 10
Gene Common Name(s) PHI, peptide histidine isoleucine; PHM27; vip/phi27;
Molecular Note A neomycin resistance gene was inserted in reverse orientation into exon 4. PCR confirmed recombination in mutant mice. Immunohistochemistry confirmed the loss of protein in homozygotes. [MGI Ref ID J:86544]

Genotyping

Genotyping Information

Genotyping Protocols

Viptm1Clw SEP PCR, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Colwell CS; Michel S; Itri J; Rodriguez W; Tam J; Lelievre V; Hu Z; Liu X; Waschek JA. 2003. Disrupted circadian rhythms in VIP- and PHI-deficient mice. Am J Physiol Regul Integr Comp Physiol 285(5):R939-49. [PubMed: 12855416]  [MGI Ref ID J:86544]

Additional References

Viptm1Clw related

Abad C; Tan YV; Cheung-Lau G; Nobuta H; Waschek JA. 2012. VIP deficient mice exhibit resistance to lipopolysaccharide induced endotoxemia with an intrinsic defect in proinflammatory cellular responses. PLoS One 7(5):e36922. [PubMed: 22615845]  [MGI Ref ID J:187234]

Abad C; Tan YV; Lopez R; Nobuta H; Dong H; Phan P; Feng JM; Campagnoni AT; Waschek JA. 2010. Vasoactive intestinal peptide loss leads to impaired CNS parenchymal T-cell infiltration and resistance to experimental autoimmune encephalomyelitis. Proc Natl Acad Sci U S A 107(45):19555-60. [PubMed: 20978211]  [MGI Ref ID J:166920]

An S; Harang R; Meeker K; Granados-Fuentes D; Tsai CA; Mazuski C; Kim J; Doyle FJ 3rd; Petzold LR; Herzog ED. 2013. A neuropeptide speeds circadian entrainment by reducing intercellular synchrony. Proc Natl Acad Sci U S A 110(46):E4355-61. [PubMed: 24167276]  [MGI Ref ID J:202892]

Aton SJ; Colwell CS; Harmar AJ; Waschek J; Herzog ED. 2005. Vasoactive intestinal polypeptide mediates circadian rhythmicity and synchrony in mammalian clock neurons. Nat Neurosci 8(4):476-83. [PubMed: 15750589]  [MGI Ref ID J:98524]

Aton SJ; Huettner JE; Straume M; Herzog ED. 2006. GABA and Gi/o differentially control circadian rhythms and synchrony in clock neurons. Proc Natl Acad Sci U S A 103(50):19188-93. [PubMed: 17138670]  [MGI Ref ID J:118298]

Bechtold DA; Brown TM; Luckman SM; Piggins HD. 2008. Metabolic rhythm abnormalities in mice lacking VIP-VPAC2 signaling. Am J Physiol Regul Integr Comp Physiol 294(2):R344-51. [PubMed: 18032467]  [MGI Ref ID J:130192]

Brown TM; Colwell CS; Waschek JA; Piggins HD. 2007. Disrupted neuronal activity rhythms in the suprachiasmatic nuclei of vasoactive intestinal polypeptide-deficient mice. J Neurophysiol 97(3):2553-8. [PubMed: 17151217]  [MGI Ref ID J:135944]

Ciarleglio CM ; Gamble KL ; Axley JC ; Strauss BR ; Cohen JY ; Colwell CS ; McMahon DG. 2009. Population encoding by circadian clock neurons organizes circadian behavior. J Neurosci 29(6):1670-6. [PubMed: 19211874]  [MGI Ref ID J:146633]

Dragich JM; Loh DH; Wang LM; Vosko AM; Kudo T; Nakamura TJ; Odom IH; Tateyama S; Hagopian A; Waschek JA; Colwell CS. 2010. The role of the neuropeptides PACAP and VIP in the photic regulation of gene expression in the suprachiasmatic nucleus. Eur J Neurosci 31(5):864-75. [PubMed: 20180841]  [MGI Ref ID J:159524]

Girard BA; Lelievre V; Braas KM; Razinia T; Vizzard MA; Ioffe Y; El Meskini R; Ronnett GV; Waschek JA; May V. 2006. Noncompensation in peptide/receptor gene expression and distinct behavioral phenotypes in VIP- and PACAP-deficient mice. J Neurochem 99(2):499-513. [PubMed: 17029602]  [MGI Ref ID J:119672]

Gomez-Arroyo J; Saleem SJ; Mizuno S; Syed AA; Bogaard HJ; Abbate A; Taraseviciene-Stewart L; Sung Y; Kraskauskas D; Farkas D; Conrad DH; Nicolls MR; Voelkel NF. 2012. A brief overview of mouse models of pulmonary arterial hypertension: problems and prospects. Am J Physiol Lung Cell Mol Physiol 302(10):L977-91. [PubMed: 22307907]  [MGI Ref ID J:190182]

Itri J; Michel S; Waschek JA; Colwell CS. 2004. Circadian rhythm in inhibitory synaptic transmission in the mouse suprachiasmatic nucleus. J Neurophysiol 92(1):311-9. [PubMed: 14973316]  [MGI Ref ID J:101989]

Keef KD; Saxton SN; McDowall RA; Kaminski RE; Duffy AM; Cobine CA. 2013. Functional role of vasoactive intestinal polypeptide in inhibitory motor innervation in the mouse internal anal sphincter. J Physiol 591(Pt 6):1489-506. [PubMed: 23339175]  [MGI Ref ID J:207354]

Lacombe A; Lelievre V; Roselli CE; Muller JM; Waschek JA; Vilain E. 2007. Lack of vasoactive intestinal peptide reduces testosterone levels and reproductive aging in mouse testis. J Endocrinol 194(1):153-60. [PubMed: 17592029]  [MGI Ref ID J:122403]

Lelievre V; Favrais G; Abad C; Adle-Biassette H; Lu Y; Germano PM; Cheung-Lau G; Pisegna JR; Gressens P; Lawson G; Waschek JA. 2007. Gastrointestinal dysfunction in mice with a targeted mutation in the gene encoding vasoactive intestinal polypeptide: a model for the study of intestinal ileus and Hirschsprung's disease. Peptides 28(9):1688-99. [PubMed: 17606312]  [MGI Ref ID J:129473]

Li JM; Hossain MS; Southerland L; Waller EK. 2013. Pharmacological inhibition of VIP signaling enhances antiviral immunity and improves survival in murine cytomegalovirus-infected allogeneic bone marrow transplant recipients. Blood 121(12):2347-51. [PubMed: 23325838]  [MGI Ref ID J:195881]

Li JM; Southerland L; Hossain MS; Giver CR; Wang Y; Darlak K; Harris W; Waschek J; Waller EK. 2011. Absence of vasoactive intestinal peptide expression in hematopoietic cells enhances Th1 polarization and antiviral immunity in mice. J Immunol 187(2):1057-65. [PubMed: 21677142]  [MGI Ref ID J:178031]

Lim MA; Stack CM; Cuasay K; Stone MM; McFarlane HG; Waschek JA; Hill JM. 2008. Regardless of genotype, offspring of VIP-deficient female mice exhibit developmental delays and deficits in social behavior. Int J Dev Neurosci 26(5):423-34. [PubMed: 18423945]  [MGI Ref ID J:139814]

Lucassen EA; van Diepen HC; Houben T; Michel S; Colwell CS; Meijer JH. 2012. Role of vasoactive intestinal peptide in seasonal encoding by the suprachiasmatic nucleus clock. Eur J Neurosci 35(9):1466-74. [PubMed: 22512278]  [MGI Ref ID J:191449]

Martin B; Shin YK; White CM; Ji S; Kim W; Carlson OD; Napora JK; Chadwick W; Chapter M; Waschek JA; Mattson MP; Maudsley S; Egan JM. 2010. Vasoactive intestinal peptide-null mice demonstrate enhanced sweet taste preference, dysglycemia, and reduced taste bud leptin receptor expression. Diabetes 59(5):1143-52. [PubMed: 20150284]  [MGI Ref ID J:164326]

Maywood ES; Chesham JE; O'Brien JA; Hastings MH. 2011. A diversity of paracrine signals sustains molecular circadian cycling in suprachiasmatic nucleus circuits. Proc Natl Acad Sci U S A 108(34):14306-11. [PubMed: 21788520]  [MGI Ref ID J:175620]

Miller JE; Granados-Fuentes D; Wang T; Marpegan L; Holy TE; Herzog ED. 2014. Vasoactive intestinal polypeptide mediates circadian rhythms in mammalian olfactory bulb and olfaction. J Neurosci 34(17):6040-6. [PubMed: 24760863]  [MGI Ref ID J:210611]

Said SI; Hamidi SA; Dickman KG; Szema AM; Lyubsky S; Lin RZ; Jiang YP; Chen JJ; Waschek JA; Kort S. 2007. Moderate pulmonary arterial hypertension in male mice lacking the vasoactive intestinal peptide gene. Circulation 115(10):1260-8. [PubMed: 17309917]  [MGI Ref ID J:132313]

Schroeder A; Loh DH; Jordan MC; Roos KP; Colwell CS. 2010. Circadian Regulation of Cardiovascular Function: a role for vasoactive intestinal peptide. Am J Physiol Heart Circ Physiol :. [PubMed: 20952671]  [MGI Ref ID J:165789]

Schroeder AM; Truong D; Loh DH; Jordan MC; Roos KP; Colwell CS. 2012. Voluntary scheduled exercise alters diurnal rhythms of behaviour, physiology and gene expression in wild-type and vasoactive intestinal peptide-deficient mice. J Physiol 590(Pt 23):6213-26. [PubMed: 22988135]  [MGI Ref ID J:203022]

Stack CM; Lim MA; Cuasay K; Stone MM; Seibert KM; Spivak-Pohis I; Crawley JN; Waschek JA; Hill JM. 2008. Deficits in social behavior and reversal learning are more prevalent in male offspring of VIP deficient female mice. Exp Neurol 211(1):67-84. [PubMed: 18316078]  [MGI Ref ID J:136552]

Szema AM; Hamidi SA; Lyubsky S; Dickman KG; Mathew S; Abdel-Razek T; Chen JJ; Waschek JA; Said SI. 2006. Mice lacking the VIP gene show airway hyperresponsiveness and airway inflammation, partially reversible by VIP. Am J Physiol Lung Cell Mol Physiol 291(5):L880-6. [PubMed: 16782752]  [MGI Ref ID J:144694]

Szema AM; Hamidi SA; Smith SD; Benveniste H. 2013. VIP gene deletion in mice causes cardiomyopathy associated with upregulation of heart failure genes. PLoS One 8(5):e61449. [PubMed: 23700405]  [MGI Ref ID J:202163]

Yusta B; Holland D; Waschek JA; Drucker DJ. 2012. Intestinotrophic glucagon-like peptide-2 (GLP-2) activates intestinal gene expression and growth factor-dependent pathways independent of the vasoactive intestinal peptide gene in mice. Endocrinology 153(6):2623-32. [PubMed: 22535770]  [MGI Ref ID J:188646]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are bred as heterozygous females and homozygous males. Homozygous females are subfertile; 15-20% of homozygous females can have litters .

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* $2140.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

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

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2782.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

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

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

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

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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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"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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