Strain Name:

129-Kcne1tm1Sfh/J

Stock Number:

003009

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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 129/Sv-Kcne1tm1Sfh/J    (Changed: 15-DEC-04 )
Type Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse

Description
This strain is characterized by inner ear defects with a phenotype similar to shaker and waltzer. There is loss of hair cells and many supporting cells in the organ of Corti as well as in all vestibular end organs. The time course of hair cell degeneration is different for each portion of the inner ear. Heart abnormalities of homozygous mutant mice included a longer QT interval at slow heart rates, a paradoxical shorter QT interval at fast heart rates, and an overall exacerbated QT-heart rate adaptation compared with wild-type controls. This mutant serves as a model for Jervell and Lange-Nielsen disease in which patients suffer cardian arrhythmias and profound bilateral deafness.

Development
A targeting vector was designed to replace exon 2 of the endogenous gene (exon 2 contains the full uninterrupted coding sequence) with a PGK promoter-driven neomyicin resistance gene. The construct was electroporated into 129S1/Sv-derived W9.5 embryonic stem (ES) cells. Properly selected ES cells were injected into C57BL/6J blastocysts and the resulting chimeric males bred to 129/Sv males.

Control Information

  Control
   Wild-type from the colony
   002448 129S1/SvImJ
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Kcne1
004820   C57BL/6J-Kcne12J/J
View Strains carrying other alleles of Kcne1     (1 strain)

Additional Web Information

New 129 Nomenclature Bulletin

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Jervell and Lange-Nielsen Syndrome 2; JLNS2
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Long QT Syndrome 5; LQT5   (KCNE1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Kcne1tm1Sfh/Kcne1tm1Sfh

        involves: 129S1/Sv
  • behavior/neurological phenotype
  • abnormal posture
    • homozygotes posture for an occipital rather than a forepaw landing when hung by the tail   (MGI Ref ID J:105528)
    • however, at rest, the S-shaped, sagittal posture of the vertebral column is identical for wild-type and mutant mice: both hold the head with the atlanto-occipital joint fully flexed, the cervico-thoracic junction fully flexed, and the cervical column upright   (MGI Ref ID J:105528)
  • absent pinna reflex   (MGI Ref ID J:105528)
    • fail to show any pinnea reflex   (MGI Ref ID J:37461)
  • absent startle reflex
    • fail to show signs of startle   (MGI Ref ID J:37461)
  • absent vestibuloocular reflex
    • vestibulo-ocular reflex (VOR) testing indicates that head rotation fails to elicit compensatory slow-phase eye movements in mutant mice; no vestibular quick phases are generated at low frequencies   (MGI Ref ID J:105528)
    • VOR gain is statistically insignificant at all frequencies and both velocities examined   (MGI Ref ID J:105528)
  • decreased startle reflex   (MGI Ref ID J:105528)
  • head tilt
    • occasional head tilt   (MGI Ref ID J:37461)
  • hyperactivity   (MGI Ref ID J:37461)
  • impaired coordination
    • when mutants begin to walk, exhibit an awkward uncoordinated movement   (MGI Ref ID J:37461)
  • impaired limb coordination
    • unlike wild-type mice which perform a symmetrical gait at 0.5 m s-1, with an equal time lag between the lay-down of the hindlimbs and forelimbs, homozygotes show episodes of circling and are incapable of following a linear trajectory   (MGI Ref ID J:105528)
  • impaired righting response
    • pups have difficulty righting themselves, however this disappears with maturation   (MGI Ref ID J:37461)
    • as early as P7, homozygotes have difficuly righting themselves when placed on their backs   (MGI Ref ID J:105528)
    • at P90, homozygotes show inhibition of righting when supine by cutaneous input to the feet   (MGI Ref ID J:105528)
    • at P90, homozygotes land on their backs when dropped supine   (MGI Ref ID J:105528)
  • impaired swimming
    • mutants rotate along their long axis and sink   (MGI Ref ID J:37461)
    • while underwater, mutants somersault while still rotating along their body length   (MGI Ref ID J:37461)
    • as early as P7, homozygotes cannot swim   (MGI Ref ID J:105528)
  • stereotypic behavior   (MGI Ref ID J:37461)
    • circling
      • following unilateral labyrinthectomy, homozygotes continue to circle instead of exhibiting the expected static postural syndromes   (MGI Ref ID J:105528)
      • unlike wild-type mice, homozygotes cannot walk or run in a straight path in an open field or on a treadmill, and exhibit episodes of spontaneous circling during which the vertebral column maintains an S-shaped posture   (MGI Ref ID J:105528)
      • bidirectional circling   (MGI Ref ID J:105528)
        • as mice mature, exhibit an intermittent bidirectional circling behavior   (MGI Ref ID J:37461)
      • unidirectional circling
        • interestingly, with time circling tends to become more unidirectional   (MGI Ref ID J:105528)
    • head bobbing   (MGI Ref ID J:37461)
      • when at rest (i.e. alert but stationary), homozygotes show intermittent episodes of head bobbing with the head oscillating in the sagittal plane about the atlanto-occipital joint by 10-30 at 3-5 Hz   (MGI Ref ID J:105528)
  • hearing/vestibular/ear phenotype
  • abnormal cochlea morphology   (MGI Ref ID J:37461)
    • abnormal cochlear sensory epithelium morphology
      • change in structure of the sensory epithelium is observed at P3   (MGI Ref ID J:37461)
      • cochlear hair cell degeneration
        • hair cells of the cochlear duct differentiate normally but degenerate postnatally, starting at around P3   (MGI Ref ID J:37461)
    • abnormal scala media morphology   (MGI Ref ID J:37461)
      • abnormal stria vascularis morphology
        • exhibit an expansion of the intercellular space between marginal and intermediate cell processes, and between marginal cell processes and blood vessels   (MGI Ref ID J:37461)
      • absent organ of Corti
        • at P20, do not contain an organ of Corti   (MGI Ref ID J:37461)
      • cochlear hair cell degeneration
        • hair cells of the cochlear duct differentiate normally but degenerate postnatally, starting at around P3   (MGI Ref ID J:37461)
      • organ of Corti degeneration
        • seen at P3 in all turns of the cochlea, however degeneration of the supporting cells outside the organ of Corti does not occur until later (around P20)   (MGI Ref ID J:37461)
    • collapsed Reissner membrane
      • at P3, but not P0, Reissner's membrane is collapsed onto the surface of the spiral limbus, along the tectorial membrane and reticular lamina, and along the lateral wall of the clochlea in close opposition to the stria vascularis   (MGI Ref ID J:37461)
  • abnormal ear physiology
    • strial marginal cells and vestibular dark cells of the inner ear are unable to generate a short circuit current in vitro, indicating a lack of transepithelial potassium secretion   (MGI Ref ID J:37461)
    • abnormal vestibular system physiology
      • as early as P7, homozygotes spontaneously roll on their backs more often than wild-type mice, have difficuly righting themselves when placed on their backs, and are unable to swim   (MGI Ref ID J:105528)
      • following unilateral labyrinthectomy, homozygotes fail to exhibit the expected oculomotor and postural changes (i.e. ocular nystagmus and static postural syndromes) observed in wild-type mice   (MGI Ref ID J:105528)
      • absent vestibuloocular reflex
        • vestibulo-ocular reflex (VOR) testing indicates that head rotation fails to elicit compensatory slow-phase eye movements in mutant mice; no vestibular quick phases are generated at low frequencies   (MGI Ref ID J:105528)
        • VOR gain is statistically insignificant at all frequencies and both velocities examined   (MGI Ref ID J:105528)
  • abnormal inner ear vestibule morphology
    • exhibit a collapse of the vestibular wall at P3, indicating a decrease in endolymph volume   (MGI Ref ID J:37461)
    • the transitional epithelium and the inner core of the cristae are degenerating by P42 and by 7 months of age, no structure is discerned within the ampullae   (MGI Ref ID J:37461)
    • the melanocyte and dark cell layer are twisted and displaced toward the epithelial surface of the cristae at P42   (MGI Ref ID J:37461)
    • loss of connective tissue that normally underlies the vestibule by P42   (MGI Ref ID J:37461)
    • vestibular dark cells begin to degenerate at P3 and connective tissue below the dark cell epithelium is less abundant   (MGI Ref ID J:37461)
    • the apical membrane surface of the dark cell epithelial layer of the vestibular labyrinth is jagged and scalloped rather than smooth   (MGI Ref ID J:37461)
    • by P69, vestibular end-organs have completely degenerated, although vestibular dark cells are still present   (MGI Ref ID J:108905)
    • abnormal vestibular dark cell morphology
      • the melanocyte and dark cell layer are twisted and displaced toward the epithelial surface of the cristae at P42   (MGI Ref ID J:77288)
      • the apical membrane surface of the dark cell epithelial layer of the vestibular labyrinth is jagged and scalloped rather than smooth   (MGI Ref ID J:77288)
      • although normal at birth, the basal membrane infoldings and size of vestibular dark cells start to increase at P7   (MGI Ref ID J:108905)
      • at P10, the height and volume of dark cells is increased, the cytoplasm and nucleus are restricted to the apical side facing the endolymph, and basolateral membrane infoldings occupy >2/3 of cell height   (MGI Ref ID J:108905)
      • at P22, dark cells show significant increases in cell size, multiplication of mitochondria and basal membrane infoldings; the cytoplasm is reduced to a tiny area around a pyknotic nucleus and extracellular spaces between the infoldings are dilated   (MGI Ref ID J:108905)
      • by P69, the cells of the roof of the ampullae are crushed onto the dark cells and the endolymphatic space has completely collapsed   (MGI Ref ID J:108905)
      • at P69, vestibular dark cells are still present but morphologically resemble those observed at 1 or 3 weeks after birth, except for a pyknotic nucleus   (MGI Ref ID J:108905)
      • vestibular dark cell degeneration
        • vestibular dark cells begin to degenerate at P3 and connective tissue below the dark cell epithelium is less abundant   (MGI Ref ID J:77288)
    • utricular macular degeneration
      • at 5 months, the macule of the utricle shows significant, though less striking, signs of degeneration   (MGI Ref ID J:105528)
    • vestibular hair cell degeneration
      • hair cells of the macula of the sacculus degenerate postnatally, beginning around 5 months of age   (MGI Ref ID J:37461)
      • by P69, most vestibular hair cells have degenerated and the space between the afferent calyx and cells is enlarged   (MGI Ref ID J:108905)
      • at P69, rare remaining sensory hair cells appear completely wrapped in a few remaining supporting cells   (MGI Ref ID J:108905)
    • vestibular saccular macula degeneration
      • at 5 months, the macule of the saccule shows significant, though less striking, signs of degeneration   (MGI Ref ID J:105528)
  • abnormal semicircular canal morphology
    • at 5 months, the semicircular canals appear largely abnormal   (MGI Ref ID J:105528)
    • abnormal crista ampullaris morphology
      • hair cells of the cristae degenerate postnatally, beginning at P10   (MGI Ref ID J:37461)
      • at 5 months, the cristae exhibit massive degeneration at the level of hair cells and in the transitional epithelium while the core of the cristae appears vacuolated   (MGI Ref ID J:105528)
      • in contrast, no degeneration in vestibular nerve fibers or cells in Scarpa's ganglion is observed   (MGI Ref ID J:105528)
      • abnormal crista ampullaris neuroepithelium morphology
        • at P22, but not earlier, the general morphology of sensory hair cells (type I and II) is relatively normal, except for the presence of intracytoplasmic rods or filaments and of a few cystic cavities surrounded by an afferent nerve calyx   (MGI Ref ID J:108905)
        • however, the nucleus is not pyknotic and hair bundles are present through scattered in some cases   (MGI Ref ID J:108905)
  • nervous system phenotype
  • cochlear ganglion degeneration
    • first signs of spiral ganglion cell degeneration in the cochlea occur at P20, with the majority degenerated by P42, however do not see loss of apical ganglion cells   (MGI Ref ID J:37461)
  • cochlear hair cell degeneration
    • hair cells of the cochlear duct differentiate normally but degenerate postnatally, starting at around P3   (MGI Ref ID J:37461)
  • vestibular hair cell degeneration
    • hair cells of the macula of the sacculus degenerate postnatally, beginning around 5 months of age   (MGI Ref ID J:37461)
    • by P69, most vestibular hair cells have degenerated and the space between the afferent calyx and cells is enlarged   (MGI Ref ID J:108905)
    • at P69, rare remaining sensory hair cells appear completely wrapped in a few remaining supporting cells   (MGI Ref ID J:108905)
  • cardiovascular system phenotype
  • prolonged QT interval   (MGI Ref ID J:77288)
  • digestive/alimentary phenotype
  • abnormal digestive system physiology
    • fecal potassium excretion increases linearly with plasma potassium concentration much more rapidly than in wild-type, indicating a dysfunction of the intestine in secreting or absorbing potassium   (MGI Ref ID J:77288)
    • abnormal feces composition
      • mutants fed a normal, high, or low potassium diet excrete per gram of feces, respectively,1.9-, 1.8-, and 1.8-fold as much sodium and 2.2-, 1.8-, or 1.4-fold as much potassium as wild-type   (MGI Ref ID J:77288)
  • hematopoietic system phenotype
  • increased hematocrit   (MGI Ref ID J:77288)
  • homeostasis/metabolism phenotype
  • abnormal circulating renin level
    • renin levels are not decreasaed by a high potassium diet as in wild-type   (MGI Ref ID J:77288)
  • dehydration
    • slightly dehydrated   (MGI Ref ID J:77288)
  • hypokalemia
    • hypokalemia is seen on a normal (0.9%) and high (3%) potassium diet, but not a low (0.05%) potassium diet   (MGI Ref ID J:77288)
  • increased blood osmolality
    • increase in plasma osmolality   (MGI Ref ID J:77288)
  • increased circulating aldosterone level
    • higher plasma levels on both a normal and high potassium diet   (MGI Ref ID J:77288)
  • increased circulating chloride level   (MGI Ref ID J:77288)
  • increased circulating sodium level   (MGI Ref ID J:77288)
View Research Applications

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

Kcne1tm1Sfh related

Cell Biology Research
Channel and Transporter Defects
      potassium

Neurobiology Research
Channel and Transporter Defects
      potassium
Hearing Defects
      Jervell and Lange-Nielsen (JLN) syndromes

Sensorineural Research
Hearing Defects
      Jervell and Lange-Nielsen (JLN) syndromes

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Kcne1tm1Sfh
Allele Name targeted mutation 1, Stephen F Heinemann
Allele Type Targeted (Null/Knockout)
Common Name(s) KCNE1-; isk-;
Mutation Made By Jacques Vetter,   CNRS/The Salk Inst for Biol Studies
Strain of Origin129S1/Sv-Oca2<+> Tyr<+> Kitl<+>
ES Cell Line NameW9.5/W95
ES Cell Line Strain129S1/Sv-Oca2<+> Tyr<+> Kitl<+>
Gene Symbol and Name Kcne1, potassium voltage-gated channel, Isk-related subfamily, member 1
Chromosome 16
Gene Common Name(s) Isk; MinK; m; neuroscience mutagenesis facility, 190; nmf190;
Molecular Note A neomycin resistance cassette replaced the entire coding region of the gene. [MGI Ref ID J:37461]

Genotyping

Genotyping Information

Genotyping Protocols

Kcne1tm1Sfh, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Kcne1tm1Sfh related

Arrighi I; Bloch-Faure M; Grahammer F; Bleich M; Warth R; Mengual R; Drici MD; Barhanin J; Meneton P. 2001. Altered potassium balance and aldosterone secretion in a mouse model of human congenital long QT syndrome. Proc Natl Acad Sci U S A 98(15):8792-7. [PubMed: 11438691]  [MGI Ref ID J:77288]

Balasubramaniam R; Grace AA; Saumarez RC; Vandenberg JI; Huang CL. 2003. Electrogram prolongation and nifedipine-suppressible ventricular arrhythmias in mice following targeted disruption of KCNE1. J Physiol 552(Pt 2):535-46. [PubMed: 14561835]  [MGI Ref ID J:105415]

Chabannes D; Barhanin J; Escande D. 2001. Mice disrupted for the KvLQT1 potassium channel regulator IsK gene accumulate mature T cells. Cell Immunol 209(1):1-9. [PubMed: 11414731]  [MGI Ref ID J:70160]

Charpentier F; Merot J; Riochet D; Le Marec H; Escande D. 1998. Adult KCNE1-knockout mice exhibit a mild cardiac cellular phenotype. Biochem Biophys Res Commun 251(3):806-10. [PubMed: 9790991]  [MGI Ref ID J:50586]

Drici MD; Arrighi I; Chouabe C; Mann JR; Lazdunski M; Romey G; Barhanin J. 1998. Involvement of IsK-associated K+ channel in heart rate control of repolarization in a murine engineered model of Jervell and Lange-Nielsen syndrome. Circ Res 83(1):95-102. [PubMed: 9670922]  [MGI Ref ID J:114194]

Eugene D; Deforges S; Guimont F; Idoux E; Vidal PP; Moore LE; Vibert N. 2007. Developmental regulation of the membrane properties of central vestibular neurons by sensory vestibular information in the mouse. J Physiol 583(Pt 3):923-43. [PubMed: 17627998]  [MGI Ref ID J:140827]

Grahammer F; Warth R; Barhanin J; Bleich M; Hug MJ. 2001. The small conductance K+ channel, KCNQ1: expression, function, and subunit composition in murine trachea. J Biol Chem 276(45):42268-75. [PubMed: 11527966]  [MGI Ref ID J:119156]

Lock H; Valverde MA. 2000. Contribution of the IsK (MinK) potassium channel subunit to regulatory volume decrease in murine tracheal epithelial cells. J Biol Chem 275(45):34849-52. [PubMed: 10995738]  [MGI Ref ID J:115346]

Millar ID; Hartley JA; Haigh C; Grace AA; White SJ; Kibble JD; Robson L. 2004. Volume regulation is defective in renal proximal tubule cells isolated from KCNE1 knockout mice. Exp Physiol 89(2):173-80. [PubMed: 15123546]  [MGI Ref ID J:105333]

Neal AM; Taylor HC; Millar ID; Kibble JD; White SJ; Robson L. 2011. Renal defects in KCNE1 knockout mice are mimicked by chromanol 293B in vivo: identification of a KCNE1-regulated K+ conductance in the proximal tubule. J Physiol 589(Pt 14):3595-609. [PubMed: 21576273]  [MGI Ref ID J:189403]

Nicolas M; Dememes D; Martin A; Kupershmidt S; Barhanin J. 2001. KCNQ1/KCNE1 potassium channels in mammalian vestibular dark cells. Hear Res 153(1-2):132-45. [PubMed: 11223304]  [MGI Ref ID J:108905]

Puchalski RB; Kelly E; Bachmanov AA; Brazier SP; Kuang J; Arrighi I; Barhanin J; Tordoff MG. 2001. NaCl consumption is attenuated in female KCNE1 null mutant mice. Physiol Behav 74(3):267-76. [PubMed: 11714488]  [MGI Ref ID J:96707]

Thomas G; Killeen MJ; Gurung IS; Hakim P; Balasubramaniam R; Goddard CA; Grace AA; Huang CL. 2007. Mechanisms of ventricular arrhythmogenesis in mice following targeted disruption of KCNE1 modelling long QT syndrome 5. J Physiol 578(Pt 1):99-114. [PubMed: 17095567]  [MGI Ref ID J:140608]

Vallon V; Grahammer F; Richter K; Bleich M; Lang F; Barhanin J; Volkl H; Warth R. 2001. Role of KCNE1-dependent K+ fluxes in mouse proximal tubule. J Am Soc Nephrol 12(10):2003-11. [PubMed: 11562398]  [MGI Ref ID J:103378]

Vetter DE; Mann JR; Wangemann P; Liu J; McLaughlin KJ; Lesage F ; Marcus DC ; Lazdunski M ; Heinemann SF ; Barhanin J. 1996. Inner ear defects induced by null mutation of the isk gene. Neuron 17(6):1251-64. [PubMed: 8982171]  [MGI Ref ID J:37461]

Vidal PP; Degallaix L; Josset P; Gasc JP; Cullen KE. 2004. Postural and locomotor control in normal and vestibularly deficient mice. J Physiol 559(Pt 2):625-38. [PubMed: 15243133]  [MGI Ref ID J:105528]

Warth R; Garcia Alzamora M; Kim JK; Zdebik A; Nitschke R; Bleich M; Gerlach U; Barhanin J; Kim SJ. 2002. The role of KCNQ1/KCNE1 K(+) channels in intestine and pancreas: lessons from the KCNE1 knockout mouse. Pflugers Arch 443(5-6):822-8. [PubMed: 11889581]  [MGI Ref ID J:106204]

Health & husbandry

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

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, heterozygous siblings can be intercrossed to generate homozygotes/heterozygotes/wildtype. Expected coat color from breeding:White Bellied Agouti, Albino, Tan w/pink eyes

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* $3300.00
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* $4290.00
Animals Provided

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

Standard Supply

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

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

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

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

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

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

Control Information

  Control
   Wild-type from the colony
   002448 129S1/SvImJ
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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

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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