Strain Name:

B6;129S4-Col1a1tm1Jae/J

Stock Number:

002495

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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

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
 
Donating InvestigatorDr. Rudolf Jaenisch,   Whitehead Institute (MIT)

Appearance
white-bellied agouti
Related Genotype: Aw/Aw

Description
Homozygous mice are viable and develop to young adulthood without obvious differences from wildtype mice. As the mice age they develop fibrosis in the dermis characterized by a thickening and roughening of the skin, which is similar to that seen in human scleroderma. Homozygous females develop postpartum abnormalities of the uterus caused by a failure of collagen resorption. They have slightly reduced litter sizes and significantly fewer litters than normal wildtype mice. A secondary collagenase cleavage site was found in the mutant protein that could be cleaved by rat collagenase but not by human collagenase.

Control Information

  Control
   Wild-type from the colony
   101045 B6129SF2/J (approximate)
 
  Considerations for Choosing Controls

Related Strains

View Strains carrying other alleles of Col1a1     (18 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Caffey Disease   (COL1A1)
Collagen, Type I, Alpha-1; COL1A1   (COL1A1)
Ehlers-Danlos Syndrome, Type I   (COL1A1)
Ehlers-Danlos Syndrome, Type VII, Autosomal Dominant   (COL1A1)
Osteogenesis Imperfecta, Type I   (COL1A1)
Osteogenesis Imperfecta, Type II   (COL1A1)
Osteogenesis Imperfecta, Type III   (COL1A1)
Osteogenesis Imperfecta, Type IV   (COL1A1)
Osteoporosis   (COL1A1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Col1a1tm1Jae/Col1a1+

        either: (involves: 129S4/SvJae * BALB/c) or (involves: 129S4/SvJae * C57BL/6)
  • reproductive system phenotype
  • abnormal uterus morphology
    • collagen accumulation in the uteri of heterozygous mutants was less pronounced relative to homozygous mutants   (MGI Ref ID J:26504)
  • decreased litter size
    • heterozygous females had slightly reduced litter sizes and significantly fewer litters than wild-type females   (MGI Ref ID J:26504)
  • integument phenotype
  • focal hair loss
    • heterozygotes developed patchy hair loss   (MGI Ref ID J:26504)
  • thick dermal layer
    • at ~7 months, heterozygotes developed dermal fibrosis, similar to scleroderma, and skin ulcerations   (MGI Ref ID J:26504)
    • mutant skin displayed a significant increase in collagen extending through to the deep dermis   (MGI Ref ID J:26504)
    • heterozygous males and females developed similar but milder skin abnormalities relative to age-matched homozygous males   (MGI Ref ID J:26504)

Col1a1tm1Jae/Col1a1tm1Jae

        either: (involves: 129S4/SvJae * BALB/c) or (involves: 129S4/SvJae * C57BL/6)
  • reproductive system phenotype
  • abnormal uterus morphology
    • homozygous females developed postpartum abnormalities of the uterus, including persistence of nodules containing type I collagen in the uterine wall, caused by a failure of collagen resorption   (MGI Ref ID J:26504)
    • abnormal myometrium morphology
      • occasionally, virgin homozygous females showed small accumulations of collagen in the myometrium of the uterus   (MGI Ref ID J:26504)
  • decreased litter size
    • mutant females had slightly reduced litter sizes and significantly fewer litters than wild-type females   (MGI Ref ID J:26504)
  • integument phenotype
  • focal hair loss
    • homozygotes developed patchy hair loss   (MGI Ref ID J:26504)
  • thick dermal layer
    • homozygotes were viable, resistant to collagenase action, and developed normally to young adulthood   (MGI Ref ID J:26504)
    • at ~7 months, homozygotes developed dermal fibrosis, similar to scleroderma, and skin ulcerations   (MGI Ref ID J:26504)
    • mutant skin displayed a significant increase in collagen extending through to the deep dermis   (MGI Ref ID J:26504)
    • homozygous females developed similar but milder skin abnormalities relative to age-matched homozygous males   (MGI Ref ID J:26504)

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

Col1a1tm1Jae/Col1a1tm1Jae

        involves: 129S4/SvJae * C57BL/6
  • craniofacial phenotype
  • abnormal neurocranium morphology
    • at >4 weeks of age, mutants showed increased bone deposition in calvariae mainly at the inner periosteal surface adjacent to the dura mater   (MGI Ref ID J:90884)
    • calvarial thickness nearly doubled by ~10 months of age   (MGI Ref ID J:90884)
    • homozygotes had normal circulating levels of PTH, but showed increased calcein labeling of calvarial surfaces   (MGI Ref ID J:90884)
  • growth/size/body phenotype
  • decreased body weight
    • homozygotes showed a normal mean body weight throughout the 36-wk observation period, except for a 9.8% reduction at 18 wks   (MGI Ref ID J:82606)
  • limbs/digits/tail phenotype
  • abnormal limb bone morphology
    • adult homozygotes showed bony deformities, particularly of long bones, with increased deposition of woven bone   (MGI Ref ID J:53079)
  • skeleton phenotype
  • *normal* skeleton phenotype
    • homozygotes showed normal tooth eruption   (MGI Ref ID J:85591)
    • abnormal joint morphology
      • adult homozygotes developed joint contractures   (MGI Ref ID J:53079)
    • abnormal limb bone morphology
      • adult homozygotes showed bony deformities, particularly of long bones, with increased deposition of woven bone   (MGI Ref ID J:53079)
    • abnormal neurocranium morphology
      • at >4 weeks of age, mutants showed increased bone deposition in calvariae mainly at the inner periosteal surface adjacent to the dura mater   (MGI Ref ID J:90884)
      • calvarial thickness nearly doubled by ~10 months of age   (MGI Ref ID J:90884)
      • homozygotes had normal circulating levels of PTH, but showed increased calcein labeling of calvarial surfaces   (MGI Ref ID J:90884)
    • abnormal osteoblast morphology
      • beginning at about 2 weeks of age, homozygotes showed increased osteoblast and osteocyte apoptosis, despite increased bone deposition   (MGI Ref ID J:90884)
      • abnormal osteoblast differentiation
        • at 4 weeks, homozygotes showed an increase in tibial trabecular bone volume despite an overall decrease in osteoblast activity in trabecular bone   (MGI Ref ID J:85591)
        • in contrast, homozygotes displayed normal tibial cortical bone thickness, and a relatively normal tibial periosteal mineral apposition rate   (MGI Ref ID J:85591)
        • at greater 4 weeks of age, mutants began to show increased bone deposition of endosteal trabecular bone in tibial/femoral bones   (MGI Ref ID J:90884)
      • abnormal osteocyte morphology
        • beginning at about 2 weeks of age, homozygotes showed increased osteoblast and osteocyte apoptosis, despite increased bone deposition   (MGI Ref ID J:90884)
        • at greater than 2 weeks of age, homozygotes showed loss of osteocytes from their lacunae in the calvariae and in the shafts of long bones   (MGI Ref ID J:90884)
        • the number of "empty" lacunae increased with age   (MGI Ref ID J:90884)
    • abnormal osteoclast physiology
      • in contrast to wild-type, homozygotes showed resistance to PTH-induced bone resorption, with only a few resorption spaces and rare osteoclasts   (MGI Ref ID J:53079)
      • the bone resorption area and the number of osteoclasts/mm2 were significantly increased (~5-fold) after PTH injection in wild-type, but not in homozygous mutant mice   (MGI Ref ID J:53079)
      • homozygotes were not resistant to other skeletal effects of PTH   (MGI Ref ID J:53079)
      • after i.p. injection of PTH, calcemic responses were significantly lower in homozygotes versus wild-type   (MGI Ref ID J:53079)
    • failure of secondary bone resorption
      • homozygotes showed impaired osteoclastic bone resorption in trabecular bone: namely, an increase in osteoclast number and surface in long bones   (MGI Ref ID J:85591)
    • osteopetrosis
      • homozygotes exhibited a mild osteopetrotic phenotype, that is, a mild, but significant, increase in tibial trabecular number and volume, and a sharp decrease in trabecular separation   (MGI Ref ID J:85591)
  • vision/eye phenotype
  • *normal* vision/eye phenotype
    • homozygotes showed no anterior segment defects: the angle was open, and the depth of the anterior chamber appeared normal   (MGI Ref ID J:82606)
    • ocular hypertension
      • homozygotes showed a significant increase in mean intraocular pressure at 18, 24, and 36 weeks (21%, 44%, and 36%, respectively)   (MGI Ref ID J:82606)
      • homozygotes displayed an increased accumulation of collagen I in conjunctiva, subconjunctival tissue, and sclera, suggesting an association between IOP regulation and fibrillar collagen turnover   (MGI Ref ID J:82606)
  • immune system phenotype
  • abnormal osteoclast physiology
    • in contrast to wild-type, homozygotes showed resistance to PTH-induced bone resorption, with only a few resorption spaces and rare osteoclasts   (MGI Ref ID J:53079)
    • the bone resorption area and the number of osteoclasts/mm2 were significantly increased (~5-fold) after PTH injection in wild-type, but not in homozygous mutant mice   (MGI Ref ID J:53079)
    • homozygotes were not resistant to other skeletal effects of PTH   (MGI Ref ID J:53079)
    • after i.p. injection of PTH, calcemic responses were significantly lower in homozygotes versus wild-type   (MGI Ref ID J:53079)
  • cellular phenotype
  • abnormal osteoblast differentiation
    • at 4 weeks, homozygotes showed an increase in tibial trabecular bone volume despite an overall decrease in osteoblast activity in trabecular bone   (MGI Ref ID J:85591)
    • in contrast, homozygotes displayed normal tibial cortical bone thickness, and a relatively normal tibial periosteal mineral apposition rate   (MGI Ref ID J:85591)
    • at greater 4 weeks of age, mutants began to show increased bone deposition of endosteal trabecular bone in tibial/femoral bones   (MGI Ref ID J:90884)
  • hematopoietic system phenotype
  • abnormal osteoclast physiology
    • in contrast to wild-type, homozygotes showed resistance to PTH-induced bone resorption, with only a few resorption spaces and rare osteoclasts   (MGI Ref ID J:53079)
    • the bone resorption area and the number of osteoclasts/mm2 were significantly increased (~5-fold) after PTH injection in wild-type, but not in homozygous mutant mice   (MGI Ref ID J:53079)
    • homozygotes were not resistant to other skeletal effects of PTH   (MGI Ref ID J:53079)
    • after i.p. injection of PTH, calcemic responses were significantly lower in homozygotes versus wild-type   (MGI Ref ID J:53079)
View Research Applications

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

Col1a1tm1Jae related

Cardiovascular Research
Heart Abnormalities
      cardiomyopathy

Dermatology Research
Skin and Hair Texture Defects

Developmental Biology Research
Defects in Extracellular Matrix Molecules
Skeletal Defects

Reproductive Biology Research
Fertility Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Col1a1tm1Jae
Allele Name targeted mutation 1, Rudolf Jaenisch
Allele Type Targeted (knock-in)
Common Name(s) Col1a1r; Col1a1tmJae; ColR; mutation IV; rr;
Mutation Made ByDr. Rudolf Jaenisch,   Whitehead Institute (MIT)
Strain of Origin129S4/SvJae
ES Cell Line NameJ1
ES Cell Line Strain129S4/SvJae
Promoter Col1a1, collagen, type I, alpha 1, mouse, laboratory
Molecular Note Several point mutations were introduced into the sequences encoding the collagenase cleavage domain by a "hit and run" targeting strategy. These mutations resulted in substitutions of proline for glutamine-774 and alanine-777 and methionine for isoleucine-776 in the encoded protein. [MGI Ref ID J:17514]

Genotyping

Genotyping Information

Genotyping Protocols

Cola1tm1Jae, Restriction Enzyme Digest


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Liu X; Wu H; Byrne M; Jeffrey J; Krane S; Jaenisch R. 1995. A targeted mutation at the known collagenase cleavage site in mouse type I collagen impairs tissue remodeling. J Cell Biol 130(1):227-37. [PubMed: 7790374]  [MGI Ref ID J:26504]

Additional References

Aihara M; Lindsey JD; Weinreb RN. 2003. Ocular hypertension in mice with a targeted type I collagen mutation. Invest Ophthalmol Vis Sci 44(4):1581-5. [PubMed: 12657595]  [MGI Ref ID J:82606]

Mabuchi F; Lindsey JD; Aihara M; Mackey MR; Weinreb RN. 2004. Optic nerve damage in mice with a targeted type I collagen mutation. Invest Ophthalmol Vis Sci 45(6):1841-5. [PubMed: 15161848]  [MGI Ref ID J:92285]

Col1a1tm1Jae related

Aihara M; Lindsey JD; Weinreb RN. 2003. Ocular hypertension in mice with a targeted type I collagen mutation. Invest Ophthalmol Vis Sci 44(4):1581-5. [PubMed: 12657595]  [MGI Ref ID J:82606]

Beare AH; Krane SM; Ferguson MW. 2005. Variable impairment of wound healing in the heterozygous collagenase-resistant mouse. Wound Repair Regen 13(1):27-40. [PubMed: 15659034]  [MGI Ref ID J:110086]

Chiusaroli R; Maier A; Knight MC; Byrne M; Calvi LM; Baron R; Krane SM; Schipani E. 2003. Collagenase cleavage of type I collagen is essential for both basal and parathyroid hormone (PTH)/PTH-related peptide receptor-induced osteoclast activation and has differential effects on discrete bone compartments. Endocrinology 144(9):4106-16. [PubMed: 12933685]  [MGI Ref ID J:85591]

Dai Y; Lindsey JD; Duong-Polk X; Nguyen D; Hofer A; Weinreb RN. 2009. Outflow facility in mice with a targeted type I collagen mutation. Invest Ophthalmol Vis Sci 50(12):5749-53. [PubMed: 19797236]  [MGI Ref ID J:158328]

Deguchi JO; Huang H; Libby P; Aikawa E; Whittaker P; Sylvan J; Lee RT; Aikawa M. 2009. Genetically engineered resistance for MMP collagenases promotes abdominal aortic aneurysm formation in mice infused with angiotensin II. Lab Invest 89(3):315-26. [PubMed: 19153555]  [MGI Ref ID J:145853]

Egeblad M; Shen HC; Behonick DJ; Wilmes L; Eichten A; Korets LV; Kheradmand F; Werb Z; Coussens LM. 2007. Type I collagen is a genetic modifier of matrix metalloproteinase 2 in murine skeletal development. Dev Dyn 236(6):1683-93. [PubMed: 17440987]  [MGI Ref ID J:121546]

Fukumoto Y; Deguchi JO; Libby P; Rabkin-Aikawa E; Sakata Y; Chin MT; Hill CC; Lawler PR; Varo N; Schoen FJ; Krane SM; Aikawa M. 2004. Genetically determined resistance to collagenase action augments interstitial collagen accumulation in atherosclerotic plaques. Circulation 110(14):1953-9. [PubMed: 15451791]  [MGI Ref ID J:146712]

Lin M; Jackson P; Tester AM; Diaconu E; Overall CM; Blalock JE; Pearlman E. 2008. Matrix metalloproteinase-8 facilitates neutrophil migration through the corneal stromal matrix by collagen degradation and production of the chemotactic peptide Pro-Gly-Pro. Am J Pathol 173(1):144-53. [PubMed: 18556780]  [MGI Ref ID J:137367]

Lindsey ML; Yoshioka J; MacGillivray C; Muangman S; Gannon J; Verghese A; Aikawa M; Libby P; Krane SM; Lee RT. 2003. Effect of a cleavage-resistant collagen mutation on left ventricular remodeling. Circ Res 93(3):238-45. [PubMed: 12855673]  [MGI Ref ID J:115673]

Mabuchi F; Lindsey JD; Aihara M; Mackey MR; Weinreb RN. 2004. Optic nerve damage in mice with a targeted type I collagen mutation. Invest Ophthalmol Vis Sci 45(6):1841-5. [PubMed: 15161848]  [MGI Ref ID J:92285]

Madsen DH; Leonard D; Masedunskas A; Moyer A; Jurgensen HJ; Peters DE; Amornphimoltham P; Selvaraj A; Yamada SS; Brenner DA; Burgdorf S; Engelholm LH; Behrendt N; Holmbeck K; Weigert R; Bugge TH. 2013. M2-like macrophages are responsible for collagen degradation through a mannose receptor-mediated pathway. J Cell Biol 202(6):951-66. [PubMed: 24019537]  [MGI Ref ID J:201738]

Nong Z; O'Neil C; Lei M; Gros R; Watson A; Rizkalla A; Mequanint K; Li S; Frontini MJ; Feng Q; Pickering JG. 2011. Type I collagen cleavage is essential for effective fibrotic repair after myocardial infarction. Am J Pathol 179(5):2189-98. [PubMed: 21907695]  [MGI Ref ID J:177382]

Ooi CY; Wang Z; Tabima DM; Eickhoff JC; Chesler NC. 2010. The role of collagen in extralobar pulmonary artery stiffening in response to hypoxia-induced pulmonary hypertension. Am J Physiol Heart Circ Physiol :. [PubMed: 20852040]  [MGI Ref ID J:164655]

Provenzano PP; Inman DR; Eliceiri KW; Knittel JG; Yan L; Rueden CT; White JG; Keely PJ. 2008. Collagen density promotes mammary tumor initiation and progression. BMC Med 6:11. [PubMed: 18442412]  [MGI Ref ID J:138535]

Sounni NE; Dehne K; van Kempen L; Egeblad M; Affara NI; Cuevas I; Wiesen J; Junankar S; Korets L; Lee J; Shen J; Morrison CJ; Overall CM; Krane SM; Werb Z; Boudreau N; Coussens LM. 2010. Stromal regulation of vessel stability by MMP14 and TGF{beta}. Dis Model Mech 3(5-6):317-32. [PubMed: 20223936]  [MGI Ref ID J:159238]

Wu H; Liu X; Jaenisch R. 1994. Double replacement: strategy for efficient introduction of subtle mutations into the murine Col1a-1 gene by homologous recombination in embryonic stem cells. Proc Natl Acad Sci U S A 91(7):2819-23. [PubMed: 8146196]  [MGI Ref ID J:17514]

Zhao W; Byrne MH; Boyce BF; Krane SM. 1999. Bone resorption induced by parathyroid hormone is strikingly diminished in collagenase-resistant mutant mice. J Clin Invest 103(4):517-24. [PubMed: 10021460]  [MGI Ref ID J:53079]

Zhao W; Byrne MH; Wang Y; Krane SM. 2000. Osteocyte and osteoblast apoptosis and excessive bone deposition accompany failure of collagenase cleavage of collagen. J Clin Invest 106(8):941-9. [PubMed: 11032854]  [MGI Ref ID J:90884]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

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* $2450.00
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.

Embryos

Price (US dollars $)
Frozen Embryo $1600.00

Standard Supply

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

Supply Notes

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

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • 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 11 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* $3185.00
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.

Embryos

Price (US dollars $)
Frozen Embryo $2080.00

Standard Supply

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

Supply Notes

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

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • 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 11 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
   101045 B6129SF2/J (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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