Strain Name:

B6.129S6-Nf1tm1Fcr/J

Stock Number:

002646

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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

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
Background Strain C57BL/6
Donor Strain 129S6 via EK.CCE ES cell line

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for the Nf1tm1Fcr targeted mutation die during embryonic development due to severe heart malformation (~E13). They also show hyperplasia of neural crest-derived sympathetic ganglia. Heterozygotes do not exhibit any overt disease symptoms. However, as noted in a another targeted mutation deleting the same exon of the Nf1 gene (Jacks, et al., Nat Genetics 7:353-361, 1994), they do show a predisposition to many types of tumors and were recently shown to have deficits in learning and memory (Silva, et al., Nat Genetics 15:281-284, 1997).

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

View Strains carrying other alleles of Nf1     (6 strains)

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).
Neurofibromatosis, Type I; NF1
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Juvenile Myelomonocytic Leukemia; JMML   (NF1)
Neurofibromatosis, Familial Spinal   (NF1)
Neurofibromatosis-Noonan Syndrome; NFNS   (NF1)
Watson Syndrome   (NF1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Nf1tm1Fcr/Nf1tm1Fcr

        either: (involves: 129S/SvEv) or (involves: 129S/SvEv * C57BL/6J)
  • mortality/aging
  • complete lethality throughout fetal growth and development
    • all die by E14.5   (MGI Ref ID J:18048)
  • cardiovascular system phenotype
  • abnormal heart development   (MGI Ref ID J:18048)
    • abnormal fetal atrioventricular canal morphology
      • at E13.5, the atrioventricular canal is composed of loosely arranged endothelial cells that lack the typical cellular density   (MGI Ref ID J:18048)
      • abnormal atrioventricular cushion morphology
        • E13.5 endocardial cushion retains a loose, myxoid appearance that is seen at E12 in wild-type, even though it merges and divides the atrioventricular canal into the left and right channels   (MGI Ref ID J:18048)
        • increased atrioventricular cushion size
          • considerably larger at E13.5   (MGI Ref ID J:18048)
  • abnormal heart shape
    • globular heart   (MGI Ref ID J:18048)
  • abnormal heart valve morphology
    • cardiac valve abnormalities at E13.5   (MGI Ref ID J:18048)
    • abnormal mitral valve cusp morphology
      • leaflets of the mitral valve remain poorly condensed at E13.5   (MGI Ref ID J:18048)
  • abnormal vein morphology
    • show distended veins   (MGI Ref ID J:18048)
  • disorganized myocardium
    • show disoriented and poorly developed myocardial fibers   (MGI Ref ID J:18048)
  • heart hypoplasia   (MGI Ref ID J:18048)
  • liver hemorrhage
    • seen at E13.5   (MGI Ref ID J:18048)
  • pericardial effusion   (MGI Ref ID J:18048)
  • persistent truncus arteriosis
    • at E13.5, have a common root of the aorta and pulmonary artery departing from the conus cordis of the right ventricle   (MGI Ref ID J:18048)
    • as the truncus proceeds cephalad, it divides into two channels, the pulmonary artery and the aorta, which are not fully separate and are joined in a common external sheath   (MGI Ref ID J:18048)
  • vasculature congestion   (MGI Ref ID J:18048)
  • ventricular septal defect
    • exhibit only a rudimentary septum near the apex that is exculsively muscular   (MGI Ref ID J:18048)
  • liver/biliary system phenotype
  • delayed hepatic development
    • 18- to 24-hr delay in hepatic development   (MGI Ref ID J:18048)
  • focal hepatic necrosis
    • seen at E13.5   (MGI Ref ID J:18048)
  • liver hemorrhage
    • seen at E13.5   (MGI Ref ID J:18048)
  • liver hypoplasia
    • seen at E13.5   (MGI Ref ID J:18048)
  • pale liver   (MGI Ref ID J:18048)
  • muscle phenotype
  • abnormal muscle morphology
    • musculature of the stomach, the three layers of the abdominal musculature, and the muscles of the shoulder girdle are thinner   (MGI Ref ID J:18048)
    • delayed muscle development
      • 18- to 24-hour delay in development of skeletal muscle   (MGI Ref ID J:18048)
    • skeletal muscle hypoplasia
      • skeletal muscle throughout the body is hypoplastic at E13.5   (MGI Ref ID J:18048)
  • renal/urinary system phenotype
  • abnormal metanephros morphology
    • a retardation of cephalad repositioning is noted at E13.5   (MGI Ref ID J:18048)
  • decreased renal glomerulus number
    • reduced number of glomeruli at E13.5, due to developmental delay   (MGI Ref ID J:18048)
  • delayed kidney development
    • 18- to 24-hr delay in renal development   (MGI Ref ID J:18048)
    • in the metanephros, display a retardation of cephalad repositioning at E13.5   (MGI Ref ID J:18048)
  • vision/eye phenotype
  • microphthalmia   (MGI Ref ID J:18048)
  • nervous system phenotype
  • exencephaly
    • seen in about 6.3% of homozygotes   (MGI Ref ID J:18048)
  • paravertebral ganglia hyperplasia   (MGI Ref ID J:18048)
  • prevertebral ganglia hyperplasia   (MGI Ref ID J:18048)
  • growth/size/body phenotype
  • enlarged chest
    • display a chest bulge   (MGI Ref ID J:18048)
  • megacephaly   (MGI Ref ID J:18048)
  • homeostasis/metabolism phenotype
  • edema
    • systemic edema   (MGI Ref ID J:18048)
  • pericardial effusion   (MGI Ref ID J:18048)
  • pleural effusion   (MGI Ref ID J:18048)
  • immune system phenotype
  • abnormal lymphatic vessel morphology
    • show distended lymphatics   (MGI Ref ID J:18048)
  • respiratory system phenotype
  • pleural effusion   (MGI Ref ID J:18048)

Nf1tm1Fcr/Nf1tm1Fcr

        involves: 129S/SvEv
  • mortality/aging
  • complete embryonic lethality during organogenesis
    • homozygotes die by E13.5   (MGI Ref ID J:114455)
  • homeostasis/metabolism phenotype
  • abnormal enzyme/coenzyme activity
    • active Ras levels are elevated in homozygotes   (MGI Ref ID J:114455)
View Research Applications

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

Nf1tm1Fcr related

Cancer Research
Increased Tumor Incidence
      Other Tissues/Organs
      Other Tissues/Organs: multiple

Cardiovascular Research
Heart Abnormalities

Developmental Biology Research
Neurodevelopmental Defects

Internal/Organ Research
Heart Abnormalities

Neurobiology Research
Behavioral and Learning Defects
Neurodevelopmental Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Nf1tm1Fcr
Allele Name targeted mutation 1, Fredrick Cancer Research and Development Center
Allele Type Targeted (Null/Knockout)
Common Name(s) Nf1-; Nf1Fcr; Nf1mut;
Mutation Made ByDr. Camilynn Brannan,   Univ of Florida College of Medicine
Strain of Origin129S/SvEv-Gpi1
ES Cell Line NameCCE/EK.CCE
ES Cell Line Strain129S/SvEv-Gpi1
Gene Symbol and Name Nf1, neurofibromatosis 1
Chromosome 11
Gene Common Name(s) AW494271; NFNS; Nf-1; VRNF; WSS; expressed sequence AW494271; neurofibromin;
General Note Phenotypic Similarity to Human Syndrome: Glioblastoma Multiforme (in combination with neuronal deletion of Trp53, J:149662)
Molecular Note Insertion of a neomycin cassette in the opposite transcriptional orientation into exon 31 of the Nf1 gene. Exon 31 was chosen as the mutation site because several point mutations exist at this site in human NF1 patients. This allele is a null allele; no RNA or protein is made from this mutated allele. [MGI Ref ID J:18048]

Genotyping

Genotyping Information

Genotyping Protocols

Nf1tm1Fcr, Melt Curve Analysis
Nf1tm1Fcr, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Brannan CI; Perkins AS; Vogel KS; Ratner N; Nordlund ML; Reid SW; Buchberg AM; Jenkins NA; Parada LF; Copeland NG. 1994. Targeted disruption of the neurofibromatosis type-1 gene leads to developmental abnormalities in heart and various neural crest-derived tissues [published erratum appears in Genes Dev 1994 Nov 15;8(22):2792] Genes Dev 8(9):1019-29. [PubMed: 7926784]  [MGI Ref ID J:18048]

Additional References

Costa RM; Federov NB; Kogan JH; Murphy GG; Stern J; Ohno M; Kucherlapati R; Jacks T; Silva AJ. 2002. Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1. Nature 415(6871):526-30. [PubMed: 11793011]  [MGI Ref ID J:74257]

Jacks T; Shih TS; Schmitt EM; Bronson RT; Bernards A; Weinberg RA. 1994. Tumour predisposition in mice heterozygous for a targeted mutation in Nf1. Nat Genet 7(3):353-61. [PubMed: 7920653]  [MGI Ref ID J:18542]

Silva AJ; Frankland PW; Marowitz Z; Friedman E; Lazlo G; Cioffi D; Jacks T; Bourtchuladze R. 1997. A mouse model for the learning and memory deficits associated with neurofibromatosis type I. Nat Genet 15(3):281-4. [PubMed: 9054942]  [MGI Ref ID J:38703]

Nf1tm1Fcr related

Atit RP; Crowe MJ; Greenhalgh DG; Wenstrup RJ; Ratner N. 1999. The Nf1 tumor suppressor regulates mouse skin wound healing, fibroblast proliferation, and collagen deposited by fibroblasts. J Invest Dermatol 112(6):835-42. [PubMed: 10383727]  [MGI Ref ID J:55742]

Atit RP; Mitchell K; Nguyen L; Warshawsky D; Ratner N. 2000. The neurofibromatosis type 1 (Nf1) tumor suppressor is a modifier of carcinogen-induced pigmentation and papilloma formation in C57BL/6 mice. J Invest Dermatol 114(6):1093-100. [PubMed: 10844550]  [MGI Ref ID J:62818]

Bajenaru ML; Donahoe J; Corral T; Reilly KM; Brophy S; Pellicer A; Gutmann DH. 2001. Neurofibromatosis 1 (NF1) heterozygosity results in a cell-autonomous growth advantage for astrocytes. Glia 33(4):314-23. [PubMed: 11246230]  [MGI Ref ID J:80411]

Bajenaru ML; Garbow JR; Perry A; Hernandez MR; Gutmann DH. 2005. Natural history of neurofibromatosis 1-associated optic nerve glioma in mice. Ann Neurol 57(1):119-27. [PubMed: 15622533]  [MGI Ref ID J:96293]

Bajenaru ML; Hernandez MR; Perry A; Zhu Y; Parada LF; Garbow JR; Gutmann DH. 2003. Optic nerve glioma in mice requires astrocyte Nf1 gene inactivation and Nf1 brain heterozygosity. Cancer Res 63(24):8573-7. [PubMed: 14695164]  [MGI Ref ID J:87063]

Bajenaru ML; Zhu Y; Hedrick NM; Donahoe J; Parada LF; Gutmann DH. 2002. Astrocyte-specific inactivation of the neurofibromatosis 1 gene (NF1) is insufficient for astrocytoma formation. Mol Cell Biol 22(14):5100-13. [PubMed: 12077339]  [MGI Ref ID J:77208]

Banerjee D; Hegedus B; Gutmann DH; Garbow JR. 2007. Detection and measurement of neurofibromatosis-1 mouse optic glioma in vivo. Neuroimage 35(4):1434-7. [PubMed: 17383899]  [MGI Ref ID J:122677]

Banerjee S; Crouse NR; Emnett RJ; Gianino SM; Gutmann DH. 2011. Neurofibromatosis-1 regulates mTOR-mediated astrocyte growth and glioma formation in a TSC/Rheb-independent manner. Proc Natl Acad Sci U S A 108(38):15996-6001. [PubMed: 21896734]  [MGI Ref ID J:176586]

Bennett MR; Rizvi TA; Karyala S; McKinnon RD; Ratner N. 2003. Aberrant growth and differentiation of oligodendrocyte progenitors in neurofibromatosis type 1 mutants. J Neurosci 23(18):7207-17. [PubMed: 12904481]  [MGI Ref ID J:84861]

Brown JA; Emnett RJ; White CR; Yuede CM; Conyers SB; O'Malley KL; Wozniak DF; Gutmann DH. 2010. Reduced striatal dopamine underlies the attention system dysfunction in neurofibromatosis-1 mutant mice. Hum Mol Genet 19(22):4515-28. [PubMed: 20826448]  [MGI Ref ID J:165138]

Chen YH; Gutmann DH. 2014. The molecular and cell biology of pediatric low-grade gliomas. Oncogene 33(16):2019-26. [PubMed: 23624918]  [MGI Ref ID J:212366]

Dasgupta B; Gutmann DH. 2005. Neurofibromin regulates neural stem cell proliferation, survival, and astroglial differentiation in vitro and in vivo. J Neurosci 25(23):5584-94. [PubMed: 15944386]  [MGI Ref ID J:98766]

Dasgupta B; Yi Y; Hegedus B; Weber JD; Gutmann DH. 2005. Cerebrospinal fluid proteomic analysis reveals dysregulation of methionine aminopeptidase-2 expression in human and mouse neurofibromatosis 1-associated glioma. Cancer Res 65(21):9843-50. [PubMed: 16267007]  [MGI Ref ID J:102692]

Diwakar G; Zhang D; Jiang S; Hornyak TJ. 2008. Neurofibromin as a regulator of melanocyte development and differentiation. J Cell Sci 121(Pt 2):167-77. [PubMed: 18089649]  [MGI Ref ID J:130856]

Garza R; Hudson RA 3rd; McMahan CA; Walter CA; Vogel KS. 2007. A mild mutator phenotype arises in a mouse model for malignancies associated with neurofibromatosis type 1. Mutat Res 615(1-2):98-110. [PubMed: 17208258]  [MGI Ref ID J:117442]

Guilding C; McNair K; Stone TW; Morris BJ. 2007. Restored plasticity in a mouse model of neurofibromatosis type 1 via inhibition of hyperactive ERK and CREB. Eur J Neurosci 25(1):99-105. [PubMed: 17241271]  [MGI Ref ID J:118619]

Gutmann DH; Loehr A; Zhang Y; Kim J; Henkemeyer M; Cashen A. 1999. Haploinsufficiency for the neurofibromatosis 1 (NF1) tumor suppressor results in increased astrocyte proliferation. Oncogene 18(31):4450-9. [PubMed: 10442636]  [MGI Ref ID J:56902]

Huse JT; Holland EC. 2009. Genetically engineered mouse models of brain cancer and the promise of preclinical testing. Brain Pathol 19(1):132-43. [PubMed: 19076778]  [MGI Ref ID J:173443]

Ingram DA; Wenning MJ; Shannon K; Clapp DW. 2003. Leukemic potential of doubly mutant Nf1 and Wv hematopoietic cells. Blood 101(5):1984-6. [PubMed: 12393498]  [MGI Ref ID J:82128]

Ismat FA; Xu J; Lu MM; Epstein JA. 2006. The neurofibromin GAP-related domain rescues endothelial but not neural crest development in Nf1 mice. J Clin Invest 116(9):2378-84. [PubMed: 16906226]  [MGI Ref ID J:114455]

Kallarackal AJ; Simard JM; Bailey AM. 2013. The effect of apamin, a small conductance calcium activated potassium (SK) channel blocker, on a mouse model of neurofibromatosis 1. Behav Brain Res 237:71-5. [PubMed: 22983217]  [MGI Ref ID J:197086]

Kim A; Morgan K; Hasz DE; Wiesner SM; Lauchle JO; Geurts JL; Diers MD; Le DT; Kogan SC; Parada LF; Shannon K; Largaespada DA. 2007. Beta common receptor inactivation attenuates myeloproliferative disease in Nf1 mutant mice. Blood 109(4):1687-91. [PubMed: 17090653]  [MGI Ref ID J:123850]

Kim KY; Ju WK; Hegedus B; Gutmann DH; Ellisman MH. 2010. Ultrastructural characterization of the optic pathway in a mouse model of neurofibromatosis-1 optic glioma. Neuroscience 170(1):178-88. [PubMed: 20600672]  [MGI Ref ID J:165209]

King D; Yang G; Thompson MA; Hiebert SW. 2002. Loss of neurofibromatosis-1 and p19(ARF) cooperate to induce a multiple tumor phenotype. Oncogene 21(32):4978-82. [PubMed: 12118376]  [MGI Ref ID J:78079]

Klesse LJ; Parada LF. 1998. p21 ras and phosphatidylinositol-3 kinase are required for survival of wild-type and NF1 mutant sensory neurons. J Neurosci 18(24):10420-8. [PubMed: 9852579]  [MGI Ref ID J:68953]

Largaespada DA; Brannan CI; Jenkins NA; Copeland NG. 1996. Nf1 deficiency causes Ras-mediated granulocyte/macrophage colony stimulating factor hypersensitivity and chronic myeloid leukaemia. Nat Genet 12(2):137-43. [PubMed: 8563750]  [MGI Ref ID J:31568]

Ling BC; Wu J; Miller SJ; Monk KR; Shamekh R; Rizvi TA; Decourten-Myers G; Vogel KS; DeClue JE; Ratner N. 2005. Role for the epidermal growth factor receptor in neurofibromatosis-related peripheral nerve tumorigenesis. Cancer Cell 7(1):65-75. [PubMed: 15652750]  [MGI Ref ID J:95933]

Mashour GA; Martuza RL; Kurtz A. 1999. Induction of melanogenic abnormalities in NF1+/- mutant mice by DMBA [letter] J Invest Dermatol 113(6):1133-4. [PubMed: 10594763]  [MGI Ref ID J:59045]

Ozerdem U. 2004. Targeting neovascular pericytes in neurofibromatosis type 1. Angiogenesis 7(4):307-11. [PubMed: 15886874]  [MGI Ref ID J:105408]

Patmore DM; Welch S; Fulkerson PC; Wu J; Choi K; Eaves D; Kordich JJ; Collins MH; Cripe TP; Ratner N. 2012. In vivo regulation of TGF-beta by R-Ras2 revealed through loss of the RasGAP protein NF1. Cancer Res 72(20):5317-27. [PubMed: 22918885]  [MGI Ref ID J:191804]

Rizvi TA; Akunuru S; de Courten-Myers G; Switzer RC 3rd; Nordlund ML ; Ratner N. 1999. Region-specific astrogliosis in brains of mice heterozygous for mutations in the neurofibromatosis type 1 (Nf1) tumor suppressor. Brain Res 816(1):111-23. [PubMed: 9878702]  [MGI Ref ID J:51953]

Rizvi TA; Huang Y; Sidani A; Atit R; Largaespada DA; Boissy RE; Ratner N. 2002. A novel cytokine pathway suppresses glial cell melanogenesis after injury to adult nerve. J Neurosci 22(22):9831-40. [PubMed: 12427839]  [MGI Ref ID J:109211]

Rosenbaum T; Engelbrecht V; Krolls W; van Dorsten FA; Hoehn-Berlage M; Lenard HG. 1999. MRI abnormalities in neurofibromatosis type 1 (NF1): a study of men and mice. Brain Dev 21(4):268-73. [PubMed: 10392751]  [MGI Ref ID J:55949]

Sandsmark DK; Zhang H; Hegedus B; Pelletier CL; Weber JD; Gutmann DH. 2007. Nucleophosmin mediates mammalian target of rapamycin-dependent actin cytoskeleton dynamics and proliferation in neurofibromin-deficient astrocytes. Cancer Res 67(10):4790-9. [PubMed: 17510408]  [MGI Ref ID J:121729]

Solga AC; Gianino SM; Gutmann DH. 2014. NG2-cells are not the cell of origin for murine neurofibromatosis-1 (Nf1) optic glioma. Oncogene 33(3):289-99. [PubMed: 23318450]  [MGI Ref ID J:204871]

Staser K; Yang FC; Clapp DW. 2010. Mast cells and the neurofibroma microenvironment. Blood 116(2):157-64. [PubMed: 20233971]  [MGI Ref ID J:162828]

Sullivan K; El-Hoss J; Quinlan KG; Deo N; Garton F; Seto JT; Gdalevitch M; Turner N; Cooney GJ; Kolanczyk M; North KN; Little DG; Schindeler A. 2014. NF1 is a critical regulator of muscle development and metabolism. Hum Mol Genet 23(5):1250-9. [PubMed: 24163128]  [MGI Ref ID J:206219]

Tong J; Hannan F; Zhu Y; Bernards A; Zhong Y. 2002. Neurofibromin regulates G protein-stimulated adenylyl cyclase activity. Nat Neurosci 5(2):95-6. [PubMed: 11788835]  [MGI Ref ID J:109327]

Verchere CB; D'Alessio DA; Palmiter RD; Weir GC; Bonner-Weir S; Baskin DG; Kahn SE. 1996. Islet amyloid formation associated with hyperglycemia in transgenic mice with pancreatic beta cell expression of human islet amyloid polypeptide. Proc Natl Acad Sci U S A 93(8):3492-6. [PubMed: 8622964]  [MGI Ref ID J:108871]

Vogel KS; Brannan CI; Jenkins NA; Copeland NG; Parada LF. 1995. Loss of neurofibromin results in neurotrophin-independent survival of embryonic sensory and sympathetic neurons. Cell 82(5):733-42. [PubMed: 7671302]  [MGI Ref ID J:68952]

Vogel KS; Klesse LJ; Velasco-Miguel S; Meyers K; Rushing EJ; Parada LF. 1999. Mouse tumor model for neurofibromatosis type 1. Science 286(5447):2176-9. [PubMed: 10591653]  [MGI Ref ID J:58877]

Vogel KS; Parada LF. 1998. Sympathetic neuron survival and proliferation are prolonged by loss of p53 and neurofibromin. Mol Cell Neurosci 11(1-2):19-28. [PubMed: 9608530]  [MGI Ref ID J:47680]

Wang Y; Yang J; Zheng H; Tomasek GJ; Zhang P; McKeever PE; Lee EY; Zhu Y. 2009. Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine model. Cancer Cell 15(6):514-26. [PubMed: 19477430]  [MGI Ref ID J:149662]

Warrington NM; Gianino SM; Jackson E; Goldhoff P; Garbow JR; Piwnica-Worms D; Gutmann DH; Rubin JB. 2010. Cyclic AMP suppression is sufficient to induce gliomagenesis in a mouse model of neurofibromatosis-1. Cancer Res 70(14):5717-27. [PubMed: 20551058]  [MGI Ref ID J:162482]

Warrington NM; Woerner BM; Daginakatte GC; Dasgupta B; Perry A; Gutmann DH; Rubin JB. 2007. Spatiotemporal Differences in CXCL12 Expression and Cyclic AMP Underlie the Unique Pattern of Optic Glioma Growth in Neurofibromatosis Type 1. Cancer Res 67(18):8588-95. [PubMed: 17875698]  [MGI Ref ID J:124875]

Wehrle-Haller B; Meller M; Weston JA. 2001. Analysis of melanocyte precursors in Nf1 mutants reveals that MGF/KIT signaling promotes directed cell migration independent of its function in cell survival. Dev Biol 232(2):471-83. [PubMed: 11401406]  [MGI Ref ID J:69377]

Weiss WA; Israel M; Cobbs C; Holland E; James CD; Louis DN; Marks C; McClatchey AI; Roberts T; Van Dyke T; Wetmore C; Chiu IM; Giovannini M; Guha A; Higgins RJ; Marino S; Radovanovic I; Reilly K; Aldape K. 2002. Neuropathology of genetically engineered mice: consensus report and recommendations from an international forum. Oncogene 21(49):7453-63. [PubMed: 12386807]  [MGI Ref ID J:79667]

Wozniak DF; Diggs-Andrews KA; Conyers S; Yuede CM; Dearborn JT; Brown JA; Tokuda K; Izumi Y; Zorumski CF; Gutmann DH. 2013. Motivational disturbances and effects of L-dopa administration in neurofibromatosis-1 model mice. PLoS One 8(6):e66024. [PubMed: 23762458]  [MGI Ref ID J:203309]

Wu J; Crimmins JT; Monk KR; Williams JP; Fitzgerald ME; Tedesco S; Ratner N. 2006. Perinatal epidermal growth factor receptor blockade prevents peripheral nerve disruption in a mouse model reminiscent of benign world health organization grade I neurofibroma. Am J Pathol 168(5):1686-96. [PubMed: 16651634]  [MGI Ref ID J:108591]

Wu M; Wallace MR; Muir D. 2006. Nf1 haploinsufficiency augments angiogenesis. Oncogene 25(16):2297-303. [PubMed: 16288202]  [MGI Ref ID J:108781]

Xu Y; Chiamvimonvat N; Vazquez AE; Akunuru S; Ratner N; Yamoah EN. 2002. Gene-targeted deletion of neurofibromin enhances the expression of a transient outward K+ current in Schwann cells: a protein kinase A-mediated mechanism. J Neurosci 22(21):9194-202. [PubMed: 12417644]  [MGI Ref ID J:123994]

Yin B; Delwel R; Valk PJ; Wallace MR; Loh ML; Shannon KM; Largaespada DA. 2009. A retroviral mutagenesis screen reveals strong cooperation between Bcl11a overexpression and loss of the Nf1 tumor suppressor gene. Blood 113(5):1075-85. [PubMed: 18948576]  [MGI Ref ID J:144622]

Zhu Y; Ghosh P; Charnay P; Burns DK; Parada LF. 2002. Neurofibromas in NF1: Schwann cell origin and role of tumor environment. Science 296(5569):920-2. [PubMed: 11988578]  [MGI Ref ID J:76359]

Zhu Y; Romero MI; Ghosh P; Ye Z; Charnay P; Rushing EJ; Marth JD; Parada LF. 2001. Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain. Genes Dev 15(7):859-76. [PubMed: 11297510]  [MGI Ref ID J:68558]

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* $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 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* $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 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
   000664 C57BL/6J
 
  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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

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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