Strain Name:

STOCK Nf1tm1Par/J

Stock Number:

017639

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Availability:

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These Nf1flox mice possess loxP sites flanking exons 31-32 of the neurofibromatosis 1 gene (Nf1), and have applications in studying cancer, neural crest development and neurofibromatosis type I.

Description

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHomozygote x Homozygote         (Female x Male)   15-JUL-13
Specieslaboratory mouse
Generation?+N3f4 (17-DEC-13)
Generation Definitions
 
Donating Investigator Luis F Parada,   UT Southwestern Medical Center

Description
Mutation in the human neurofibromin gene, NF1, is the cause of the autosomal dominant disorder Type I Neurofibromatosis. These mice possess loxP sites on either side of exons 31 and 32 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 31 and 32 deleted in the cre-expressing tissue(s).

When bred to a strain with Cre recombinase expression in the developing neural tube (see Stock No. 009107 for example), this mutant mouse strain may be useful in studies of Type I Neurofibromatosis.

When bred to a strain with Cre recombinase expression in neuronal cells (see Stock No. 003966 for example), this mutant mouse strain may be useful in studies of cerebral cortex development and reactive astrogliosis.

When bred to a strain with Cre recombinase expression in endothelial cells (see Stock No. 008863 for example), this mutant mouse strain may be useful in studies of neural crest development.

When bred to B6.Cg-Tg(Prrx1-cre)1Cjt/J mice (Stock No. 005584), mesenchyme-specific cre-expression results in mice that exhibit an increase in the amount of connective tissue, as well as muscle dystrophy characterized by fibrosis, a reduced number of muscle fibers, and reduced muscle force.

When bred to mice carrying Tg(Mx1-cre)1Cgn (Stock No. 003556), interferon-induced Cre-mediated recombination results in a progressive myeloproliferative disorder.

This allele is also part of the MADM-TG,p53KO,NF1-flox strain (Stock No. 017530), which is a genetic mosaicism model for cancer.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
A targeting vector containing a loxP site and a PGKNeo cassette was inserted upstream of exon 31. A second loxP site was inserted downstream of exon 32. The construct was electroporated into 129 derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6 mice. The mice were then crossed to several other mutant lines. The combination mutant strain, with a mix of CD1, C57BL/6 and 129 genetic backgrounds, was crossed to C57BL/6J to separate the Nf1tm1Par allele.

Control Information

  Control
   101045 B6129SF2/J (approximate)
   000664 C57BL/6J (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Nf1tm1Par allele
017640   B6.129(Cg)-Nf1tm1Par/J
017530   STOCK Igs2tm2(ACTB-tdTomato,-EGFP)Luo Trp53tm1Tyj Nf1tm1Par/J
View Strains carrying   Nf1tm1Par     (2 strains)

Strains carrying other alleles of Nf1
007923   B6.129S1-Nf1tm1Cbr/J
008192   B6.129S2-Nf1tm1Tyj/J
002646   B6.129S6-Nf1tm1Fcr/J
008191   B6;129S2-Trp53tm1Tyj Nf1tm1Tyj/J
View Strains carrying other alleles of Nf1     (4 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).
Juvenile Myelomonocytic Leukemia; JMML
Neurofibromatosis, Type I; NF1
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
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.

Nf1tm1Par/Nf1tm1Par

        involves: 129S1/Sv * 129X1/SvJ   (conditional)
  • nervous system phenotype
  • abnormal astrocyte physiology
    • astrocytes transfected with a cre-expresing adenovirus exhibit increased proliferation compared to in control cells   (MGI Ref ID J:176586)

The following phenotype relates to a compound genotype created using this strain.
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Nf1tm1Par/Nf1tm1Par Tg(Gfap-cre)77.6Mvs/0

        involves: 129S1/Sv * 129X1/SvJ * BALB/c * C57BL/6NHsd   (conditional)
  • tumorigenesis
  • *normal* tumorigenesis
    • mutants do not develop tumors   (MGI Ref ID J:154673)

Nf1tm1Par/Nf1tm1Par Tg(Mx1-cre)1Cgn/0

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA   (conditional)
  • mortality/aging
  • premature death
    • 50% of pIpC treated mice die by 7.5 months of age   (MGI Ref ID J:90973)
  • hematopoietic system phenotype
  • abnormal bone marrow cell morphology/development
    • apoptosis is reduced in the bone marrow of pIpC injected mice   (MGI Ref ID J:90973)
    • bone marrow from pIpC injected mice is highly cellular, comprised of myeloid cells at various stages of differentiation   (MGI Ref ID J:90973)
    • increase in numbers of immature monocytic cells in the bone marrow of pIpC treated mice   (MGI Ref ID J:90973)
    • bone marrow from pIpC injected mice contains elevated numbers of CFU-GM and an increase in the numbers of CFU-GM that are hypersensitive to granulocyte-macrophage colony stimulating factor (GM-CSF) and CFU-GM colonies are larger than normal and show abnormal spreading morphology   (MGI Ref ID J:90973)
    • abnormal common myeloid progenitor cell morphology
      • myeloid progenitors from pIpC injected mice show increased proliferation   (MGI Ref ID J:90973)
  • abnormal hematopoiesis
    • pIpC injected mice at 3 to 5 days of age develop overt signs of myeloproliferative disease beginning between 5 and 6 months of age   (MGI Ref ID J:90973)
    • pIpC injected mice show a shift in hematopoiesis from the marrow to the spleen   (MGI Ref ID J:90973)
    • abnormal common myeloid progenitor cell morphology
      • myeloid progenitors from pIpC injected mice show increased proliferation   (MGI Ref ID J:90973)
    • abnormal hematopoietic cell number
      • pIpC injected mice at 3 to 5 days of age exhibit elevated numbers of differentiated lymphoid cells by 3 months of age   (MGI Ref ID J:90973)
      • increased leukocyte cell number
        • pIpC injected mice at 3 to 5 days of age exhibit elevated leukocyte counts by 3 months of age   (MGI Ref ID J:90973)
        • cultures from pIpC injected mice show an increase in the percentage of monocyte-macrophage cells   (MGI Ref ID J:90973)
        • increased granulocyte number
          • pIpC injected mice show an increase in numbers of differentiated granulocytic cells   (MGI Ref ID J:90973)
          • increased neutrophil cell number
            • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal neutrophils by 3 months of age   (MGI Ref ID J:90973)
        • increased lymphocyte cell number
          • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal lymphocytes by 3 months of age   (MGI Ref ID J:90973)
        • increased monocyte cell number
          • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal monocytes by 3 months of age   (MGI Ref ID J:90973)
          • pIpC injected mice show an increase in numbers of immature monocytic cells in the bone marrow   (MGI Ref ID J:90973)
    • abnormal myeloid leukocyte morphology
      • pIpC injected mice at 3 to 5 days of age exhibit elevated numbers of differentiated myeloid cells by 3 months of age   (MGI Ref ID J:90973)
    • abnormal myelopoiesis
      • spleen from pIpC injected mice shows a massive increase in myelopoiesis   (MGI Ref ID J:90973)
  • abnormal spleen morphology
    • spleens from pIpC injected mice contain large numbers of CFU-GM   (MGI Ref ID J:90973)
    • enlarged spleen
      • pIpC injected mice at 3 to 5 days of age exhibit progressive splenomegaly with extensive infiltration of myeloid cells at various stages of maturation   (MGI Ref ID J:90973)
  • behavior/neurological phenotype
  • abnormal gait
    • pIpC injected mice at 3 to 5 days of age exhibit hunching by 5-6 months of age   (MGI Ref ID J:90973)
  • hunched posture
    • pIpC injected mice at 3 to 5 days of age exhibit abnormal gait by 5-6 months of age   (MGI Ref ID J:90973)
  • immune system phenotype
  • abnormal myeloid leukocyte morphology
    • pIpC injected mice at 3 to 5 days of age exhibit elevated numbers of differentiated myeloid cells by 3 months of age   (MGI Ref ID J:90973)
    • increased granulocyte number
      • pIpC injected mice show an increase in numbers of differentiated granulocytic cells   (MGI Ref ID J:90973)
      • increased neutrophil cell number
        • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal neutrophils by 3 months of age   (MGI Ref ID J:90973)
    • increased monocyte cell number
      • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal monocytes by 3 months of age   (MGI Ref ID J:90973)
      • pIpC injected mice show an increase in numbers of immature monocytic cells in the bone marrow   (MGI Ref ID J:90973)
  • abnormal myelopoiesis
    • spleen from pIpC injected mice shows a massive increase in myelopoiesis   (MGI Ref ID J:90973)
  • abnormal spleen morphology
    • spleens from pIpC injected mice contain large numbers of CFU-GM   (MGI Ref ID J:90973)
    • enlarged spleen
      • pIpC injected mice at 3 to 5 days of age exhibit progressive splenomegaly with extensive infiltration of myeloid cells at various stages of maturation   (MGI Ref ID J:90973)
  • increased leukocyte cell number
    • pIpC injected mice at 3 to 5 days of age exhibit elevated leukocyte counts by 3 months of age   (MGI Ref ID J:90973)
    • cultures from pIpC injected mice show an increase in the percentage of monocyte-macrophage cells   (MGI Ref ID J:90973)
    • increased granulocyte number
      • pIpC injected mice show an increase in numbers of differentiated granulocytic cells   (MGI Ref ID J:90973)
      • increased neutrophil cell number
        • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal neutrophils by 3 months of age   (MGI Ref ID J:90973)
    • increased lymphocyte cell number
      • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal lymphocytes by 3 months of age   (MGI Ref ID J:90973)
    • increased monocyte cell number
      • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal monocytes by 3 months of age   (MGI Ref ID J:90973)
      • pIpC injected mice show an increase in numbers of immature monocytic cells in the bone marrow   (MGI Ref ID J:90973)
  • integument phenotype
  • disheveled coat
    • pIpC injected mice at 3 to 5 days of age have a disheveled appearance by 5-6 months of age   (MGI Ref ID J:90973)

Nf1tm1Par/Nf1tm1Par Tg(Prrx1-cre)1Cjt/0

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL/J   (conditional)
  • growth/size/body phenotype
  • decreased body weight
    • weight is on average reduced by 25%   (MGI Ref ID J:173779)
  • limbs/digits/tail phenotype
  • short limbs
    • short-limbed dwarfism, with mutants showing a reduction in entire limb size   (MGI Ref ID J:173779)
  • muscle phenotype
  • abnormal muscle morphology
    • mutants exhibit muscle dystrophy   (MGI Ref ID J:173779)
    • large areas of dystrophic musculature are occupied by fat tissue   (MGI Ref ID J:173779)
    • muscle connective tissue shows increased proliferation at E14.5 and an increase in connective tissue in muscles is already seen at E16.5   (MGI Ref ID J:173779)
    • muscle fibers are thinned out at E16.5   (MGI Ref ID J:173779)
    • abnormal muscle development
      • marker analysis indicates a defect in muscle formation at E13.5, with specific muscle primordial reduced in size or entirely missing; approximate 30% reduction in the m. triceps size and about 50% reduction in the m. gluteus maximus size of E13.5 embryos   (MGI Ref ID J:173779)
      • the m. latissimus dorsi appears smaller and shows rarefaction of muscle fibers   (MGI Ref ID J:173779)
      • distal muscle groups in the extremities are most affected, with some muscles completely missing, indicating that the muscle differentiation process is disturbed   (MGI Ref ID J:173779)
      • abnormal myogenesis
        • defect in myogenesis affecting the terminal differentiation of myoblasts between E12.5 and E14.5   (MGI Ref ID J:173779)
        • abnormal myoblast differentiation
          • maker analysis indicates a severe disruption of myoblast terminal differentiation   (MGI Ref ID J:173779)
          • marker analysis indicates that migration and proliferation of pre-muscle cells at E11.5 are normal but increased proliferation of myoblasts in ventral muscle masses is seen   (MGI Ref ID J:173779)
    • abnormal muscle fiber morphology
      • muscles show a 20% increase in the number of fibers with cleft-like invaginations (split fibers)   (MGI Ref ID J:173779)
      • muscle fiber size appears more variable than in controls, however no overt muscle regeneration is seen   (MGI Ref ID J:173779)
      • decreased skeletal muscle fiber number
        • total number of muscle fibers is reduced by 50% in the triceps   (MGI Ref ID J:173779)
    • decreased muscle weight
      • weight of triceps muscle is reduced by more than 50%   (MGI Ref ID J:173779)
    • decreased skeletal muscle mass
      • reduction in muscle size and mass   (MGI Ref ID J:173779)
    • skeletal muscle fibrosis
      • generalized muscle fibrosis, characterized by expansion of collagen-rich connective tissue, and reduction in total number of muscle fibers   (MGI Ref ID J:173779)
  • abnormal muscle physiology
    • in the force gauge pull test, mice show a dramatic reduction in muscle force   (MGI Ref ID J:173779)
    • satellite cells exhibit normal self-renewal but impaired differentiation as indicated by diminished myotube formatio   (MGI Ref ID J:173779)
  • cellular phenotype
  • abnormal myoblast differentiation
    • maker analysis indicates a severe disruption of myoblast terminal differentiation   (MGI Ref ID J:173779)
    • marker analysis indicates that migration and proliferation of pre-muscle cells at E11.5 are normal but increased proliferation of myoblasts in ventral muscle masses is seen   (MGI Ref ID J:173779)
  • homeostasis/metabolism phenotype
  • skeletal muscle fibrosis
    • generalized muscle fibrosis, characterized by expansion of collagen-rich connective tissue, and reduction in total number of muscle fibers   (MGI Ref ID J:173779)

Nf1tm1Par/Nf1tm1Par Tg(Prrx1-cre)1Cjt/0

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * C57BL/6N * SJL/J   (conditional)
  • skeleton phenotype
  • abnormal bone healing
    • mutants exhibit delayed and defective fracture healing characterized by diminished cartilaginous callus formation, increased bone formation near the cortical bone on the periosteum but not in the fracture gap, and persistence of cartilage at day 21 such that bony bridging is not observed   (MGI Ref ID J:193350)
    • while total callus volume following fracture is larger in mutants at day 7 and 10 due to rapid initial growth of fibrous tissue (desmal type ossification), by day 14 and 21, the total callus volume is significantly smaller   (MGI Ref ID J:193350)
    • accumulation and persistence of fibrous tissue in the fracture gap, with increased numbers of osteoclasts   (MGI Ref ID J:193350)
    • increase in number of blood vessels in mutant fractures (in callus) compared to controls, indicating increased vascularization of the fracture tissue, however no osteogenesis results from this increased vascularization   (MGI Ref ID J:193350)
    • ectopic fat tissue is seen in the fracture site   (MGI Ref ID J:193350)
  • abnormal cartilage morphology
    • bone fractures exhibit impaired cartilage formation and increased periosteal ossification at the cortices   (MGI Ref ID J:193350)
  • abnormal endochondral bone ossification
    • endochondrial formation is impaired following fracture but periosteal bone formation is enhanced   (MGI Ref ID J:193350)
  • abnormal osteoblast cell number
    • fewer osteoblasts are seen within the fracture gap throughout healing compared to controls, however, osteoblast number is increased at the periosteal surface   (MGI Ref ID J:193350)
  • abnormal osteoid morphology
    • presence of large areas of non-mineralized osteoid in the fracture gap, indicating decreased mineralization of the extracellular matrix   (MGI Ref ID J:193350)
    • increased osteoid thickness
      • thickening of the osteoid layer in the periosteal region following fracture   (MGI Ref ID J:193350)
  • decreased bone mineral density
    • decrease of regenerative tissue bone mineral density following fracture   (MGI Ref ID J:193350)
  • fragile skeleton
    • bones are weaker; femora show lower torsional stiffness and ultimate torque at failure compared to controls   (MGI Ref ID J:193350)
    • fractured bones of mutants that are allowed to heal also exhibit a lower torsional stiffness and ultimate torque at failure compared to controls   (MGI Ref ID J:193350)
  • increased compact bone volume
    • dramatic cortical bone thickening following fracture   (MGI Ref ID J:193350)
  • increased osteoclast cell number
    • callus following fracture shows increased number of osteoclasts; most osteoclasts are localized within fibrous tissue and not on the bone surface as in controls   (MGI Ref ID J:193350)
  • homeostasis/metabolism phenotype
  • abnormal bone healing
    • mutants exhibit delayed and defective fracture healing characterized by diminished cartilaginous callus formation, increased bone formation near the cortical bone on the periosteum but not in the fracture gap, and persistence of cartilage at day 21 such that bony bridging is not observed   (MGI Ref ID J:193350)
    • while total callus volume following fracture is larger in mutants at day 7 and 10 due to rapid initial growth of fibrous tissue (desmal type ossification), by day 14 and 21, the total callus volume is significantly smaller   (MGI Ref ID J:193350)
    • accumulation and persistence of fibrous tissue in the fracture gap, with increased numbers of osteoclasts   (MGI Ref ID J:193350)
    • increase in number of blood vessels in mutant fractures (in callus) compared to controls, indicating increased vascularization of the fracture tissue, however no osteogenesis results from this increased vascularization   (MGI Ref ID J:193350)
    • ectopic fat tissue is seen in the fracture site   (MGI Ref ID J:193350)
  • hematopoietic system phenotype
  • increased osteoclast cell number
    • callus following fracture shows increased number of osteoclasts; most osteoclasts are localized within fibrous tissue and not on the bone surface as in controls   (MGI Ref ID J:193350)
  • immune system phenotype
  • increased osteoclast cell number
    • callus following fracture shows increased number of osteoclasts; most osteoclasts are localized within fibrous tissue and not on the bone surface as in controls   (MGI Ref ID J:193350)

Nf1tm1Par/Nf1tm1Par Tg(Syn1-cre)671Jxm/0

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA   (conditional)
  • growth/size/body phenotype
  • decreased body weight
    • body weight and size are about 50% of normal   (MGI Ref ID J:68558)
  • postnatal growth retardation
    • 3-4 days after birth, mice begin to exhibit growth retardation that is sustained into adulthood   (MGI Ref ID J:68558)
  • nervous system phenotype
  • abnormal cerebral cortex morphology
    • increase in cell density in the cerebral cortex, often resulting in less apparent lamination   (MGI Ref ID J:68558)
    • thin cerebral cortex
      • about 20% reduction in coritcal thickness   (MGI Ref ID J:68558)
  • astrocytosis
    • mice display astrogliosis in various brain regions, however do not develop neuronal degeneration or microgliosis   (MGI Ref ID J:68558)
  • decreased forebrain size
    • forebrain, but not the rest of the brain, is reduced in size, however mice exhibit normal neuronal development   (MGI Ref ID J:68558)
  • behavior/neurological phenotype
  • abnormal learning/memory/conditioning
    • mice display severe learning disability   (MGI Ref ID J:68558)
  • tumorigenesis
  • *normal* tumorigenesis
    • no evidence of tumors; optic gliomas, astrocytomas, or neurofibroma are not observed   (MGI Ref ID J:68558)

Nf1tm1Par/Nf1tm1Par Tg(Tek-cre)1Ywa/0

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL   (conditional)
  • cardiovascular system phenotype
  • double outlet right ventricle
    • seen in 8 of 11 embryos   (MGI Ref ID J:80323)
  • increased atrioventricular cushion size
    • 8 of 11 embryos show an enlarged atrioventricular cushion   (MGI Ref ID J:80323)
  • pericardial effusion   (MGI Ref ID J:80323)
  • thin myocardium compact layer   (MGI Ref ID J:80323)
  • thin myocardium
    • 8 of 11 embryos exhibit a thinned myocardium   (MGI Ref ID J:80323)
  • ventricular septal defect
    • 10 of 11 embryos exhibit ventricular septal defects   (MGI Ref ID J:80323)
  • homeostasis/metabolism phenotype
  • pericardial effusion   (MGI Ref ID J:80323)
View Research Applications

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

Cancer Research
Increased Tumor Incidence
      Other Tissues/Organs: brain

Neurobiology Research
Cre-lox System
      loxP-flanked Sequences

Research Tools
Cre-lox System
      loxP-flanked Sequences

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Nf1tm1Par
Allele Name targeted mutation 1, Luis F Parada
Allele Type Targeted (Conditional ready (e.g. floxed), No functional change)
Common Name(s) Nf1flox; Nf1flox;
Mutation Made By Steven McKinnon,   UT Southwestern Medical Center
Strain of Origin(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Site of ExpressionWhen mice carrying this allele are mated to a Synapsin I promoter driven Cre transgenic mouse strain, NF1 function is abated in most differentiated neuronal populations, resulting in abnormal development of the cerebral cortex.
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: Astrocytoma (J:134611)
Molecular Note A loxP-neomycin selection cassette was inserted into intron 30 and a single loxP site was inserted into intron 32. [MGI Ref ID J:68558]

Genotyping

Genotyping Information

Genotyping Protocols

Nf1tm1Par,

Separated MCA


Nf1tm1Par, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Liu C; Sage JC; Miller MR; Verhaak RG; Hippenmeyer S; Vogel H; Foreman O; Bronson RT; Nishiyama A; Luo L; Zong H. 2011. Mosaic analysis with double markers reveals tumor cell of origin in glioma. Cell 146(2):209-21. [PubMed: 21737130]  [MGI Ref ID J:174616]

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]

Additional References

Nf1tm1Par related

Alanne MH; Siljamaki E; Peltonen S; Vaananen K; Windle JJ; Parada LF; Maatta JA; Peltonen J. 2012. Phenotypic characterization of transgenic mice harboring Nf1+/- or Nf1-/- osteoclasts in otherwise Nf1+/+ background. J Cell Biochem 113(6):2136-46. [PubMed: 22307743]  [MGI Ref ID J:211765]

Alcantara Llaguno S; Chen J; Kwon CH; Jackson EL; Li Y; Burns DK; Alvarez-Buylla A; Parada LF. 2009. Malignant astrocytomas originate from neural stem/progenitor cells in a somatic tumor suppressor mouse model. Cancer Cell 15(1):45-56. [PubMed: 19111880]  [MGI Ref ID J:143505]

Baek ST; Tallquist MD. 2012. Nf1 limits epicardial derivative expansion by regulating epithelial to mesenchymal transition and proliferation. Development 139(11):2040-9. [PubMed: 22535408]  [MGI Ref ID J:183991]

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; Byrd JN; Gianino SM; Harpstrite SE; Rodriguez FJ; Tuskan RG; Reilly KM; Piwnica-Worms DR; Gutmann DH. 2010. The Neurofibromatosis Type 1 Tumor Suppressor Controls Cell Growth by Regulating Signal Transducer and Activator of Transcription-3 Activity In vitro and In vivo. Cancer Res 70(4):1356-66. [PubMed: 20124472]  [MGI Ref ID J:157155]

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]

Brown JA; Diggs-Andrews KA; Gianino SM; Gutmann DH. 2012. Neurofibromatosis-1 heterozygosity impairs CNS neuronal morphology in a cAMP/PKA/ROCK-dependent manner. Mol Cell Neurosci 49(1):13-22. [PubMed: 21903164]  [MGI Ref ID J:189363]

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]

Brown JA; Gianino SM; Gutmann DH. 2010. Defective cAMP generation underlies the sensitivity of CNS neurons to neurofibromatosis-1 heterozygosity. J Neurosci 30(16):5579-89. [PubMed: 20410111]  [MGI Ref ID J:159840]

Brown JA; Xu J; Diggs-Andrews KA; Wozniak DF; Mach RH; Gutmann DH. 2011. PET imaging for attention deficit preclinical drug testing in neurofibromatosis-1 mice. Exp Neurol 232(2):333-8. [PubMed: 21963652]  [MGI Ref ID J:178468]

Chang T; Krisman K; Theobald EH; Xu J; Akutagawa J; Lauchle JO; Kogan S; Braun BS; Shannon K. 2013. Sustained MEK inhibition abrogates myeloproliferative disease in Nf1 mutant mice. J Clin Invest 123(1):335-9. [PubMed: 23221337]  [MGI Ref ID J:194161]

Chen J; Li Y; Yu TS; McKay RM; Burns DK; Kernie SG; Parada LF. 2012. A restricted cell population propagates glioblastoma growth after chemotherapy. Nature 488(7412):522-6. [PubMed: 22854781]  [MGI Ref ID J:186769]

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]

Cui Y; Costa RM; Murphy GG; Elgersma Y; Zhu Y; Gutmann DH; Parada LF; Mody I; Silva AJ. 2008. Neurofibromin regulation of ERK signaling modulates GABA release and learning. Cell 135(3):549-60. [PubMed: 18984165]  [MGI Ref ID J:147614]

Cutts BA; Sjogren AK; Andersson KM; Wahlstrom AM; Karlsson C; Swolin B; Bergo MO. 2009. Nf1 deficiency cooperates with oncogenic K-RAS to induce acute myeloid leukemia in mice. Blood 114(17):3629-32. [PubMed: 19710506]  [MGI Ref ID J:153839]

Dasgupta B; Dugan LL; Gutmann DH. 2003. The neurofibromatosis 1 gene product neurofibromin regulates pituitary adenylate cyclase-activating polypeptide-mediated signaling in astrocytes. J Neurosci 23(26):8949-54. [PubMed: 14523097]  [MGI Ref ID J:120166]

Dasgupta B; Li W; Perry A; Gutmann DH. 2005. Glioma formation in neurofibromatosis 1 reflects preferential activation of K-RAS in astrocytes. Cancer Res 65(1):236-45. [PubMed: 15665300]  [MGI Ref ID J:95509]

Dasgupta B; Yi Y; Chen DY; Weber JD; Gutmann DH. 2005. Proteomic analysis reveals hyperactivation of the mammalian target of rapamycin pathway in neurofibromatosis 1-associated human and mouse brain tumors. Cancer Res 65(7):2755-60. [PubMed: 15805275]  [MGI Ref ID J:97360]

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]

Deo M; Huang JL; Fuchs H; de Angelis MH; Van Raamsdonk CD. 2013. Differential effects of neurofibromin gene dosage on melanocyte development. J Invest Dermatol 133(1):49-58. [PubMed: 22810304]  [MGI Ref ID J:196495]

El Khassawna T; Toben D; Kolanczyk M; Schmidt-Bleek K; Koennecke I; Schell H; Mundlos S; Duda GN. 2012. Deterioration of fracture healing in the mouse model of NF1 long bone dysplasia. Bone 51(4):651-60. [PubMed: 22868293]  [MGI Ref ID J:193350]

Elefteriou F; Benson MD; Sowa H; Starbuck M; Liu X; Ron D; Parada LF; Karsenty G. 2006. ATF4 mediation of NF1 functions in osteoblast reveals a nutritional basis for congenital skeletal dysplasiae. Cell Metab 4(6):441-51. [PubMed: 17141628]  [MGI Ref ID J:129752]

Gitler AD; Kong Y; Choi JK; Zhu Y; Pear WS; Epstein JA. 2004. Tie2-Cre-induced inactivation of a conditional mutant Nf1 allele in mouse results in a myeloproliferative disorder that models juvenile myelomonocytic leukemia. Pediatr Res 55(4):581-4. [PubMed: 14739366]  [MGI Ref ID J:88133]

Gitler AD; Zhu Y; Ismat FA; Lu MM; Yamauchi Y; Parada LF; Epstein JA. 2003. Nf1 has an essential role in endothelial cells. Nat Genet 33(1):75-9. [PubMed: 12469121]  [MGI Ref ID J:80323]

Gregorian C; Nakashima J; Dry SM; Nghiemphu PL; Smith KB; Ao Y; Dang J; Lawson G; Mellinghoff IK; Mischel PS; Phelps M; Parada LF; Liu X; Sofroniew MV; Eilber FC; Wu H. 2009. PTEN dosage is essential for neurofibroma development and malignant transformation. Proc Natl Acad Sci U S A 106(46):19479-84. [PubMed: 19846776]  [MGI Ref ID J:154673]

Hegedus B; Banerjee D; Yeh TH; Rothermich S; Perry A; Rubin JB; Garbow JR; Gutmann DH. 2008. Preclinical cancer therapy in a mouse model of neurofibromatosis-1 optic glioma. Cancer Res 68(5):1520-8. [PubMed: 18316617]  [MGI Ref ID J:132860]

Hegedus B; Dasgupta B; Shin JE; Emnett RJ; Hart-Mahon EK; Elghazi L; Bernal-Mizrachi E; Gutmann DH. 2007. Neurofibromatosis-1 regulates neuronal and glial cell differentiation from neuroglial progenitors in vivo by both cAMP- and Ras-dependent mechanisms. Cell Stem Cell 1(4):443-57. [PubMed: 18371380]  [MGI Ref ID J:139866]

Hegedus B; Yeh TH; Lee da Y; Emnett RJ; Li J; Gutmann DH. 2008. Neurofibromin regulates somatic growth through the hypothalamic-pituitary axis. Hum Mol Genet 17(19):2956-66. [PubMed: 18614544]  [MGI Ref ID J:138868]

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]

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]

Jessen WJ; Miller SJ; Jousma E; Wu J; Rizvi TA; Brundage ME; Eaves D; Widemann B; Kim MO; Dombi E; Sabo J; Hardiman Dudley A; Niwa-Kawakita M; Page GP; Giovannini M; Aronow BJ; Cripe TP; Ratner N. 2013. MEK inhibition exhibits efficacy in human and mouse neurofibromatosis tumors. J Clin Invest 123(1):340-7. [PubMed: 23221341]  [MGI Ref ID J:194157]

Joseph NM; Mosher JT; Buchstaller J; Snider P; McKeever PE; Lim M; Conway SJ; Parada LF; Zhu Y; Morrison SJ. 2008. The loss of Nf1 transiently promotes self-renewal but not tumorigenesis by neural crest stem cells. Cancer Cell 13(2):129-40. [PubMed: 18242513]  [MGI Ref ID J:131914]

Keng VW; Rahrmann EP; Watson AL; Tschida BR; Moertel CL; Jessen WJ; Rizvi TA; Collins MH; Ratner N; Largaespada DA. 2012. PTEN and NF1 inactivation in Schwann cells produces a severe phenotype in the peripheral nervous system that promotes the development and malignant progression of peripheral nerve sheath tumors. Cancer Res 72(13):3405-13. [PubMed: 22700876]  [MGI Ref ID J:189280]

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]

Kolanczyk M; Kossler N; Kuhnisch J; Lavitas L; Stricker S; Wilkening U; Manjubala I; Fratzl P; Sporle R; Herrmann BG; Parada LF; Kornak U; Mundlos S. 2007. Multiple roles for neurofibromin in skeletal development and growth. Hum Mol Genet 16(8):874-86. [PubMed: 17317783]  [MGI Ref ID J:121700]

Kossler N; Stricker S; Rodelsperger C; Robinson PN; Kim J; Dietrich C; Osswald M; Kuhnisch J; Stevenson DA; Braun T; Mundlos S; Kolanczyk M. 2011. Neurofibromin (Nf1) is required for skeletal muscle development. Hum Mol Genet 20(14):2697-709. [PubMed: 21478499]  [MGI Ref ID J:173779]

Kuhnisch J; Seto J; Lange C; Schrof S; Stumpp S; Kobus K; Grohmann J; Kossler N; Varga P; Osswald M; Emmerich D; Tinschert S; Thielemann F; Duda G; Seifert W; El Khassawna T; Stevenson DA; Elefteriou F; Kornak U; Raum K; Fratzl P; Mundlos S; Kolanczyk M. 2014. Multiscale, converging defects of macro-porosity, microstructure and matrix mineralization impact long bone fragility in NF1. PLoS One 9(1):e86115. [PubMed: 24465906]  [MGI Ref ID J:212331]

Kwon CH; Zhao D; Chen J; Alcantara S; Li Y; Burns DK; Mason RP; Lee EY; Wu H; Parada LF. 2008. Pten haploinsufficiency accelerates formation of high-grade astrocytomas. Cancer Res 68(9):3286-94. [PubMed: 18451155]  [MGI Ref ID J:134611]

Lasater EA; Li F; Bessler WK; Estes ML; Vemula S; Hingtgen CM; Dinauer MC; Kapur R; Conway SJ; Ingram DA Jr. 2010. Genetic and cellular evidence of vascular inflammation in neurofibromin-deficient mice and humans. J Clin Invest 120(3):859-70. [PubMed: 20160346]  [MGI Ref ID J:158570]

Lauchle JO; Kim D; Le DT; Akagi K; Crone M; Krisman K; Warner K; Bonifas JM; Li Q; Coakley KM; Diaz-Flores E; Gorman M; Przybranowski S; Tran M; Kogan SC; Roose JP; Copeland NG; Jenkins NA; Parada L; Wolff L; Sebolt-Leopold J; Shannon K. 2009. Response and resistance to MEK inhibition in leukaemias initiated by hyperactive Ras. Nature 461(7262):411-4. [PubMed: 19727076]  [MGI Ref ID J:152381]

Le DT; Kong N; Zhu Y; Lauchle JO; Aiyigari A; Braun BS; Wang E; Kogan SC; Le Beau MM; Parada L; Shannon KM. 2004. Somatic inactivation of Nf1 in hematopoietic cells results in a progressive myeloproliferative disorder. Blood 103(11):4243-50. [PubMed: 14982883]  [MGI Ref ID J:90973]

Le LQ; Liu C; Shipman T; Chen Z; Suter U; Parada LF. 2011. Susceptible Stages in Schwann Cells for NF1-Associated Plexiform Neurofibroma Development. Cancer Res 71(13):4686-95. [PubMed: 21551250]  [MGI Ref ID J:173624]

Le LQ; Shipman T; Burns DK; Parada LF. 2009. Cell of origin and microenvironment contribution for NF1-associated dermal neurofibromas. Cell Stem Cell 4(5):453-63. [PubMed: 19427294]  [MGI Ref ID J:149832]

Lee da Y; Gianino SM; Gutmann DH. 2012. Innate neural stem cell heterogeneity determines the patterning of glioma formation in children. Cancer Cell 22(1):131-8. [PubMed: 22789544]  [MGI Ref ID J:191011]

Lee da Y; Yeh TH; Emnett RJ; White CR; Gutmann DH. 2010. Neurofibromatosis-1 regulates neuroglial progenitor proliferation and glial differentiation in a brain region-specific manner. Genes Dev 24(20):2317-29. [PubMed: 20876733]  [MGI Ref ID J:164880]

Li Y; Li Y; McKay RM; Riethmacher D; Parada LF. 2012. Neurofibromin modulates adult hippocampal neurogenesis and behavioral effects of antidepressants. J Neurosci 32(10):3529-39. [PubMed: 22399775]  [MGI Ref ID J:182728]

Li YJ; Takizawa H; Azuma A; Kohyama T; Yamauchi Y; Takahashi S; Yamamoto M; Kawada T; Kudoh S; Sugawara I. 2008. Disruption of Nrf2 enhances susceptibility to airway inflammatory responses induced by low-dose diesel exhaust particles in mice. Clin Immunol 128(3):366-73. [PubMed: 18614404]  [MGI Ref ID J:138869]

Lin L; Chen J; Richardson JA; Parada LF. 2009. Mice lacking neurofibromin develop gastric hyperplasia. Am J Physiol Gastrointest Liver Physiol 297(4):G751-61. [PubMed: 19661150]  [MGI Ref ID J:209264]

Lush ME; Li Y; Kwon CH; Chen J; Parada LF. 2008. Neurofibromin is required for barrel formation in the mouse somatosensory cortex. J Neurosci 28(7):1580-7. [PubMed: 18272679]  [MGI Ref ID J:132220]

Maertens O; Johnson B; Hollstein P; Frederick DT; Cooper ZA; Messiaen L; Bronson RT; McMahon M; Granter S; Flaherty K; Wargo JA; Marais R; Cichowski K. 2013. Elucidating distinct roles for NF1 in melanomagenesis. Cancer Discov 3(3):338-49. [PubMed: 23171796]  [MGI Ref ID J:198252]

Mayes DA; Rizvi TA; Cancelas JA; Kolasinski NT; Ciraolo GM; Stemmer-Rachamimov AO; Ratner N. 2011. Perinatal or Adult Nf1 Inactivation Using Tamoxifen-Inducible PlpCre Each Cause Neurofibroma Formation. Cancer Res 71(13):4675-85. [PubMed: 21551249]  [MGI Ref ID J:173625]

Mo W; Chen J; Patel A; Zhang L; Chau V; Li Y; Cho W; Lim K; Xu J; Lazar AJ; Creighton CJ; Bolshakov S; McKay RM; Lev D; Le LQ; Parada LF. 2013. CXCR4/CXCL12 Mediate Autocrine Cell- Cycle Progression in NF1-Associated Malignant Peripheral Nerve Sheath Tumors. Cell 152(5):1077-90. [PubMed: 23434321]  [MGI Ref ID J:193957]

Oliver JA; Lapinski PE; Lubeck BA; Turner JS; Parada LF; Zhu Y; King PD. 2013. The Ras GTPase-activating protein neurofibromin 1 promotes the positive selection of thymocytes. Mol Immunol 55(3-4):292-302. [PubMed: 23522726]  [MGI Ref ID J:202145]

Ono K; Karolak MR; Ndong Jde L; Wang W; Yang X; Elefteriou F. 2013. The Ras-GTPase activity of neurofibromin restrains ERK-dependent FGFR signaling during endochondral bone formation. Hum Mol Genet 22(15):3048-62. [PubMed: 23571107]  [MGI Ref ID J:198529]

Parrinello S; Noon LA; Harrisingh MC; Digby PW; Rosenberg LH; Cremona CA; Echave P; Flanagan AM; Parada LF; Lloyd AC. 2008. NF1 loss disrupts Schwann cell-axonal interactions: a novel role for semaphorin 4F. Genes Dev 22(23):3335-48. [PubMed: 19056885]  [MGI Ref ID J:142040]

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]

Prada CE; Jousma E; Rizvi TA; Wu J; Dunn RS; Mayes DA; Cancelas JA; Dombi E; Kim MO; West BL; Bollag G; Ratner N. 2013. Neurofibroma-associated macrophages play roles in tumor growth and response to pharmacological inhibition. Acta Neuropathol 125(1):159-68. [PubMed: 23099891]  [MGI Ref ID J:211760]

Price RL; Song J; Bingmer K; Kim TH; Yi JY; Nowicki MO; Mo X; Hollon T; Murnan E; Alvarez-Breckenridge C; Fernandez S; Kaur B; Rivera A; Oglesbee M; Cook C; Chiocca EA; Kwon CH. 2013. Cytomegalovirus contributes to glioblastoma in the context of tumor suppressor mutations. Cancer Res 73(11):3441-50. [PubMed: 23729642]  [MGI Ref ID J:199096]

Ribeiro S; Napoli I; White IJ; Parrinello S; Flanagan AM; Suter U; Parada LF; Lloyd AC. 2013. Injury signals cooperate with Nf1 loss to relieve the tumor-suppressive environment of adult peripheral nerve. Cell Rep 5(1):126-36. [PubMed: 24075988]  [MGI Ref ID J:203786]

Romero MI; Lin L; Lush ME; Lei L; Parada LF; Zhu Y. 2007. Deletion of Nf1 in neurons induces increased axon collateral branching after dorsal root injury. J Neurosci 27(8):2124-34. [PubMed: 17314307]  [MGI Ref ID J:118374]

Sharma R; Wu X; Rhodes SD; Chen S; He Y; Yuan J; Li J; Yang X; Li X; Jiang L; Kim ET; Stevenson DA; Viskochil D; Xu M; Yang FC. 2013. Hyperactive Ras/MAPK signaling is critical for tibial nonunion fracture in neurofibromin-deficient mice. Hum Mol Genet 22(23):4818-28. [PubMed: 23863460]  [MGI Ref ID J:202235]

Shilyansky C; Karlsgodt KH; Cummings DM; Sidiropoulou K; Hardt M; James AS; Ehninger D; Bearden CE; Poirazi P; Jentsch JD; Cannon TD; Levine MS; Silva AJ. 2010. Neurofibromin regulates corticostriatal inhibitory networks during working memory performance. Proc Natl Acad Sci U S A 107(29):13141-6. [PubMed: 20624961]  [MGI Ref ID J:162376]

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]

Stansfield BK; Bessler WK; Mali R; Mund JA; Downing B; Li F; Sarchet KN; Distasi MR; Conway SJ; Kapur R; Ingram DA Jr. 2013. Heterozygous inactivation of the Nf1 gene in myeloid cells enhances neointima formation via a rosuvastatin-sensitive cellular pathway. Hum Mol Genet 22(5):977-88. [PubMed: 23197650]  [MGI Ref ID J:192569]

Staser K; Park SJ; Rhodes SD; Zeng Y; He YZ; Shew MA; Gehlhausen JR; Cerabona D; Menon K; Chen S; Sun Z; Yuan J; Ingram DA; Nalepa G; Yang FC; Clapp DW. 2013. Normal hematopoiesis and neurofibromin-deficient myeloproliferative disease require Erk. J Clin Invest 123(1):329-34. [PubMed: 23221339]  [MGI Ref ID J:194159]

Su W; Xing R; Guha A; Gutmann DH; Sherman LS. 2007. Mice with GFAP-targeted loss of neurofibromin demonstrate increased axonal MET expression with aging. Glia 55(7):723-33. [PubMed: 17348023]  [MGI Ref ID J:156097]

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]

Tan M; Zhao Y; Kim SJ; Liu M; Jia L; Saunders TL; Zhu Y; Sun Y. 2011. SAG/RBX2/ROC2 E3 Ubiquitin Ligase Is Essential for Vascular and Neural Development by Targeting NF1 for Degradation. Dev Cell 21(6):1062-76. [PubMed: 22118770]  [MGI Ref ID J:178926]

Wang W; Nyman JS; Moss HE; Gutierrez G; Mundy GR; Yang X; Elefteriou F. 2010. Local low-dose lovastatin delivery improves the bone-healing defect caused by Nf1 loss of function in osteoblasts. J Bone Miner Res 25(7):1658-67. [PubMed: 20200958]  [MGI Ref ID J:183363]

Wang W; Nyman JS; Ono K; Stevenson DA; Yang X; Elefteriou F. 2011. Mice lacking Nf1 in osteochondroprogenitor cells display skeletal dysplasia similar to patients with neurofibromatosis type I. Hum Mol Genet 20(20):3910-24. [PubMed: 21757497]  [MGI Ref ID J:175684]

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]

Wong JC; Zhang Y; Lieuw KH; Tran MT; Forgo E; Weinfurtner K; Alzamora P; Kogan SC; Akagi K; Wolff L; Le Beau MM; Killeen N; Shannon K. 2010. Use of chromosome engineering to model a segmental deletion of chromosome band 7q22 found in myeloid malignancies. Blood 115(22):4524-32. [PubMed: 20233966]  [MGI Ref ID J:161558]

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; Patmore DM; Jousma E; Eaves DW; Breving K; Patel AV; Schwartz EB; Fuchs JR; Cripe TP; Stemmer-Rachamimov AO; Ratner N. 2014. EGFR-STAT3 signaling promotes formation of malignant peripheral nerve sheath tumors. Oncogene 33(2):173-80. [PubMed: 23318430]  [MGI Ref ID J:204875]

Wu J; Williams JP; Rizvi TA; Kordich JJ; Witte D; Meijer D; Stemmer-Rachamimov AO; Cancelas JA; Ratner N. 2008. Plexiform and dermal neurofibromas and pigmentation are caused by Nf1 loss in desert hedgehog-expressing cells. Cancer Cell 13(2):105-16. [PubMed: 18242511]  [MGI Ref ID J:131916]

Xu J; Ismat FA; Wang T; Lu MM; Antonucci N; Epstein JA. 2009. Cardiomyocyte-specific loss of neurofibromin promotes cardiac hypertrophy and dysfunction. Circ Res 105(3):304-11. [PubMed: 19574548]  [MGI Ref ID J:164937]

Xu J; Ismat FA; Wang T; Yang J; Epstein JA. 2007. NF1 regulates a Ras-dependent vascular smooth muscle proliferative injury response. Circulation 116(19):2148-56. [PubMed: 17967772]  [MGI Ref ID J:142994]

Yeh TH; Lee da Y; Gianino SM; Gutmann DH. 2009. Microarray analyses reveal regional astrocyte heterogeneity with implications for neurofibromatosis type 1 (NF1)-regulated glial proliferation. Glia 57(11):1239-49. [PubMed: 19191334]  [MGI Ref ID J:156205]

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]

Zhang W; Rhodes SD; Zhao L; He Y; Zhang Y; Shen Y; Yang D; Wu X; Li X; Yang X; Park SJ; Chen S; Turner C; Yang FC. 2011. Primary osteopathy of vertebrae in a neurofibromatosis type 1 murine model. Bone 48(6):1378-87. [PubMed: 21439418]  [MGI Ref ID J:172512]

Zheng H; Chang L; Patel N; Yang J; Lowe L; Burns DK; Zhu Y. 2008. Induction of abnormal proliferation by nonmyelinating schwann cells triggers neurofibroma formation. Cancer Cell 13(2):117-28. [PubMed: 18242512]  [MGI Ref ID J:131915]

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; Guignard F; Zhao D; Liu L; Burns DK; Mason RP; Messing A; Parada LF. 2005. Early inactivation of p53 tumor suppressor gene cooperating with NF1 loss induces malignant astrocytoma. Cancer Cell 8(2):119-30. [PubMed: 16098465]  [MGI Ref ID J:101868]

Zhu Y; Harada T; Liu L; Lush ME; Guignard F; Harada C; Burns DK; Bajenaru ML; Gutmann DH; Parada LF. 2005. Inactivation of NF1 in CNS causes increased glial progenitor proliferation and optic glioma formation. Development 132(24):5577-88. [PubMed: 16314489]  [MGI Ref ID J:104342]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX12

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice can be bred as homozygotes.
Mating SystemHomozygote x Homozygote         (Female x Male)   15-JUL-13

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $232.00Female or MaleHomozygous for Nf1tm1Par  
Price per Pair (US dollars $)Pair Genotype
$464.00Homozygous for Nf1tm1Par x Homozygous for Nf1tm1Par  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $301.60Female or MaleHomozygous for Nf1tm1Par  
Price per Pair (US dollars $)Pair Genotype
$603.20Homozygous for Nf1tm1Par x Homozygous for Nf1tm1Par  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   101045 B6129SF2/J (approximate)
   000664 C57BL/6J (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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JAX® Mice
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Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

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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