Overview

Also Known As:Nf1flox

These Nf1^flox 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.

Donating Investigator

Luis F Parada, UT Southwestern Medical Center

Genetic overview

Genetic Background	Generation

Nf1^tm1Par

Allele Type	Gene Symbol	Gene Name
Targeted (Conditional ready (e.g. floxed), No functional change)	Nf1	neurofibromin 1

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Research Applications

Neurobiology Research
Research Tools
Mouse/Human Gene Homologs
Cancer Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed 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 Nf1^tm1Par allele.

Control Suggestions

Approximate Controls

Additional Information

Considerations for Choosing Controls

Selected References

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):209-21PubMed: 21737130 MGI: 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):859-76PubMed: 11297510 MGI: J:68558

View All References

Genetics

Nf1^tm1Par

Allele Symbol: Nf1^tm1Par

Allele Name	targeted mutation 1, Luis F Parada
Allele Type	Targeted (Conditional ready (e.g. floxed), No functional change)
Allele Synonym(s)	Nf1^flox; Nf1flox
Gene Symbol and Name	Nf1, neurofibromin 1
Gene Synonym(s)
Site of Expression	When 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.
Strain of Origin	(129X1/SvJ x 129S1/Sv)F1-Kitl⁺
Chromosome	11
Molecular Note	A loxP-neomycin selection cassette was inserted into intron 30 and a single loxP site was inserted into intron 32.
Mutations Made By	Steven McKinnon, UT Southwestern Medical Center

Disease/Phenotype

Disease Terms

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).

Research Areas By Phenotype

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

Neurobiology Research
- Cre-lox System
  - loxP-flanked Sequences
Research Tools
- Cre-lox System
  - loxP-flanked Sequences
Mouse/Human Gene Homologs
- Neurofibromatosis Type I
Cancer Research
- Increased Tumor Incidence
  - Other Tissues/Organs: brain

Mammalian Phenotype Terms by Genotype

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

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Syn1-cre)671Jxm/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

behavior/neurological phenotype

abnormal learning/memory/conditioning
- mice display severe learning disability

growth/size/body region phenotype

decreased body weight
- body weight and size are about 50% of normal

postnatal growth retardation
- 3-4 days after birth, mice begin to exhibit growth retardation that is sustained into adulthood

mammalian phenotype

neoplasm
- Normal - no evidence of tumors; optic gliomas, astrocytomas, or neurofibroma are not observed

nervous system phenotype

abnormal cerebral cortex morphology
- increase in cell density in the cerebral cortex, often resulting in less apparent lamination

astrocytosis
- mice display astrogliosis in various brain regions, however do not develop neuronal degeneration or microgliosis

decreased forebrain size
- forebrain, but not the rest of the brain, is reduced in size, however mice exhibit normal neuronal development

thin cerebral cortex
- about 20% reduction in coritcal thickness

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

cardiovascular system phenotype

double outlet right ventricle
- seen in 8 of 11 embryos

increased atrioventricular cushion size
- 8 of 11 embryos show an enlarged atrioventricular cushion

pericardial effusion

thin myocardium
- 8 of 11 embryos exhibit a thinned myocardium

thin myocardium compact layer

ventricular septal defect
- 10 of 11 embryos exhibit ventricular septal defects

homeostasis/metabolism phenotype

pericardial effusion

muscle phenotype

thin myocardium
- 8 of 11 embryos exhibit a thinned myocardium

thin myocardium compact layer

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Gfap-cre)77.6Mvs/0
involves: 129S1/Sv * 129X1/SvJ * BALB/c * C57BL/6NHsd

mammalian phenotype

neoplasm
- Normal - mutants do not develop tumors

Genotype: Nf1^tm1Par/Nf1^tm1Par
involves: 129S1/Sv * 129X1/SvJ

nervous system phenotype

abnormal astrocyte physiology
- astrocytes transfected with a cre-expresing adenovirus exhibit increased proliferation compared to in control cells

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Prrx1-cre)1Cjt/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL/J

cellular phenotype

abnormal myoblast differentiation
- maker analysis indicates a severe disruption of myoblast terminal differentiation

increased myoblast proliferation
- 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

growth/size/body region phenotype

decreased body weight
- weight is on average reduced by 25%

limbs/digits/tail phenotype

short limbs
- short-limbed dwarfism, with mutants showing a reduction in entire limb size

muscle phenotype

abnormal muscle development
- distal muscle groups in the extremities are most affected, with some muscles completely missing, indicating that the muscle differentiation process is disturbed
- 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
- the m. latissimus dorsi appears smaller and shows rarefaction of muscle fibers

abnormal muscle fiber morphology
- muscle fiber size appears more variable than in controls, however no overt muscle regeneration is seen
- muscles show a 20% increase in the number of fibers with cleft-like invaginations (split fibers)

abnormal muscle morphology
- large areas of dystrophic musculature are occupied by fat tissue
- muscle connective tissue shows increased proliferation at E14.5 and an increase in connective tissue in muscles is already seen at E16.5
- muscle fibers are thinned out at E16.5
- mutants exhibit muscle dystrophy

abnormal muscle physiology
- in the force gauge pull test, mice show a dramatic reduction in muscle force
- satellite cells exhibit normal self-renewal but impaired differentiation as indicated by diminished myotube formatio

abnormal myoblast differentiation
- maker analysis indicates a severe disruption of myoblast terminal differentiation

abnormal myogenesis
- defect in myogenesis affecting the terminal differentiation of myoblasts between E12.5 and E14.5

decreased muscle weight
- weight of triceps muscle is reduced by more than 50%

decreased skeletal muscle fiber number
- total number of muscle fibers is reduced by 50% in the triceps

decreased skeletal muscle mass
- reduction in muscle size and mass

increased myoblast proliferation
- 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

skeletal muscle fibrosis
- generalized muscle fibrosis, characterized by expansion of collagen-rich connective tissue, and reduction in total number of muscle fibers

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Prrx1-cre)1Cjt/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * C57BL/6N * SJL/J

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

homeostasis/metabolism phenotype

abnormal bone healing
- accumulation and persistence of fibrous tissue in the fracture gap, with increased numbers of osteoclasts
- ectopic fat tissue is seen in the fracture site
- hat bony bridging is not observed
- 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
- 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
- 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

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

skeleton phenotype

abnormal bone healing
- accumulation and persistence of fibrous tissue in the fracture gap, with increased numbers of osteoclasts
- ectopic fat tissue is seen in the fracture site
- hat bony bridging is not observed
- 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
- 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
- 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

abnormal cartilage morphology
- bone fractures exhibit impaired cartilage formation and increased periosteal ossification at the cortices

abnormal endochondral bone ossification
- endochondrial formation is impaired following fracture but periosteal bone formation is enhanced

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

abnormal osteoid morphology
- presence of large areas of non-mineralized osteoid in the fracture gap, indicating decreased mineralization of the extracellular matrix

decreased bone mineral density
- decrease of regenerative tissue bone mineral density following fracture

fragile skeleton
- bones are weaker; femora show lower torsional stiffness and ultimate torque at failure compared to controls
- fractured bones of mutants that are allowed to heal also exhibit a lower torsional stiffness and ultimate torque at failure compared to controls

increased compact bone volume
- dramatic cortical bone thickening following fracture

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

increased osteoid thickness
- thickening of the osteoid layer in the periosteal region following fracture

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Mx1-cre)1Cgn/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

behavior/neurological phenotype

abnormal gait
- pIpC injected mice at 3 to 5 days of age exhibit hunching by 5-6 months of age

hunched posture
- pIpC injected mice at 3 to 5 days of age exhibit abnormal gait by 5-6 months of age

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

abnormal myelopoiesis
- spleen from pIpC injected mice shows a massive increase in myelopoiesis

abnormal spleen morphology
- spleens from pIpC injected mice contain large numbers of CFU-GM

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

increased granulocyte number
- pIpC injected mice show an increase in numbers of differentiated granulocytic cells

increased leukocyte cell number
- cultures from pIpC injected mice show an increase in the percentage of monocyte-macrophage cells
- pIpC injected mice at 3 to 5 days of age exhibit elevated leukocyte counts by 3 months of age

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

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
- pIpC injected mice show an increase in numbers of immature monocytic cells in the bone marrow

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

growth/size/body region phenotype

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

integument phenotype

disheveled coat
- pIpC injected mice at 3 to 5 days of age have a disheveled appearance by 5-6 months of age

mortality/aging

premature death
- 50% of pIpC treated mice die by 7.5 months of age

hematopoietic system phenotype

abnormal bone marrow cell morphology/development
- apoptosis is reduced in the bone marrow of pIpC injected mice
- 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
- bone marrow from pIpC injected mice is highly cellular, comprised of myeloid cells at various stages of differentiation
- increase in numbers of immature monocytic cells in the bone marrow of pIpC treated mice
- mal spreading morphology

abnormal common myeloid progenitor cell morphology
- myeloid progenitors from pIpC injected mice show increased proliferation

abnormal definitive 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
- pIpC injected mice show a shift in hematopoiesis from the marrow to the spleen

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

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

abnormal myelopoiesis
- spleen from pIpC injected mice shows a massive increase in myelopoiesis

abnormal spleen morphology
- spleens from pIpC injected mice contain large numbers of CFU-GM

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

increased granulocyte number
- pIpC injected mice show an increase in numbers of differentiated granulocytic cells

increased leukocyte cell number
- cultures from pIpC injected mice show an increase in the percentage of monocyte-macrophage cells
- pIpC injected mice at 3 to 5 days of age exhibit elevated leukocyte counts by 3 months of age

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

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
- pIpC injected mice show an increase in numbers of immature monocytic cells in the bone marrow

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

References

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):209-21PubMed: 21737130 MGI: 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):859-76PubMed: 11297510 MGI: J:68558

Additional - Nf1^tm1Par related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Separated MCA:Nf1
- Separated PCR:Nf1
- Genotyping resources and troubleshooting
Breeding Considerations

When maintaining a live colony, these mice can be bred as homozygotes.
- Additional Breeding and Husbandry Support
Citation
When using the Nf1flox mouse strain in a publication, please cite the originating article(s) and include JAX stock #017639 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous for Nf1<tm1Par>

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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.

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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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General Terms and Conditions

Questions about Terms of Use

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Licensing Information

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Also Known As:Nf1flox

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Nf1tm1Par

Allele Symbol: Nf1tm1Par

Disease Terms

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).

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Nf1tm1Par/Nf1tm1Par Tg(Syn1-cre)671Jxm/0involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

behavior/neurological phenotype

growth/size/body region phenotype

mammalian phenotype

nervous system phenotype

Genotype: Nf1tm1Par/Nf1tm1Par Tg(Tek-cre)1Ywa/0involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

cardiovascular system phenotype

homeostasis/metabolism phenotype

muscle phenotype

Genotype: Nf1tm1Par/Nf1tm1Par Tg(Gfap-cre)77.6Mvs/0involves: 129S1/Sv * 129X1/SvJ * BALB/c * C57BL/6NHsd

mammalian phenotype

Genotype: Nf1tm1Par/Nf1tm1Parinvolves: 129S1/Sv * 129X1/SvJ

nervous system phenotype

Genotype: Nf1tm1Par/Nf1tm1Par Tg(Prrx1-cre)1Cjt/0involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL/J

cellular phenotype

growth/size/body region phenotype

limbs/digits/tail phenotype

muscle phenotype

Genotype: Nf1tm1Par/Nf1tm1Par Tg(Prrx1-cre)1Cjt/0involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * C57BL/6N * SJL/J

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

skeleton phenotype

Genotype: Nf1tm1Par/Nf1tm1Par Tg(Mx1-cre)1Cgn/0involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

behavior/neurological phenotype

immune system phenotype

growth/size/body region phenotype

integument phenotype

mortality/aging

hematopoietic system phenotype

References

Additional - Nf1tm1Par related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Nf1^tm1Par

Allele Symbol: Nf1^tm1Par

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Syn1-cre)671Jxm/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Gfap-cre)77.6Mvs/0
involves: 129S1/Sv * 129X1/SvJ * BALB/c * C57BL/6NHsd

Genotype: Nf1^tm1Par/Nf1^tm1Par
involves: 129S1/Sv * 129X1/SvJ

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Prrx1-cre)1Cjt/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL/J

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Prrx1-cre)1Cjt/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * C57BL/6N * SJL/J

Genotype: Nf1^tm1Par/Nf1^tm1Par Tg(Mx1-cre)1Cgn/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Additional - Nf1^tm1Par related