Strain Name:

B6;129S2-Trp53tm1Tyj Nf1tm1Tyj/J

Stock Number:


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These mice carry Trp53 and Nf1 targeted mutations on the same homolog of chromosome 11 (in cis). These mutations are approximately 10 Mbp apart and may segregate independently of one another. Double heterozygotes survive an average of five months and exhibit a significant increase in the percentage of soft tissue sarcomas. About 30% of tumors from the Nf1/Trp53 cis animals stain positively for S100 (consistent with glial cell origin) and exhibit classic histological features of malignant peripheral nerve sheath tumors (MPNSTs). This strain may be useful in studies of astrocytomas/glioblastomas and tumor suppressor genes.


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 Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
Generation Definitions
Donating InvestigatorDr. Tyler Jacks,   Massachusetts Institute of Technology

These mice carry Trp53 and Nf1 targeted mutations (in cis) on chromosome 11. These mutations are approximately 10 Mbp apart and may segregate independently of one another. Double homozygotes are embryonic lethal. Double heterozygotes survive an average of five months and exhibit a significant increase in the percentage of soft tissue sarcomas compared with mice of other genotypes (Nf1 +/-, 5%; p53, 57%; Nf1/Trp53 trans, 36%; Nf1/Trp53 cis, 81%). Furthermore, although Nf1/Trp53 trans mice exclusively develop osteo-, fibro-, rhabdomyo-, and hemangiosarcomas, about 30% of tumors from the Nf1/Trp53 cis animals stain positively for S100 (consistent with glial cell origin) and exhibit classic histological features of malignant peripheral nerve sheath tumors (MPNSTs). This strain may be useful in studies of astrocytomas/glioblastomas and tumor suppressor genes.

These mice carry two independently-created targeted mutations, Trp53tm1Tjy and Nf1tm1Tyj, that are approximately 10 Mbp apart on the same homolog of chromosome 11 (in cis). To create the Trp53 mutation, a targeting vector was designed to replace approximately 40% of the coding sequences (involving exons 2-6) with a neomycin resistance cassette. To create the Nf1 mutation, a targeting vector was designed to insert a neomycin resistance cassette and delete the first 42 codons of exon 31, the exon 31 splice acceptor site, and approximately 2 kb of intron 30. Each of the targeting vectors was independently electroporated into 129S2/SvPas-derived D3 embryonic stem (ES) cells. Independent strains carrying germline mutations in Trp53 and Nf1 were generated on a mixed 129S2/SvPas and C57BL/6 genetic background, and then then intercrossed. Mice that underwent meiotic recombination events placing both mutations on the same homolog of chromosome 11 (in cis) were selected. This double mutant strain was maintained on a mixed 129S2/SvPas and C57BL/6 genetic background by the donating laboratory prior to sending to The Jackson Laboratory Repository. Upon arrival, males that were heterozygous for both mutations were identified and used to cryopreserve sperm.

Related Strains

Strains carrying   Nf1tm1Tyj allele
008192   B6.129S2-Nf1tm1Tyj/J
View Strains carrying   Nf1tm1Tyj     (1 strain)

View Strains carrying   Trp53tm1Tyj     (7 strains)

Strains carrying other alleles of Nf1
017640   B6.129(Cg)-Nf1tm1Par/J
007923   B6.129S1-Nf1tm1Cbr/J
002646   B6.129S6-Nf1tm1Fcr/J
017530   STOCK Igs2tm2(ACTB-tdTomato,-EGFP)Luo Trp53tm1Tyj Nf1tm1Par/J
017639   STOCK Nf1tm1Par/J
View Strains carrying other alleles of Nf1     (5 strains)

View Strains carrying other alleles of Trp53     (19 strains)


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.
Adrenocortical Carcinoma, Hereditary; ADCC   (TP53)
Basal Cell Carcinoma, Susceptibility to, 7; BCC7   (TP53)
Breast Cancer   (TP53)
Colorectal Cancer; CRC   (TP53)
Glioma Susceptibility 1; GLM1   (TP53)
Hepatocellular Carcinoma   (TP53)
Juvenile Myelomonocytic Leukemia; JMML   (NF1)
Li-Fraumeni Syndrome 1; LFS1   (TP53)
Nasopharyngeal Carcinoma   (TP53)
Neurofibromatosis, Familial Spinal   (NF1)
Neurofibromatosis-Noonan Syndrome; NFNS   (NF1)
Osteogenic Sarcoma   (TP53)
Pancreatic Cancer   (TP53)
Papilloma of Choroid Plexus; CPP   (TP53)
Watson Syndrome   (NF1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Nf1tm1Tyj/Nf1+ Trp53tm1Tyj/Trp53+

        involves: 129/Sv * C57BL/6
  • mortality/aging
  • premature death
    • cis-double heterozygotes die by 5 months of age and trans-double heterozygotes survive to the average age of 10 months   (MGI Ref ID J:58876)
  • tumorigenesis
  • increased tumor incidence
    • cis-double heterozygotes exhibit greater incidence of tumors than trans-double heterozygotes   (MGI Ref ID J:58876)
    • increased sarcoma incidence
      • developed in both cis- and trans-double heterozygotes   (MGI Ref ID J:58876)
      • sarcomas in trans-double heterozygotes were similar to those found in mice with either single mutation and were usually correlated with loss of one chromosome   (MGI Ref ID J:58876)
      • increased neurofibrosarcoma incidence
        • develop in cis-double heterozygotes, usually correlated with loss of one chromosome   (MGI Ref ID J:58876)

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

Nf1tm1Tyj/Nf1+ Trp53tm1Tyj/Trp53+

        involves: 129S2/SvPas
  • nervous system phenotype
  • *normal* nervous system phenotype
    • neural crest stem cells do not abnormally persist in the peripheral nervous system in adult mice   (MGI Ref ID J:131914)
  • tumorigenesis
  • increased neurofibrosarcoma incidence
    • form by 6 months of age   (MGI Ref ID J:131914)
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
      Other Tissues/Organs: brain
Tumor Suppressor Genes

Developmental Biology Research
Embryonic Lethality (Homozygous)

Trp53tm1Tyj related

Apoptosis Research
Endogenous Regulators

Cancer Research
Increased Tumor Incidence
      Other Tissues/Organs
      Other Tissues/Organs: osteosarcoma
Tumor Suppressor Genes

Immunology, Inflammation and Autoimmunity Research
Intracellular Signaling Molecules

Research Tools
Toxicology Research
      B and T cell deficiency, xenograft transplant host
      drug/compound testing

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol Nf1tm1Tyj
Allele Name targeted mutation 1, Tyler Jacks
Allele Type Targeted (Null/Knockout)
Common Name(s) Nf1-; Nf1n31;
Mutation Made ByDr. Tyler Jacks,   Massachusetts Institute of Technology
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
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:64364)
Molecular Note A neomycin resistance cassette replaced the first 42 codons of exon 31, the exon 31 splice acceptor site, and approximately 2 kb of intron 30. This allele is a null allele; no stable full-length protein is made. [MGI Ref ID J:18542]
Allele Symbol Trp53tm1Tyj
Allele Name targeted mutation 1, Tyler Jacks
Allele Type Targeted (Null/Knockout)
Common Name(s) Trp53-; Trp53KO; p53-; p53delta; p53null; p53KO;
Mutation Made ByDr. Tyler Jacks,   Massachusetts Institute of Technology
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
Gene Symbol and Name Trp53, transformation related protein 53
Chromosome 11
Gene Common Name(s) BCC7; LFS1; P53; p44;
General Note This mutant allele was produced by a targeted neo insertion into the Trp53 locus. Homozygotes show no visible phenotype but develop tumors at 3-6 months of age. Heterozygotes develop tumors at 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome (OMIM 151623), a form of familial breast cancer with mutations in TRP53 (J:16022)(J:16023) A specific human mutation found in hepatocellular carcinomas caused by hepatitis B infection or by aflatoxin exposure has been created in amouse model, resulting in a similar gene product (J:27363).
Phenotypic Similarity to Human Syndrome: Glioblastoma Multiforme (J:149662)
Phenotypic Similarity to Human Syndrome: Astrocytoma (J:64364 and J:134611)
Phenotypic Similarity to Human Syndrome: activated B-cell diffuse large-cell lymphoma in mice hemizygous for Tg(Ly6e-MALT1)#Isg and homozygous for this allele (ABC-DLBCL, J:185590)
Molecular Note A neomycin cassette replaced 40% of the coding sequences beginning with exon 2 (upstream of the translation start site) and extending into exon 6. [MGI Ref ID J:17728]


Genotyping Information

Genotyping Protocols

Trp53tm1Tyj Alternate2, Melt Curve Analysis
Nf1tm1Tyj, Standard PCR

Helpful Links

Genotyping resources and troubleshooting


References provided by MGI

Selected Reference(s)

Reilly KM; Loisel DA; Bronson RT; McLaughlin ME; Jacks T. 2000. Nf1;Trp53 mutant mice develop glioblastoma with evidence of strain-specific effects Nat Genet 26(1):109-13. [PubMed: 10973261]  [MGI Ref ID J:64364]

Additional References

Nf1tm1Tyj related

Amlin-Van Schaick JC; Kim S; DiFabio C; Lee MH; Broman KW; Reilly KM. 2012. Arlm1 is a male-specific modifier of astrocytoma resistance on mouse Chr 12. Neuro Oncol 14(2):160-74. [PubMed: 22234937]  [MGI Ref ID J:186764]

Birnbaum RA; O'Marcaigh A; Wardak Z; Zhang YY; Dranoff G; Jacks T; Clapp DW; Shannon KM. 2000. Nf1 and Gmcsf interact in myeloid leukemogenesis. Mol Cell 5(1):189-95. [PubMed: 10678181]  [MGI Ref ID J:60155]

Boyanapalli M; Lahoud OB; Messiaen L; Kim B; Anderle de Sylor MS; Duckett SJ; Somara S; Mikol DD. 2006. Neurofibromin binds to caveolin-1 and regulates ras, FAK, and Akt. Biochem Biophys Res Commun 340(4):1200-8. [PubMed: 16405917]  [MGI Ref ID J:104986]

Buchstaller J; McKeever PE; Morrison SJ. 2012. Tumorigenic Cells Are Common in Mouse MPNSTs but Their Frequency Depends upon Tumor Genotype and Assay Conditions. Cancer Cell 21(2):240-52. [PubMed: 22340596]  [MGI Ref ID J:181460]

Carbe C; Zhang X. 2011. Lens induction requires attenuation of ERK signaling by Nf1. Hum Mol Genet 20(7):1315-23. [PubMed: 21233129]  [MGI Ref ID J:169235]

Chao RC; Pyzel U; Fridlyand J; Kuo YM; Teel L; Haaga J; Borowsky A; Horvai A; Kogan SC; Bonifas J; Huey B; Jacks TE; Albertson DG; Shannon KM. 2005. Therapy-induced malignant neoplasms in Nf1 mutant mice. Cancer Cell 8(4):337-48. [PubMed: 16226708]  [MGI Ref ID J:103509]

Chen S; Burgin S; McDaniel A; Li X; Yuan J; Chen M; Khalaf W; Clapp DW; Yang FC. 2010. Nf1-/- Schwann cell-conditioned medium modulates mast cell degranulation by c-Kit-mediated hyperactivation of phosphatidylinositol 3-kinase. Am J Pathol 177(6):3125-32. [PubMed: 21037083]  [MGI Ref ID J:167633]

Choi G; Huang B; Pinarbasi E; Braunstein SE; Horvai AE; Kogan S; Bhatia S; Faddegon B; Nakamura JL. 2012. Genetically mediated Nf1 loss in mice promotes diverse radiation-induced tumors modeling second malignant neoplasms. Cancer Res 72(24):6425-34. [PubMed: 23071067]  [MGI Ref ID J:193638]

Cichowski K; Shih TS; Schmitt E; Santiago S; Reilly K; McLaughlin ME; Bronson RT; Jacks T. 1999. Mouse models of tumor development in neurofibromatosis type 1. Science 286(5447):2172-6. [PubMed: 10591652]  [MGI Ref ID J:58876]

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]

Dai C; Santagata S; Tang Z; Shi J; Cao J; Kwon H; Bronson RT; Whitesell L; Lindquist S. 2012. Loss of tumor suppressor NF1 activates HSF1 to promote carcinogenesis. J Clin Invest 122(10):3742-54. [PubMed: 22945628]  [MGI Ref ID J:191670]

De Raedt T; Beert E; Pasmant E; Luscan A; Brems H; Ortonne N; Helin K; Hornick JL; Mautner V; Kehrer-Sawatzki H; Clapp W; Bradner J; Vidaud M; Upadhyaya M; Legius E; Cichowski K. 2014. PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies. Nature 514(7521):247-51. [PubMed: 25119042]  [MGI Ref ID J:217077]

De Raedt T; Walton Z; Yecies JL; Li D; Chen Y; Malone CF; Maertens O; Jeong SM; Bronson RT; Lebleu V; Kalluri R; Normant E; Haigis MC; Manning BD; Wong KK; Macleod KF; Cichowski K. 2011. Exploiting cancer cell vulnerabilities to develop a combination therapy for ras-driven tumors. Cancer Cell 20(3):400-13. [PubMed: 21907929]  [MGI Ref ID J:175966]

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]

Duan JH; Hodgdon KE; Hingtgen CM; Nicol GD. 2014. N-type calcium current, Cav2.2, is enhanced in small-diameter sensory neurons isolated from Nf1+/- mice. Neuroscience 270:192-202. [PubMed: 24755485]  [MGI Ref ID J:210619]

Gutmann DH; Winkeler E; Kabbarah O; Hedrick N; Dudley S; Goodfellow PJ; Liskay RM. 2003. Mlh1 deficiency accelerates myeloid leukemogenesis in neurofibromatosis 1 (Nf1) heterozygous mice. Oncogene 22(29):4581-5. [PubMed: 12881715]  [MGI Ref ID J:84658]

Hawes JJ; Tuskan RG; Reilly KM. 2007. Nf1 expression is dependent on strain background: implications for tumor suppressor haploinsufficiency studies. Neurogenetics 8(2):121-30. [PubMed: 17216419]  [MGI Ref ID J:121636]

He Y; Rhodes SD; Chen S; Wu X; Yuan J; Yang X; Jiang L; Li X; Takahashi N; Xu M; Mohammad KS; Guise TA; Yang FC. 2012. c-Fms signaling mediates neurofibromatosis Type-1 osteoclast gain-in-functions. PLoS One 7(11):e46900. [PubMed: 23144792]  [MGI Ref ID J:194861]

Henkemeyer M; Rossi DJ; Holmyard DP; Puri MC; Mbamalu G; Harpal K; Shih TS; Jacks T; Pawson T. 1995. Vascular system defects and neuronal apoptosis in mice lacking ras GTPase-activating protein. Nature 377(6551):695-701. [PubMed: 7477259]  [MGI Ref ID J:29825]

Hiatt K; Ingram DA; Huddleston H; Spandau DF; Kapur R; Clapp DW. 2004. Loss of the nf1 tumor suppressor gene decreases fas antigen expression in myeloid cells. Am J Pathol 164(4):1471-9. [PubMed: 15039234]  [MGI Ref ID J:89131]

Hingtgen CM; Roy SL; Clapp DW. 2006. Stimulus-evoked release of neuropeptides is enhanced in sensory neurons from mice with a heterozygous mutation of the Nf1 gene. Neuroscience 137(2):637-645. [PubMed: 16298082]  [MGI Ref ID J:104588]

Hodgdon KE; Hingtgen CM; Nicol GD. 2012. Dorsal root ganglia isolated from Nf1+/- mice exhibit increased levels of mRNA expression of voltage-dependent sodium channels. Neuroscience 206:237-44. [PubMed: 22260870]  [MGI Ref ID J:184640]

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; Hiatt K; King AJ; Fisher L; Shivakumar R; Derstine C; Wenning MJ; Diaz B; Travers JB; Hood A; Marshall M; Williams DA; Clapp DW. 2001. Hyperactivation of p21(ras) and the hematopoietic-specific Rho GTPase, Rac2, cooperate to alter the proliferation of neurofibromin-deficient mast cells in vivo and in vitro. J Exp Med 194(1):57-69. [PubMed: 11435472]  [MGI Ref ID J:71331]

Ingram DA; Yang FC; Travers JB; Wenning MJ; Hiatt K; New S; Hood A; Shannon K; Williams DA; Clapp DW. 2000. Genetic and biochemical evidence that haploinsufficiency of the Nf1 tumor suppressor gene modulates melanocyte and mast cell fates in vivo. J Exp Med 191(1):181-8. [PubMed: 10620616]  [MGI Ref ID J:59248]

Ingram DA; Zhang L; McCarthy J; Wenning MJ; Fisher L; Yang FC; Clapp DW; Kapur R. 2002. Lymphoproliferative defects in mice lacking the expression of neurofibromin: functional and biochemical consequences of Nf1 deficiency in T-cell development and function. Blood 100(10):3656-62. [PubMed: 12393709]  [MGI Ref ID J:79702]

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]

Johannessen CM; Johnson BW; Williams SM; Chan AW; Reczek EE; Lynch RC; Rioth MJ; McClatchey A; Ryeom S; Cichowski K. 2008. TORC1 is essential for NF1-associated malignancies. Curr Biol 18(1):56-62. [PubMed: 18164202]  [MGI Ref ID J:144615]

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]

Khalaf WF; Yang FC; Chen S; White H; Bessler W; Ingram DA; Clapp DW. 2007. K-ras is critical for modulating multiple c-kit-mediated cellular functions in wild-type and Nf1+/- mast cells. J Immunol 178(4):2527-34. [PubMed: 17277161]  [MGI Ref ID J:143972]

Koenigsmann J; Rudolph C; Sander S; Kershaw O; Gruber AD; Bullinger L; Schlegelberger B; Carstanjen D. 2009. Nf1 haploinsufficiency and Icsbp deficiency synergize in the development of leukemias. Blood 113(19):4690-701. [PubMed: 19228926]  [MGI Ref ID J:148716]

Lakkis MM; Epstein JA. 1998. Neurofibromin modulation of ras activity is required for normal endocardial-mesenchymal transformation in the developing heart. Development 125(22):4359-67. [PubMed: 9778496]  [MGI Ref ID J:50306]

Lakkis MM; Golden JA; O'Shea KS; Epstein JA. 1999. Neurofibromin deficiency in mice causes exencephaly and is a modifier for Splotch neural tube defects. Dev Biol 212(1):80-92. [PubMed: 10419687]  [MGI Ref ID J:56680]

Lasater EA; Bessler WK; Mead LE; Horn WE; Clapp DW; Conway SJ; Ingram DA; Li F. 2008. Nf1+/- mice have increased neointima formation via hyperactivation of a Gleevec sensitive molecular pathway. Hum Mol Genet 17(15):2336-44. [PubMed: 18442999]  [MGI Ref ID J:137662]

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]

Li F; Munchhof AM; White HA; Mead LE; Krier TR; Fenoglio A; Chen S; Wu X; Cai S; Yang FC; Ingram DA. 2006. Neurofibromin is a novel regulator of RAS-induced signals in primary vascular smooth muscle cells. Hum Mol Genet 15(11):1921-30. [PubMed: 16644864]  [MGI Ref ID J:109530]

Li W; Cui Y; Kushner SA; Brown RA; Jentsch JD; Frankland PW; Cannon TD; Silva AJ. 2005. The HMG-CoA reductase inhibitor lovastatin reverses the learning and attention deficits in a mouse model of neurofibromatosis type 1. Curr Biol 15(21):1961-7. [PubMed: 16271875]  [MGI Ref ID J:103691]

Mahgoub N; Taylor BR; Gratiot M; Kohl NE; Gibbs JB; Jacks T; Shannon KM. 1999. In vitro and in vivo effects of a farnesyltransferase inhibitor on Nf1-deficient hematopoietic cells. Blood 94(7):2469-76. [PubMed: 10498620]  [MGI Ref ID J:57842]

Mahgoub N; Taylor BR; Le Beau MM; Gratiot M; Carlson KM; Atwater SK ; Jacks T ; Shannon KM. 1999. Myeloid malignancies induced by alkylating agents in Nf1 mice. Blood 93(11):3617-23. [PubMed: 10339466]  [MGI Ref ID J:55413]

Malone CF; Fromm JA; Maertens O; DeRaedt T; Ingraham R; Cichowski K. 2014. Defining key signaling nodes and therapeutic biomarkers in NF1-mutant cancers. Cancer Discov 4(9):1062-73. [PubMed: 24913553]  [MGI Ref ID J:217840]

Mangues R; Corral T; Lu S; Symmans WF; Liu L; Pellicer A. 1998. NF1 inactivation cooperates with N-ras in in vivo lymphogenesis activating Erk by a mechanism independent of its Ras-GTPase accelerating activity. Oncogene 17(13):1705-16. [PubMed: 9796699]  [MGI Ref ID J:52704]

McDaniel AS; Allen JD; Park SJ; Jaffer ZM; Michels EG; Burgin SJ; Chen S; Bessler WK; Hofmann C; Ingram DA; Chernoff J; Clapp DW. 2008. Pak1 regulates multiple c-Kit mediated Ras-MAPK gain-in-function phenotypes in Nf1+/- mast cells. Blood 112(12):4646-54. [PubMed: 18768391]  [MGI Ref ID J:142439]

Molosh AI; Johnson PL; Spence JP; Arendt D; Federici LM; Bernabe C; Janasik SP; Segu ZM; Khanna R; Goswami C; Zhu W; Park SJ; Li L; Mechref YS; Clapp DW; Shekhar A. 2014. Social learning and amygdala disruptions in Nf1 mice are rescued by blocking p21-activated kinase. Nat Neurosci 17(11):1583-90. [PubMed: 25242307]  [MGI Ref ID J:219424]

Munchhof AM; Li F; White HA; Mead LE; Krier TR; Fenoglio A; Li X; Yuan J; Yang FC; Ingram DA. 2006. Neurofibroma-associated growth factors activate a distinct signaling network to alter the function of neurofibromin-deficient endothelial cells. Hum Mol Genet 15(11):1858-69. [PubMed: 16648142]  [MGI Ref ID J:109532]

Nagasubramanian R; Hansen RJ; Delaney SM; Cherian MM; Samson LD; Kogan SC; Dolan ME. 2008. Survival and tumorigenesis in O6-methylguanine DNA methyltransferase-deficient mice following cyclophosphamide exposure. Mutagenesis 23(5):341-6. [PubMed: 18477655]  [MGI Ref ID J:152129]

Nakamura JL; Phong C; Pinarbasi E; Kogan SC; Vandenberg S; Horvai AE; Faddegon BA; Fiedler D; Shokat K; Houseman BT; Chao R; Pieper RO; Shannon K. 2011. Dose-dependent effects of focal fractionated irradiation on secondary malignant neoplasms in Nf1 mutant mice. Cancer Res 71(1):106-15. [PubMed: 21199799]  [MGI Ref ID J:167772]

Nebesio TD; Ming W; Chen S; Clegg T; Yuan J; Yang Y; Estwick SA; Li Y; Li X; Hingtgen CM; Yang FC. 2007. Neurofibromin-deficient Schwann cells have increased lysophosphatidic acid dependent survival and migration-implications for increased neurofibroma formation during pregnancy. Glia 55(5):527-36. [PubMed: 17236191]  [MGI Ref ID J:156102]

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]

Pemov A; Park C; Reilly KM; Stewart DR. 2010. Evidence of perturbations of cell cycle and DNA repair pathways as a consequence of human and murine NF1-haploinsufficiency. BMC Genomics 11:194. [PubMed: 20307317]  [MGI Ref ID J:159679]

Reilly KM; Broman KW; Bronson RT; Tsang S; Loisel DA; Christy ES; Sun Z; Diehl J; Munroe DJ; Tuskan RG. 2006. An imprinted locus epistatically influences Nstr1 and Nstr2 to control resistance to nerve sheath tumors in a neurofibromatosis type 1 mouse model. Cancer Res 66(1):62-8. [PubMed: 16397217]  [MGI Ref ID J:105038]

Reilly KM; Tuskan RG; Christy E; Loisel DA; Ledger J; Bronson RT; Smith CD; Tsang S; Munroe DJ; Jacks T. 2004. Susceptibility to astrocytoma in mice mutant for Nf1 and Trp53 is linked to chromosome 11 and subject to epigenetic effects. Proc Natl Acad Sci U S A 101(35):13008-13. [PubMed: 15319471]  [MGI Ref ID J:92444]

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]

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]

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]

Silvestre DC; Gil GA; Tomasini N; Bussolino DF; Caputto BL. 2010. Growth of peripheral and central nervous system tumors is supported by cytoplasmic c-Fos in humans and mice. PLoS One 5(3):e9544. [PubMed: 20209053]  [MGI Ref ID J:158701]

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]

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van Oostrom CT; Boeve M; van Den Berg J; de Vries A; Dolle ME; Beems RB; van Kreijl CF; Vijg J; van Steeg H. 1999. Effect of heterozygous loss of p53 on benzo[a]pyrene-induced mutations and tumors in DNA repair-deficient XPA mice. Environ Mol Mutagen 34(2-3):124-30. [PubMed: 10529736]  [MGI Ref ID J:59517]

van de Wetering CI; Knudson CM. 2007. Chromosomal instability and supernumerary centrosomes represent precursor defects in a mouse model of T-cell lymphoma. Cancer Res 67(17):8081-8. [PubMed: 17804719]  [MGI Ref ID J:124884]

van der Pluijm I; Garinis GA; Brandt RM; Gorgels TG; Wijnhoven SW; Diderich KE; de Wit J; Mitchell JR; van Oostrom C; Beems R; Niedernhofer LJ; Velasco S; Friedberg EC; Tanaka K; van Steeg H; Hoeijmakers JH; van der Horst GT. 2006. Impaired genome maintenance suppresses the growth hormone--insulin-like growth factor 1 axis in mice with Cockayne syndrome. PLoS Biol 5(1):e2. [PubMed: 17326724]  [MGI Ref ID J:122013]

Health & husbandry

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

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryThese mice carry Trp53 and Nf1 targeted mutations approximately 10 Mbp apart on the same homolog of chromosome 11 (in cis). When maintained as a live colony, double heterozygotes may be bred. Heterozygotes have shortened lifespans (~5 months) due to tumor formation, however. Double homozygotes are embryonic lethal. If breeding double mutant mice to wildtype mice, the resulting offspring may be segregating for each mutation.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

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


Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2225.00
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 Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2892.50
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.

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

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


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


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.