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| The MADM-TG,p53KO,NF1-flox strain may be used as a genetic mosaicism model for different types of cancers when bred to the companion MADAM strain (Stock No. 013749), and to a Cre recombinase expressing strain. | |||||||||||||||||||
- Description
- Disease & phenotype
- Genes & alleles
- Genotyping
- Health & care
- References
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- Terms of use
Description
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Strain Information
Former Names STOCK Tg(ACTB-tdTomato,-EGFP)11Luo Trp53tm1Tyj Nf1tm1Par/J (Changed: 01-FEB-13 ) STOCK Trp53tm1Tyj Nf1tm1Par Tg(ACTB-tdTomato,-EGFP)11Luo/J (Changed: 07-FEB-12 ) STOCK Nf1tm1Par Trp53tm1Tyj Tg(ACTB-tdTomato,-EGFP)11Luo/J (Changed: 03-FEB-12 ) Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation +pN1
Generation DefinitionsDonating Investigator Hui Zong, University of Oregon Description
Mice that are heterozygous for the Nf1tm1Par Trp53tm1Tyj alleles and homozygous for the Tg(ACTB-tdTomato,-EGFP)11Luo transgene are viable and fertile. The mosaic analysis with double markers (MADM) system (MADAM strains, Stock No. 013751 and Stock No. 013749), plus the Nf1tm1Par Trp53tm1Tyj alleles, coupled with a Cre recombinase expressing strain allows fluorescent labeling and tracking of cancer cells of origin, which are normal cells that acquire the first cancer conducive mutation(s) and initiate tumorigenesis. Cre-mediated inter-chromosomal recombination in the MADAM system generates a small number of cells homozygous for the double reporter and the mutations, mimicking the intermittent loss of heterozygosity of tumor suppressor genes observed in human cancer. The system also labels the mutant daughter cells with Green Fluorescent Protein, while the sibling wildtype cells are labeled with Red Fluorescent Protein. Initially, mutant and wildtype sibling cells are produced in equal numbers. The mutant cell (cell of origin) population expansion can be quantified by the change in ratio of green to red fluorescently labeled cells.When bred to the companion MADAM strain (Stock No. 013749), and to the strain expressing Cre recombinase under the control of the human glial fibrillary acidic protein, GFAP, promoter (Stock No. 004600) the resulting mutant mice are a genetic mosaicism model for glioma.
Development
This triple mutant strain was generated by crossing Stock No. 013751, Stock No. 002101 and mice carrying the Nf1tm1Par targeted mutation.For the Nf1tm1Par targeted mutation, 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 Donating Investigator maintained the triple mutant line on the CD1 background. Upon arrival at The Jackson Laboratory, the triple mutant mice were crossed to (Stock No. 013751) females to establish the colony.
Control Information
| Control | ||
|---|---|---|
| None Available | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying Iis2tm2(ACTB-tdTomato,-EGFP)Luo allele
013751 STOCK Iis2tm2(ACTB-tdTomato,-EGFP)Luo/J View Strains carrying Iis2tm2(ACTB-tdTomato,-EGFP)Luo (1 strain)
017639 STOCK Nf1tm1Par/J
002080 129-Trp53tm1Tyj/J 002101 B6.129S2-Trp53tm1Tyj/J 008191 B6;129S2-Trp53tm1Tyj Nf1tm1Tyj/J 002103 B6;129S2-Trp53tm1Tyj/J 002526 C.129S2(B6)-Trp53tm1Tyj/J 002547 C3Ou.129S2(B6)-Trp53tm1Tyj/J 002899 FVB.129S2(B6)-Trp53tm1Tyj/J
010939 B6.Cg-Tg(ACTB-UPF1*R844C)581Hcd/J 005703 B6.Cg-Tg(ACTFLPe)9205Dym/J 009686 B6.Cg-Tg(Actb-TNFRSF6B)754Jwu/J 008226 B6.FVB-Tg(CAG-EGFP,-ALPP)2.6Ggc/J 003800 B6;SJL-Tg(ACTFLPe)9205Dym/J 005145 C57BL/6-Tg(CAG-OVA)916Jen/J 005863 C57BL/6J-Tg(ACTB-DDAH1)1Jpck/J 002981 DBA/2-Tg(xstpx-lacZ)36And/J 003376 FVB/N-Tg(ACTB-cre)2Mrt/J 008200 FVB/N-Tg(CAG-EGFP,-ALPP)2.6Ggc/J 013749 STOCK Iis2tm1(ACTB-EGFP,-tdTomato)Luo/J 005438 STOCK Tg(CAG-Bgeo,-DsRed*MST)1Nagy/J
013749 STOCK Iis2tm1(ACTB-EGFP,-tdTomato)Luo/J
007923 B6.129S1-Nf1tm1Cbr/J 008192 B6.129S2-Nf1tm1Tyj/J 002646 B6.129S6-Nf1tm1Fcr/J 008191 B6;129S2-Trp53tm1Tyj Nf1tm1Tyj/J
004301 129-Trp53tm1Holl/J 008652 129S-Trp53tm2Tyj/J 008651 129S-Trp53tm3Tyj/J 008462 B6.129P2-Trp53tm1Brn/J 008183 B6.129S4(Cg)-Trp53tm2.1Tyj/J 008182 B6.129S4-Trp53tm3.1Tyj/J 007218 B6.129S6-Trp53tm2Xu/J 011109 B6.Cg-Trp53tm2Glo/Kvm 007962 B6.FVB-Tg(MMTV-neu/OT-I/OT-II)CBnel Tg(Trp53R172H)8512Jmr/J 017767 B6;129-Trp53tm1.1Dgk/J 008045 B6;129-Trp53tm2Holl/J 006980 B6;129-Trp53tm2Xu/J 008181 B6;129S4-Trp53tm4Tyj/J 008361 B6;129S4-Trp53tm5Tyj/J 002659 FVB/N-Tg(Trp53R172H)8512Jmr/J 002660 FVB/N-Tg(Trp53R172L)4491Jmr/J 012620 STOCK Trp53tm1Brd Brca1tm1Aash Tg(LGB-cre)74Acl/J 003262 STOCK Tg(Trp53A135V)L3Ber/J
Phenotype
Phenotype Information
- 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, Type I; NF1 (NF1)
Neurofibromatosis-Noonan Syndrome; NFNS (NF1)
Osteogenic Sarcoma (TP53)
Pancreatic Cancer (TP53)
Papilloma of Choroid Plexus (TP53)
Watson Syndrome (NF1)
This mouse can be used to support research in many areas including:
GFP relatedCancer Research
Other
Neurobiology Research
Cre-lox System
loxP-flanked Sequences
loxP-flanked Sequences: Test/Reporter
Fluorescent protein expression in neural tissue
Research Tools
Cancer Research
Cre-lox System
loxP-flanked Sequences
Fluorescent Proteins
Genetics Research
Mutagenesis and Transgenesis: Cre-lox System
Tissue/Cell Markers: Cre-lox System
Trp53tm1Tyj relatedResearch Tools
Fluorescent Proteins
Apoptosis Research
Endogenous Regulators
Cancer Research
Increased Tumor Incidence
Lymphomas
Other Tissues/Organs
Other Tissues/Organs: osteosarcoma
Toxicology
Tumor Suppressor Genes
Immunology, Inflammation and Autoimmunity Research
Intracellular Signaling Molecules
Mouse/Human Gene Homologs
Li-Fraumeni syndrome
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 | Iis2tm2(ACTB-tdTomato,-EGFP)Luo | ||
|---|---|---|---|
| Allele Name | targeted mutation 2, Liqun Luo | ||
| Allele Type | Targeted (Reporter) | ||
| Common Name(s) | MADM-11-TG; MADM-11TG; TG: tdTN-termGFPC-term; Tg(ACTB-tdTomato,-EGFP)11Luo; | ||
| Mutation Made By | Dr. Liqun Luo, Stanford University, HHMI | ||
| Strain of Origin | (129X1/SvJ x 129S1/Sv)F1-Kitl<+> | ||
| Site of Expression | Mutant daughter cells express GFP, while the sibling wildtype cells are labeled with RFP. | ||
| Expressed Gene | GFP, Green Fluorescent Protein, jellyfish | ||
| Green Fluorescent Protein (GFP), derived from the jellyfish Aequorea victoria, is a versatile reporter molecule which has found use in many biological applications. In some constructs the original molecule has been modified in order to enhance its fluorescence intensity (EGFP, enhanced GFP). When utilized in a transgenic construct, tissue expressing sufficient amounts of GFP will fluoresce when exposed to a 488 nm light source. | |||
| Expressed Gene | RFP, Red Fluorescent Protein, coral | ||
| Red Fluorescent Protein (RFP), derived from marine invertebrate organisms such as the soft coral Discosoma spp and reef coral, Heteractis crispa, is a versatile reporter molecule which has found use in many biological applications. The wild type protein, which is an obligate tetramer, is not well tolerated in mammalian systems. The original molecule has been modified in order to optimize expression to mammalian physiology (examples include monomeric RFP, mRFP1, DsRed, etc). | |||
| Promoter | ACTB, actin, beta, human | ||
| Molecular Note | The TG MADM targeting construct was designed with a CMV enhancer/chicken beta-actin core promoter (pCA), the N-terminal portion of a red fluorescent protein (tdTomato; aa 1-3), a beta-globin intronic sequence containing an frt site and loxP-flanked neomycin resistance gene, the C-terminal portion of a mutant enhanced green fluorescent protein (mut4-EGFP; aa 274-724), and an SV40 T-antigen poly(A) signal. This entire TG MADM construct was inserted into the "Hipp11" locus on chromosome 11 (cytoband A1 at ~3cM between the Eif4enif1 and Drg1 loci). [MGI Ref ID J:166047] | ||
| Gene Symbol and Name | Iis2, intergenic insertion site 2 | ||
| Chromosome | 11 | ||
| Gene Common Name(s) | H11; Hipp11; | ||
| Allele Symbol | Nf1tm1Par | ||
| Allele Name | targeted mutation 1, Luis F Parada | ||
| Allele Type | Targeted (Floxed/Frt) | ||
| Common Name(s) | Nf1flox; Nf1flox; | ||
| Mutation Made By | Steven McKinnon, UT Southwestern | ||
| Strain of Origin | (129X1/SvJ x 129S1/Sv)F1-Kitl<+> | ||
| 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. | ||
| 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] | ||
| Allele Symbol | Trp53tm1Tyj | ||
| Allele Name | targeted mutation 1, Tyler Jacks | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | Trp53-; Trp53KO; p53-; p53delta; p53null; p53KO; | ||
| Mutation Made By | Dr. Tyler Jacks, Massachusetts Institute of Technology | ||
| Strain of Origin | 129S2/SvPas | ||
| ES Cell Line Name | D3 | ||
| ES Cell Line Strain | 129S2/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
Genotyping Information
Genotyping Protocols
Generic GFP/EGFP qPCR, QPCR
Nf1tm1Par,Separated MCA
Tg(ACTB-tdTomato,-EGFP)11Luo, Melt Curve Analysis
Trp53tm1Tyj, Standard PCR
Nf1tm1Par, Separated PCR
Tg(ACTB-tdTomato,-EGFP)11Luo, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Additional References
Iis2tm2(ACTB-tdTomato,-EGFP)Luo relatedNf1tm1Par relatedHippenmeyer S; Youn YH; Moon HM; Miyamichi K; Zong H; Wynshaw-Boris A; Luo L. 2010. Genetic mosaic dissection of lis1 and ndel1 in neuronal migration. Neuron 68(4):695-709. [PubMed: 21092859] [MGI Ref ID J:166047]
Liang H; Xiao G; Yin H; Hippenmeyer S; Horowitz JM; Ghashghaei HT. 2013. Neural development is dependent on the function of specificity protein 2 in cell cycle progression. Development 140(3):552-61. [PubMed: 23293287] [MGI Ref ID J:194076]
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]
Liu S; Liu Y; Hao W; Wolf L; Kiliaan AJ; Penke B; Rube CE; Walter J; Heneka MT; Hartmann T; Menger MD; Fassbender K. 2012. TLR2 is a primary receptor for Alzheimer's amyloid beta peptide to trigger neuroinflammatory activation. J Immunol 188(3):1098-107. [PubMed: 22198949] [MGI Ref ID J:180762]
Trp53tm1Tyj relatedAlcantara 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]
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]
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]
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]
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]
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]
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Yamanishi Y; Boyle DL; Pinkoski MJ; Mahboubi A; Lin T; Han Z; Zvaifler NJ; Green DR; Firestein GS. 2002. Regulation of Joint Destruction and Inflammation by p53 in Collagen-Induced Arthritis. Am J Pathol 160(1):123-30. [PubMed: 11786406] [MGI Ref ID J:73730]
Yan CT; Boboila C; Souza EK; Franco S; Hickernell TR; Murphy M; Gumaste S; Geyer M; Zarrin AA; Manis JP; Rajewsky K; Alt FW. 2007. IgH class switching and translocations use a robust non-classical end-joining pathway. Nature 449(7161):478-82. [PubMed: 17713479] [MGI Ref ID J:126758]
Yan H; Blackburn AC; McLary SC; Tao L; Roberts AL; Xavier EA; Dickinson ES; Seo JH; Arenas RB; Otis CN; Cao QJ; Lawlor RG; Osborne BA; Kittrell FS; Medina D; Jerry DJ. 2010. Pathways contributing to development of spontaneous mammary tumors in BALB/c-Trp53+/- mice. Am J Pathol 176(3):1421-32. [PubMed: 20110418] [MGI Ref ID J:158515]
Yan J; Di Y; Shi H; Rao H; Huo K. 2010. Overexpression of SCYL1-BP1 stabilizes functional p53 by suppressing MDM2-mediated ubiquitination. FEBS Lett 584(20):4319-24. [PubMed: 20849854] [MGI Ref ID J:165421]
Yang A; Reeves RH. 2011. Increased Survival following Tumorigenesis in Ts65Dn Mice That Model Down Syndrome. Cancer Res 71(10):3573-81. [PubMed: 21467166] [MGI Ref ID J:171978]
Yang DH; Fazili Z; Smith ER; Cai KQ; Klein-Szanto A; Cohen C; Horowitz IR; Xu XX. 2006. Disabled-2 Heterozygous Mice Are Predisposed to Endometrial and Ovarian Tumorigenesis and Exhibit Sex-Biased Embryonic Lethality in a p53-Null Background. Am J Pathol 169(1):258-67. [PubMed: 16816378] [MGI Ref ID J:110173]
Yang X; Klein R; Tian X; Cheng HT; Kopan R; Shen J. 2004. Notch activation induces apoptosis in neural progenitor cells through a p53-dependent pathway. Dev Biol 269(1):81-94. [PubMed: 15081359] [MGI Ref ID J:90392]
Yao R; Natsume Y; Saiki Y; Shioya H; Takeuchi K; Yamori T; Toki H; Aoki I; Saga T; Noda T. 2012. Disruption of Tacc3 function leads to in vivo tumor regression. Oncogene 31(2):135-48. [PubMed: 21685933] [MGI Ref ID J:179414]
Yazinski SA; Westcott PM; Ong K; Pinkas J; Peters RM; Weiss RS. 2009. Dual inactivation of Hus1 and p53 in the mouse mammary gland results in accumulation of damaged cells and impaired tissue regeneration. Proc Natl Acad Sci U S A 106(50):21282-7. [PubMed: 19918068] [MGI Ref ID J:155573]
Yeh JR; Ju R; Brdlik CM; Zhang W; Zhang Y; Matyskiela ME; Shotwell JD; Crews CM. 2006. Targeted gene disruption of methionine aminopeptidase 2 results in an embryonic gastrulation defect and endothelial cell growth arrest. Proc Natl Acad Sci U S A 103(27):10379-84. [PubMed: 16790550] [MGI Ref ID J:111701]
Yin C; Knudson CM; Korsmeyer SJ; Van Dyke T. 1997. Bax suppresses tumorigenesis and stimulates apoptosis in vivo. Nature 385(6617):637-40. [PubMed: 9024662] [MGI Ref ID J:38331]
Yin Y; Stahl BC; DeWolf WC; Morgentaler A. 2002. P53 and Fas are sequential mechanisms of testicular germ cell apoptosis. J Androl 23(1):64-70. [PubMed: 11780924] [MGI Ref ID J:105850]
Yin Y; Stahl BC; DeWolf WC; Morgentaler A. 1998. p53-mediated germ cell quality control in spermatogenesis. Dev Biol 204(1):165-71. [PubMed: 9851850] [MGI Ref ID J:110639]
Yin Z; Menendez D; Resnick MA; French JE; Janardhan KS; Jetten AM. 2012. RAP80 is critical in maintaining genomic stability and suppressing tumor development. Cancer Res 72(19):5080-90. [PubMed: 22896338] [MGI Ref ID J:191827]
Young LC; Keuling AM; Lai R; Nation PN; Tron VA; Andrew SE. 2007. The associated contributions of p53 and the DNA mismatch repair protein Msh6 to spontaneous tumorigenesis. Carcinogenesis 28(10):2131-8. [PubMed: 17615258] [MGI Ref ID J:125800]
Yuan L; Liu JG; Hoja MR; Lightfoot DA; Hoog C. 2001. The checkpoint monitoring chromosomal pairing in male meiotic cells is p53-independent. Cell Death Differ 8(3):316-7. [PubMed: 11319615] [MGI Ref ID J:105790]
Zeini M; Traves PG; Lopez-Fontal R; Pantoja C; Matheu A; Serrano M; Bosca L; Hortelano S. 2006. Specific contribution of p19(ARF) to nitric oxide-dependent apoptosis. J Immunol 177(5):3327-36. [PubMed: 16920973] [MGI Ref ID J:139500]
Zelazny E; Li B; Anagnostopoulos AM; Coleman A; Perkins AS. 2001. Cooperating Oncogenic Events in Murine Mammary Tumorigenesis: Assessment of ErbB2, Mutant p53, and Mouse Mammary Tumor Virus. Exp Mol Pathol 70(3):183-93. [PubMed: 11417997] [MGI Ref ID J:70644]
Zeng Q; Oakley B. 1999. p53 and Bax: putative death factors in taste cell turnover. J Comp Neurol 413(1):168-80. [PubMed: 10464378] [MGI Ref ID J:57477]
Zhang J; Cho SJ; Shu L; Yan W; Guerrero T; Kent M; Skorupski K; Chen H; Chen X. 2011. Translational repression of p53 by RNPC1, a p53 target overexpressed in lymphomas. Genes Dev 25(14):1528-43. [PubMed: 21764855] [MGI Ref ID J:174192]
Zhang J; Schweers B; Dyer MA. 2004. The first knockout mouse model of retinoblastoma. Cell Cycle 3(7):952-9. [PubMed: 15190215] [MGI Ref ID J:103618]
Zhang L; Anglesio MS; O'sullivan M; Zhang F; Yang G; Sarao R; Nghiem MP; Cronin S; Hara H; Melnyk N; Li L; Wada T; Liu PP; Farrar J; Arceci RJ; Sorensen PH; Penninger JM. 2007. The E3 ligase HACE1 is a critical chromosome 6q21 tumor suppressor involved in multiple cancers. Nat Med 13(9):1060-1069. [PubMed: 17694067] [MGI Ref ID J:125183]
Zhang L; Reynolds TL; Shan X; Desiderio S. 2011. Coupling of v(d)j recombination to the cell cycle suppresses genomic instability and lymphoid tumorigenesis. Immunity 34(2):163-74. [PubMed: 21349429] [MGI Ref ID J:168974]
Zhang Q; He X; Chen L; Zhang C; Gao X; Yang Z; Liu G. 2012. Synergistic regulation of p53 by Mdm2 and Mdm4 is critical in cardiac endocardial cushion morphogenesis during heart development. J Pathol 228(3):416-28. [PubMed: 22821713] [MGI Ref ID J:188490]
Zhang S; Zheng M; Kibe R; Huang Y; Marrero L; Warren S; Zieske AW; Iwakuma T; Kolls JK; Cui Y. 2011. Trp53 negatively regulates autoimmunity via the STAT3-Th17 axis. FASEB J 25(7):2387-98. [PubMed: 21471252] [MGI Ref ID J:174321]
Zhang X; Podsypanina K; Huang S; Mohsin SK; Chamness GC; Hatsell S; Cowin P; Schiff R; Li Y. 2005. Estrogen receptor positivity in mammary tumors of Wnt-1 transgenic mice is influenced by collaborating oncogenic mutations. Oncogene 24(26):4220-31. [PubMed: 15824740] [MGI Ref ID J:99546]
Zhao F; Obermann S; von Wasielewski R; Haile L; Manns MP; Korangy F; Greten TF. 2009. Increase in frequency of myeloid-derived suppressor cells in mice with spontaneous pancreatic carcinoma. Immunology 128(1):141-9. [PubMed: 19689743] [MGI Ref ID J:162293]
Zhou S; Gu L; He J; Zhang H; Zhou M. 2011. MDM2 Regulates Vascular Endothelial Growth Factor mRNA Stabilization in Hypoxia. Mol Cell Biol 31(24):4928-37. [PubMed: 21986500] [MGI Ref ID J:178311]
Zhu F; Dolle ME; Berton TR; Kuiper RV; Capps C; Espejo A; McArthur MJ; Bedford MT; van Steeg H; de Vries A; Johnson DG. 2010. Mouse models for the p53 R72P polymorphism mimic human phenotypes. Cancer Res 70(14):5851-9. [PubMed: 20587514] [MGI Ref ID J:162466]
Zhu M; Weiss RS. 2007. Increased common fragile site expression, cell proliferation defects, and apoptosis following conditional inactivation of mouse Hus1 in primary cultured cells. Mol Biol Cell 18(3):1044-55. [PubMed: 17215515] [MGI Ref ID J:123894]
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]
Zindy F; Nilsson LM; Nguyen L; Meunier C; Smeyne RJ; Rehg JE; Eberhart C; Sherr CJ; Roussel MF. 2003. Hemangiosarcomas, medulloblastomas, and other tumors in Ink4c/p53-null mice. Cancer Res 63(17):5420-7. [PubMed: 14500377] [MGI Ref ID J:85515]
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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 & Husbandry When maintaining a live colony, mice homozygous for the Tg(ACTB-tdTomato,-EGFP)11Luo transgene, heterozygous for Trp53tm1Tyj allele, and homozygous for the Nf1tm1Par allele may be bred to mice homozygous for the Tg(ACTB-tdTomato,-EGFP)11Luo transgene, wildtype at the Trp53 locus, and homozygous for the Nf1tm1Par allele.
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $1980.00 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 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
| Pricing for International shipping destinations |
|
Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2574.00 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 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
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|
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Control Information
| Control | ||
|---|---|---|
| None Available | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
Payment Terms and Conditions
Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.
See Terms of Use tab for General Terms and Conditions
The Jackson Laboratory's Genotype Promise
The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
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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.
- Strain(s) not available to companies or for-profit entities.
- Strain(s) not available to companies or for-profit entities.
- Use of MICE by companies or for-profit entities requires a license prior to shipping.
Contact information
General inquiries regarding Terms of UseContracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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.