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Former Names NOD.129S2(B6)-C2tatm1Ccum/FlvJ (Changed: 26-MAR-07 ) Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Background Strain NOD Donor Strain 129S2 via D3 ES cell line H2 Haplotype g7 Generation N10F?+2p
Generation DefinitionsDonating Investigator Dr. Richard A. Flavell, Yale University School of Medicine Appearance
albino, pink-eyed
Related Genotype: A/A TyrcTyrcDescription
In humans, a non-functional C2ta (or Ciita) gene causes bare lymphocyte syndrome (BLS), which is characterized by the lack of HLA class II gene expression and a reduced number of mature CD4+ T cells in the periphery.On the C57BL/6 congenic background (see Stock No. 003239) disruption of C2ta results in a lack of MHC Class II expression by splenic B cells, dendridic cells, and both resting and interferon gamma stimulated macrophages. However, thymic epithelium retains MHC class II expression. Homozygotes also exhibit a significant decrease in the levels of invariant chain and H-2M gene transcripts. Non-conventional MHC Class II molecules such as H-2O alpha and H-2O beta, are not affected by the disruption of C2ta. Despite the continued expression of MHC Class II molecules on cells of the thymic epithilium, few CD4 positive cells exist in the periphery of homozygotes. (Chang et al 1996)
Because of the role of CD4+ T cells in the onset of diabetes, the mutation was backcrossed onto the NOD/ShiLtJ background to characterize its impact on diabetes development. The resulting congenic mice (Stock No. 004448) homozygous for the mutation are completely protected from diabetes after 35 weeks of age. However, they do exhibit perivascular infiltration or periinsulitis at 15 weeks of age.. Like their C57BL/6 counterparts, NOD homozygotes exhibit a ten-fold decrease in CD4+ T cells in the periphery, while the number of CD8+ T cells in the spleen remains normal. Homozygous mice do not show defects in B cell function, as measured by immunoglobulin production after stimulation of B cells with Il4 in vitro. (Mora et al. 1999)
Development
The C2ta (or Ciita) gene was isolated from a 129S2/SvPas genomic library and disrupted by replacement of exons critical for gene function with a neomycin resistance cassette. The vector containing disrupted C2ta was transfected into D3 ES cells (129S2/SvPas derived). Positive clones were injected into C57BL/6 blastocysts, and resulting chimeric mice were intercrossed to produce homozygotes. These homozygous individuals were backcrossed to C57BL/6 for at least 2 generations before being backcrossed to NOD/LtJ for 11 generations using PCR-assisted selection for NOD diabetes susceptibility loci. (Chang et al 1996, Mora et al 1999)
| Control | ||
|---|---|---|
| 001976 NOD/ShiLtJ | ||
| Considerations for Choosing Controls | ||
Strains carrying Ciitatm1Ccum allele
003239 B6.129S2-Ciitatm1Ccum/J 003238 C.129S2(B6)-Ciitatm1Ccum/J 005356 NOD.129(B6)-B2mtm1Unc Ciitatm1Ccum/BhsJ View Strains carrying Ciitatm1Ccum (3 strains)
View Related Disease (OMIM) Terms
Related Disease (OMIM) Terms provided by MGI
- No similarity to the expected human disease phenotype was found. One or more human genes are associated with this human disease. The mouse genotype may involve mutations to orthologs of one or more of these genes, but the phenotype did not resemble the disease.
Diabetes Mellitus, Insulin-Dependent; IDDM
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Bare Lymphocyte Syndrome, Type II (CIITA)
Rheumatoid Arthritis; RA (CIITA)
View Mammalian Phenotype Terms
Mammalian Phenotype Terms provided by MGI
assigned by genotype
Ciitatm1Ccum/Ciitatm1Ccum
NOD.129S2(B6)-Ciitatm1Ccum
- homeostasis/metabolism phenotype
- abnormal circulating glucose level
- on the NOD background, by 35 weeks of age and later, no mutants show hyperglycemia while 40% of NOD-sufficient mice develop diabetes by 35 weeks of age (MGI Ref ID J:106081)
- immune system phenotype
- abnormal T cell differentiation (MGI Ref ID J:106081)
- abnormal inflammatory response (MGI Ref ID J:106081)
- pancreas inflammation
- female mutants show pancreatic infiltration by 15 weeks of age (MGI Ref ID J:106081)
- insulitis
- when recovered from NOD diabetic female recipients, islet grafts obtained from these class II-deficient NOD mice show severe infiltration and lack almost all insulin production (MGI Ref ID J:107051)
- periinsulitis
- at 15 weeks of age, around 2% of islets in female mutants show perinsulitis or insulitis compared with 75% in pre-diabetic and diabetic mice (MGI Ref ID J:106081)
- abnormal level of surface class II molecules
- MHC class II molecule expression is almost completely absent from spleen cells (MGI Ref ID J:106081)
- decreased CD4-positive T cell number
- a 10-fold reduction in levels of peripheral CD4+ T cells is observed compared to controls (MGI Ref ID J:106081)
- decreased susceptibility to autoimmune diabetes
- mice do not develop diabetes (2 consecutive blood glucose measures >16.5 nM) up to 30 weeks of age (MGI Ref ID J:107051)
- increased CD8-positive T cell number
- CD8+ T cells are slightly over-represented in mutants (25%) compared to controls (16%) (MGI Ref ID J:106081)
- hematopoietic system phenotype
- abnormal T cell differentiation (MGI Ref ID J:106081)
- decreased CD4-positive T cell number
- a 10-fold reduction in levels of peripheral CD4+ T cells is observed compared to controls (MGI Ref ID J:106081)
- increased CD8-positive T cell number
- CD8+ T cells are slightly over-represented in mutants (25%) compared to controls (16%) (MGI Ref ID J:106081)
- endocrine/exocrine gland phenotype
- pancreas inflammation
- female mutants show pancreatic infiltration by 15 weeks of age (MGI Ref ID J:106081)
- insulitis
- when recovered from NOD diabetic female recipients, islet grafts obtained from these class II-deficient NOD mice show severe infiltration and lack almost all insulin production (MGI Ref ID J:107051)
- periinsulitis
- at 15 weeks of age, around 2% of islets in female mutants show perinsulitis or insulitis compared with 75% in pre-diabetic and diabetic mice (MGI Ref ID J:106081)
- cellular phenotype
- abnormal T cell differentiation (MGI Ref ID J:106081)
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:
Ciitatm1Ccum relatedDiabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains
NOD/ShiLtJ Non-MHC Congenics
Immunology, Inflammation and Autoimmunity Research
Immunodeficiency
MHC class II associated invariant chain deficient
MHC class II defects
MHC class II deficient
T cell deficiency
Internal/Organ Research
Lymphoid Tissue Defects
T cell deficiency
Research Tools
Immunology and Inflammation Research
MHC class II associated invariant chain deficiency
MHC class II defects
T cell deficiency
Immunology, Inflammation and Autoimmunity Research
Immunodeficiency
Research Tools
Immunology and Inflammation Research
MHC class II defects
| Allele Symbol | Ciitatm1Ccum | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Cheong-Hee Chang | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | CIITA C-; CIITA-; MHC classII-; | ||
| Mutation Made By | Dr. Cheong-Hee Chang, Indiana University | ||
| Strain of Origin | 129S2/SvPas | ||
| ES Cell Line Name | D3 | ||
| ES Cell Line Strain | 129S2/SvPas | ||
| Gene Symbol and Name | Ciita, class II transactivator | ||
| Chromosome | 16 | ||
| Gene Common Name(s) | C2TA; C2ta; CIITAIV; EG669998; Gm9475; MHC2TA; NLRA; predicted gene 9475; predicted gene, EG669998; | ||
| Molecular Note | A genomic fragment containing exons which encode critical regions of the protein was replaced with a neomycin selection gene. Northern blot analysis on RNA derived from homozygous mice demonstrated that no detectable protein was produced from this allele. [MGI Ref ID J:31601] | ||
Genotyping Protocols
Ciitatm1Ccum, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
Chang CH; Guerder S; Hong SC; van Ewijk W; Flavell RA. 1996. Mice lacking the MHC class II transactivator (CIITA) show tissue-specific impairment of MHC class II expression. Immunity 4(2):167-78. [PubMed: 8624807] [MGI Ref ID J:31601]
Muhlethaler-Mottet A; Otten LA; Steimle V; Mach B. 1997. Expression of MHC class II molecules in different cellular and functional compartments is controlled by differential usage of multiple promoters of the transactivator CIITA. EMBO J 16(10):2851-60. [PubMed: 9184229] [MGI Ref ID J:40766]
Ciitatm1Ccum relatedBenito AI; Milner LA; Leisenring W; Deeg HJ; Woolfrey AE. 2001. Absence of major histocompatibility class II expression does not impair hematopoiesis in mice. Exp Hematol 29(9):1070-5. [PubMed: 11532347] [MGI Ref ID J:111611]
Benlagha K; Park SH; Guinamard R; Forestier C; Karlsson L; Chang CH; Bendelac A. 2004. Mechanisms governing B cell developmental defects in invariant chain-deficient mice. J Immunol 172(4):2076-83. [PubMed: 14764672] [MGI Ref ID J:87989]
Broxmeyer HE; Cooper S; Hangoc G; Chang CH. 2006. Class II transactivator-mediated regulation of major histocompatibility complex class II antigen expression is important for hematopoietic progenitor cell suppression by chemokines and iron-binding proteins. Exp Hematol 34(8):1078-84. [PubMed: 16863914] [MGI Ref ID J:111903]
Buch T; Polic B; Clausen BE; Weiss S; Akilli-Ozturk O; Chang CH; Flavell R; Schulz A; Jonjic S; Waisman A; Forster I. 2006. MHC class II expression through a hitherto unknown pathway supports T helper cell-dependent immune responses: implications for MHC class II deficiency. Blood 107(4):1434-44. [PubMed: 16254146] [MGI Ref ID J:129309]
Chang CH; Guerder S; Hong SC; van Ewijk W; Flavell RA. 1996. Mice lacking the MHC class II transactivator (CIITA) show tissue-specific impairment of MHC class II expression. Immunity 4(2):167-78. [PubMed: 8624807] [MGI Ref ID J:31601]
Chen L; Jay DC; Fairbanks JD; He X; Jensen PE. 2011. An MHC class Ib-restricted CD8+ T cell response to lymphocytic choriomeningitis virus. J Immunol 187(12):6463-72. [PubMed: 22084437] [MGI Ref ID J:180389]
Choi EY; Jung KC; Park HJ; Chung DH; Song JS; Yang SD; Simpson E; Park SH. 2005. Thymocyte-thymocyte interaction for efficient positive selection and maturation of CD4 T cells. Immunity 23(4):387-96. [PubMed: 16226504] [MGI Ref ID J:113276]
Chou SD; Khan AN; Magner WJ; Tomasi TB. 2005. Histone acetylation regulates the cell type specific CIITA promoters, MHC class II expression and antigen presentation in tumor cells. Int Immunol 17(11):1483-94. [PubMed: 16210330] [MGI Ref ID J:104221]
Clausen BE; Waldburger JM; Schwenk F; Barras E; Mach B; Rajewsky K; Forster I; Reith W. 1998. Residual MHC class II expression on mature dendritic cells and activated B cells in RFX5-deficient mice. Immunity 8(2):143-55. [PubMed: 9491996] [MGI Ref ID J:67941]
Creusot RJ; Yaghoubi SS; Kodama K; Dang DN; Dang VH; Breckpot K; Thielemans K; Gambhir SS; Fathman CG. 2008. Tissue-targeted therapy of autoimmune diabetes using dendritic cells transduced to express IL-4 in NOD mice. Clin Immunol 127(2):176-87. [PubMed: 18337172] [MGI Ref ID J:133579]
Das G; Das J; Eynott P; Zhang Y; Bothwell AL; Van Kaer L; Shi Y. 2006. Pivotal roles of CD8+ T cells restricted by MHC class I-like molecules in autoimmune diseases. J Exp Med 203(12):2603-11. [PubMed: 17088432] [MGI Ref ID J:124622]
Devoss JJ; Shum AK; Johannes KP; Lu W; Krawisz AK; Wang P; Yang T; Leclair NP; Austin C; Strauss EC; Anderson MS. 2008. Effector mechanisms of the autoimmune syndrome in the murine model of autoimmune polyglandular syndrome type 1. J Immunol 181(6):4072-9. [PubMed: 18768863] [MGI Ref ID J:139094]
Elliott EA; Drake JR; Amigorena S; Elsemore J; Webster P; Mellman I; Flavell RA. 1994. The invariant chain is required for intracellular transport and function of major histocompatibility complex class II molecules. J Exp Med 179(2):681-94. [PubMed: 8294875] [MGI Ref ID J:65917]
Eppert BL; Wortham BW; Flury JL; Borchers MT. 2013. Functional characterization of T cell populations in a mouse model of chronic obstructive pulmonary disease. J Immunol 190(3):1331-40. [PubMed: 23264660] [MGI Ref ID J:192605]
Fikrig E; Barthold SW; Chen M; Chang CH; Flavell RA. 1997. Protective antibodies develop, and murine Lyme arthritis regresses, in the absence of MHC class II and CD4+ T cells. J Immunol 159(11):5682-6. [PubMed: 9548512] [MGI Ref ID J:109903]
Gourley T; Roys S; Lukacs NW; Kunkel SL; Flavell RA; Chang CH. 1999. A novel role for the major histocompatibility complex class II transactivator CIITA in the repression of IL-4 production. Immunity 10(3):377-86. [PubMed: 10204493] [MGI Ref ID J:54057]
Gourley TS; Patel DR; Nickerson K; Hong SC; Chang CH. 2002. Aberrant expression of Fas ligand in mice deficient for the MHC class II transactivator. J Immunol 168(9):4414-9. [PubMed: 11970984] [MGI Ref ID J:112146]
Green EA; Wong FS; Eshima K; Mora C; Flavell RA. 2000. Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8(+) T cells. J Exp Med 191(2):225-38. [PubMed: 10637268] [MGI Ref ID J:59409]
Guleria I; Gubbels Bupp M; Dada S; Fife B; Tang Q; Ansari MJ; Trikudanathan S; Vadivel N; Fiorina P; Yagita H; Azuma M; Atkinson M; Bluestone JA; Sayegh MH. 2007. Mechanisms of PDL1-mediated regulation of autoimmune diabetes. Clin Immunol 125(1):16-25. [PubMed: 17627890] [MGI Ref ID J:125272]
Hinterberger M; Aichinger M; da Costa OP; Voehringer D; Hoffmann R; Klein L. 2010. Autonomous role of medullary thymic epithelial cells in central CD4(+) T cell tolerance. Nat Immunol 11(6):512-9. [PubMed: 20431619] [MGI Ref ID J:160615]
Jay DC; Reed-Loisel LM; Jensen PE. 2008. Polyclonal MHC Ib-Restricted CD8+ T Cells Undergo Homeostatic Expansion in the Absence of Conventional MHC-Restricted T Cells. J Immunol 180(5):2805-14. [PubMed: 18292501] [MGI Ref ID J:131725]
Kuipers H; Soullie T; Hammad H; Willart M; Kool M; Hijdra D; Hoogsteden HC; Lambrecht BN. 2009. Sensitization by intratracheally injected dendritic cells is independent of antigen presentation by host antigen-presenting cells. J Leukoc Biol 85(1):64-70. [PubMed: 18923103] [MGI Ref ID J:143272]
Kupfer TM; Crawford ML; Pham K; Gill RG. 2005. MHC-mismatched islet allografts are vulnerable to autoimmune recognition in vivo. J Immunol 175(4):2309-16. [PubMed: 16081800] [MGI Ref ID J:107508]
Lauvau G; Vijh S; Kong P; Horng T; Kerksiek K; Serbina N; Tuma RA; Pamer EG. 2001. Priming of memory but not effector CD8 T cells by a killed bacterial vaccine. Science 294(5547):1735-9. [PubMed: 11721060] [MGI Ref ID J:133596]
Lee YJ; Jeon YK; Kang BH; Chung DH; Park CG; Shin HY; Jung KC; Park SH. 2010. Generation of PLZF+ CD4+ T cells via MHC class II-dependent thymocyte-thymocyte interaction is a physiological process in humans. J Exp Med 207(1):237-46, S1-7. [PubMed: 20038602] [MGI Ref ID J:156545]
Li W; Kim MG; Gourley TS; McCarthy BP; Sant'Angelo DB; Chang CH. 2005. An alternate pathway for CD4 T cell development: thymocyte-expressed MHC class II selects a distinct T cell population. Immunity 23(4):375-86. [PubMed: 16226503] [MGI Ref ID J:113275]
Li W; Sofi MH; Yeh N; Sehra S; McCarthy BP; Patel DR; Brutkiewicz RR; Kaplan MH; Chang CH. 2007. Thymic selection pathway regulates the effector function of CD4 T cells. J Exp Med 204(9):2145-57. [PubMed: 17724129] [MGI Ref ID J:126084]
Mora C; Wong FS; Chang CH; Flavell RA. 1999. Pancreatic infiltration but not diabetes occurs in the relative absence of MHC class II-restricted CD4 T cells: studies using NOD/CIITA-deficient mice. J Immunol 162(8):4576-88. [PubMed: 10201997] [MGI Ref ID J:106081]
Ochi A; Nguyen AH; Bedrosian AS; Mushlin HM; Zarbakhsh S; Barilla R; Zambirinis CP; Fallon NC; Rehman A; Pylayeva-Gupta Y; Badar S; Hajdu CH; Frey AB; Bar-Sagi D; Miller G. 2012. MyD88 inhibition amplifies dendritic cell capacity to promote pancreatic carcinogenesis via Th2 cells. J Exp Med 209(9):1671-87. [PubMed: 22908323] [MGI Ref ID J:191814]
Otten LA; Leibundgut-Landmann S; Huarte J; Kos-Braun IC; Lavanchy C; Barras E; Borisch B; Steimle V; Acha-Orbea H; Reith W. 2006. Revisiting the specificity of the MHC class II transactivator CIITA in vivo. Eur J Immunol 36(6):1548-58. [PubMed: 16703565] [MGI Ref ID J:152061]
Patel DR; Kaplan MH; Chang CH. 2004. Altered Th1 cell differentiation programming by CIITA deficiency. J Immunol 173(9):5501-8. [PubMed: 15494498] [MGI Ref ID J:93745]
Pihlgren M; Silva AB; Madani R; Giriens V; Waeckerle-Men Y; Fettelschoss A; Hickman DT; Lopez-Deber MP; Ndao DM; Vukicevic M; Buccarello AL; Gafner V; Chuard N; Reis P; Piorkowska K; Pfeifer A; Kundig TM; Muhs A; Johansen P. 2013. TLR4- and TRIF-dependent stimulation of B lymphocytes by peptide liposomes enables T cell-independent isotype switch in mice. Blood 121(1):85-94. [PubMed: 23144170] [MGI Ref ID J:192819]
Qiao Y; Zhu L; Sofi H; Lapinski PE; Horai R; Mueller K; Stritesky GL; He X; Teh HS; Wiest DL; Kappes DJ; King PD; Hogquist KA; Schwartzberg PL; Sant'Angelo DB; Chang CH. 2012. Development of promyelocytic leukemia zinc finger-expressing innate CD4 T cells requires stronger T-cell receptor signals than conventional CD4 T cells. Proc Natl Acad Sci U S A 109(40):16264-9. [PubMed: 22988097] [MGI Ref ID J:190112]
Sawa S; Kamimura D; Jin GH; Morikawa H; Kamon H; Nishihara M; Ishihara K; Murakami M; Hirano T. 2006. Autoimmune arthritis associated with mutated interleukin (IL)-6 receptor gp130 is driven by STAT3/IL-7-dependent homeostatic proliferation of CD4+ T cells. J Exp Med 203(6):1459-70. [PubMed: 16717113] [MGI Ref ID J:124381]
Sofi MH; Liu Z; Zhu L; Yu Q; Kaplan MH; Chang CH. 2010. Regulation of IL-17 expression by the developmental pathway of CD4 T cells in the thymus. Mol Immunol 47(6):1262-8. [PubMed: 20080304] [MGI Ref ID J:158374]
Soong L; Chang CH; Sun J; Longley BJ Jr; Ruddle NH; Flavell RA; McMahon-Pratt D. 1997. Role of CD4+ T cells in pathogenesis associated with Leishmania amazonensis infection. J Immunol 158(11):5374-83. [PubMed: 9164958] [MGI Ref ID J:64283]
Taniguchi RT; Devoss JJ; Moon JJ; Sidney J; Sette A; Jenkins MK; Anderson MS. 2012. Detection of an autoreactive T-cell population within the polyclonal repertoire that undergoes distinct autoimmune regulator (Aire)-mediated selection. Proc Natl Acad Sci U S A 109(20):7847-52. [PubMed: 22552229] [MGI Ref ID J:184783]
Winer DA; Winer S; Shen L; Wadia PP; Yantha J; Paltser G; Tsui H; Wu P; Davidson MG; Alonso MN; Leong HX; Glassford A; Caimol M; Kenkel JA; Tedder TF; McLaughlin T; Miklos DB; Dosch HM; Engleman EG. 2011. B cells promote insulin resistance through modulation of T cells and production of pathogenic IgG antibodies. Nat Med 17(5):610-7. [PubMed: 21499269] [MGI Ref ID J:171607]
Xu Y; Luchsinger L; Lucey EC; Smith BD. 2011. The effect of class II transactivator mutations on bleomycin-induced lung inflammation and fibrosis. Am J Respir Cell Mol Biol 44(6):898-905. [PubMed: 20705943] [MGI Ref ID J:185026]
Xu Y; McDonald J; Perloff E; Buttice G; Schreiber BM; Smith BD. 2007. Collagen and major histocompatibility class II expression in mesenchymal cells from CIITA hypomorphic mice. Mol Immunol 44(7):1720-32. [PubMed: 16982097] [MGI Ref ID J:115938]
Yang SJ; Ahn S; Park CS; Holmes KL; Westrup J; Chang CH; Kim MG. 2006. The quantitative assessment of MHC II on thymic epithelium: implications in cortical thymocyte development. Int Immunol 18(5):729-39. [PubMed: 16569676] [MGI Ref ID J:108547]
Yee CS; Yao Y; Li P; Klemsz MJ; Blum JS; Chang CH. 2004. Cathepsin E: a novel target for regulation by class II transactivator. J Immunol 172(9):5528-34. [PubMed: 15100295] [MGI Ref ID J:89650]
Yee CS; Yao Y; Xu Q; McCarthy B; Sun-Lin D; Tone M; Waldmann H; Chang CH. 2005. Enhanced production of IL-10 by dendritic cells deficient in CIITA. J Immunol 174(3):1222-9. [PubMed: 15661876] [MGI Ref ID J:96421]
Young HY; Zucker P; Flavell RA; Jevnikar AM; Singh B. 2004. Characterization of the role of major histocompatibility complex in type 1 diabetes recurrence after islet transplantation. Transplantation 78(4):509-15. [PubMed: 15446308] [MGI Ref ID J:107051]
Zhang B; Kracker S; Yasuda T; Casola S; Vanneman M; Homig-Holzel C; Wang Z; Derudder E; Li S; Chakraborty T; Cotter SE; Koyama S; Currie T; Freeman GJ; Kutok JL; Rodig SJ; Dranoff G; Rajewsky K. 2012. Immune Surveillance and Therapy of Lymphomas Driven by Epstein-Barr Virus Protein LMP1 in a Mouse Model. Cell 148(4):739-51. [PubMed: 22341446] [MGI Ref ID J:181546]
Animal Health Reports
Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.
| Pricing for USA, Canada and Mexico shipping destinations |
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Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $3175.00 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 Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $4127.50 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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Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
| Control | ||
|---|---|---|
| 001976 NOD/ShiLtJ | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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