Type Coisogenic; Mutant Strain; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse H2 Haplotype b Appearance
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Related Genotype: a/aDescription
Mice homozygous for this spontaneous mutation develop a severe, chronic, inflammatory skin disease beginning at 3-5 weeks of age. Mice appear runted and life span is shortened. In addition to dermatitis, homozygotes exhibit multi-organ inflammation with eosinophilia, defective TH1 cytokine production, splenomegaly, absent Peyer's patches (adult), diminished serum immunoglobulins, and an absence of B cell follicles, follicular dendritic cells, and germinal centers in secondary lymph organs. This mutant mouse strain may be useful in studies related to eosinophilic dermatitis, inflammation, and secondary lymphoid organ deveopment.Development
This cpdm spontaneous mutation arose in a colony of C57BL/KaLawRij held at TNO-Institute in the Netherlands. Mice from the cpdm colony were sent to Dr. John Sundberg at The Jackson Laboratory in 1993, and were maintained by sibling matings in a private research colony until they were donated to The Jackson Laboratory Repository in 2007.
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| Considerations for Choosing Controls | ||
View Related Disease (OMIM) Terms
Related Disease (OMIM) Terms provided by MGI
Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.
Dermatitis, Atopic
View Mammalian Phenotype Terms
Mammalian Phenotype Terms provided by MGI
assigned by genotype
Sharpincpdm/Sharpincpdm
C57BL/KaLawRij-Sharpincpdm
- immune system phenotype
- abnormal humoral immune response
- 4 weeks after immunization with DNP-KLH (DNP-keyhole limpet hemocyanin), DNP-specific antibody titers are lower in mutants than control (MGI Ref ID J:53575)
- decreased immunoglobulin level
- after immunization with DNP-KLH, reductions in DNP-specific IgM (2-fold), IgG3 (4-fold), IgG1 (12-fold), IgG2a (37-fold) and IgG2b (7-fold) antibodies is observed in mutants (MGI Ref ID J:53575)
- increased IgM level
- levels in feces are significantly increased compared to controls (MGI Ref ID J:53575)
- abnormal immune system organ morphology
- atrophy of lymphoid tissue with increasing age is observed (MGI Ref ID J:14539)
- abnormal lymph node morphology
- abnormal mesenteric lymph node morphology
- nodes are small, with medulla and occasionally entire lymph node replaced with connective tissue (MGI Ref ID J:53575)
- abnormal spleen morphology (MGI Ref ID J:53575)
- absent Peyer's patches
- absent but controls have 5-7; no rudimentary PPs are found in the small intestine of mutants (MGI Ref ID J:53575)
- large lymphoid organs
- at age of 3 weeks, deep and superficial cervical, thoracic, axillary and brachial lymph nodes and spleen are mildly enlarged (MGI Ref ID J:31745)
- decreased B cell number
- numbers of B lymphocytes are slightly decreased in mutant spleen at 6-12 weeks of age (MGI Ref ID J:53575)
- decreased T cell number
- numbers are moderately decreased in mutant spleen (MGI Ref ID J:53575)
- decreased CD4-positive T cell number
- percentage of cell is significantly reduced (16.8% in control vs 8.5%) (MGI Ref ID J:53575)
- dermatitis
- mice develop dermatitis with associated skin lesions starting at 2-3 weeks of age (MGI Ref ID J:14539)
- esophageal inflammation
- lesions, lesions comparable to skin lesions, are observed starting at 4 weeks; lesions are immediately moderate to severe (MGI Ref ID J:31745)
- folliculitis
- folliculitis with some degenerated hair shafts is observed at 3 weeks of age (MGI Ref ID J:31745)
- increased eosinophil cell number
- increased mast cell number
- joint inflammation
- at 20 weeks of age, synovia and periarticular and peritendinous connective tissues are infiltrated by low to moderate number of macrophages and neutrophils, frequently affecting coxofemoral, tibiofemoral, and invertebral joints, and knee tendons; more common in female mice (MGI Ref ID J:14539)
- lung inflammation
- lesions are observed from 1 week of age; inflammatory cells are mainly eosinophils with some monocytes (MGI Ref ID J:31745)
- lymph node inflammation
- at 1 week of age, deep and superficial cervical, thoracic, axillary and brachial lymph nodes display acute lymphadenitis and perilymphadenitis with eosinophil infiltration of cortex and medulla, varying from mild to severe (MGI Ref ID J:31745)
- stomach inflammation
- lesions, lesions comparable to skin lesions but no parakeratosis, are observed starting at 4 weeks; most severe at junction of forestomach and glandular stomach, but not as severe as in esophagus (MGI Ref ID J:31745)
- infliltrating eosinophils form intraepithelial and intracorneal pustules (MGI Ref ID J:31745)
- hematopoietic system phenotype
- abnormal spleen morphology (MGI Ref ID J:53575)
- decreased B cell number
- numbers of B lymphocytes are slightly decreased in mutant spleen at 6-12 weeks of age (MGI Ref ID J:53575)
- decreased T cell number
- numbers are moderately decreased in mutant spleen (MGI Ref ID J:53575)
- decreased CD4-positive T cell number
- percentage of cell is significantly reduced (16.8% in control vs 8.5%) (MGI Ref ID J:53575)
- extramedullary hematopoiesis (MGI Ref ID J:53575)
- increased bone marrow cell number
- bone marrow is hyperplastic with extensive myelopoiesis (MGI Ref ID J:14539)
- increased eosinophil cell number
- increased mast cell number
- growth/size phenotype
- postnatal growth retardation
- mice show moderate growth retardation with aging (MGI Ref ID J:14539)
- weight loss
- weight reduction is observed from age of 5 weeks (7%) and at 6 weeks reduction of 12% is observed (MGI Ref ID J:31745)
- homeostasis/metabolism phenotype
- skin edema
- mild spongiosis (intracellular edema) of the epidermis is seen occasionally (MGI Ref ID J:14539)
- digestive/alimentary phenotype
- abnormal esophageal epithelium morphology
- at 20 weeks, similar changes to those seen in epidermis are found, with exception of parakeratosis (MGI Ref ID J:14539)
- thickness of esophageal epithelium is increased from 38.2 um to 75.4 um in mutants; less severe in aged mice (MGI Ref ID J:14539)
- lesions are prominent, with spongiform pustules occurring in esophagus (MGI Ref ID J:14539)
- lesions, lesions comparable to skin lesions, are observed starting at 4 weeks; lesions are immediately moderate to severe (MGI Ref ID J:31745)
- abnormal stomach epithelium morphology
- abnormal tongue squamous epithelium morphology
- at 2 weeks of age, first lesions of epithelium are seen; lesions are immediately moderate to severe (MGI Ref ID J:31745)
- esophageal inflammation
- lesions, lesions comparable to skin lesions, are observed starting at 4 weeks; lesions are immediately moderate to severe (MGI Ref ID J:31745)
- stomach inflammation
- lesions, lesions comparable to skin lesions but no parakeratosis, are observed starting at 4 weeks; most severe at junction of forestomach and glandular stomach, but not as severe as in esophagus (MGI Ref ID J:31745)
- infliltrating eosinophils form intraepithelial and intracorneal pustules (MGI Ref ID J:31745)
- liver/biliary system phenotype
- abnormal liver morphology
- reproductive system phenotype
- female infertility
- females are infertile (MGI Ref ID J:14539)
- reduced male fertility
- males older than 11 weeks show reduced fertility (MGI Ref ID J:31745)
- respiratory system phenotype
- abnormal lung interstitium morphology
- perivascular and peribronchiolar connective tissues of lung show similar, but less conspicuous infiltrations (MGI Ref ID J:14539)
- lung inflammation
- lesions are observed from 1 week of age; inflammatory cells are mainly eosinophils with some monocytes (MGI Ref ID J:31745)
- skeleton phenotype
- abnormal joint capsule morphology
- synovial space is often dilated, containing some neutrophils and proteinaceous material (MGI Ref ID J:14539)
- joint inflammation
- at 20 weeks of age, synovia and periarticular and peritendinous connective tissues are infiltrated by low to moderate number of macrophages and neutrophils, frequently affecting coxofemoral, tibiofemoral, and invertebral joints, and knee tendons; more common in female mice (MGI Ref ID J:14539)
- cardiovascular system phenotype
- abnormal angiogenesis
- blood vessel proliferation in dermis is observed, with tortuous dilated capillaries present in superficial dermis (MGI Ref ID J:14539)
- vision/eye phenotype
- thick eyelids
- first sign of phenotypic change is thickening of eyelids, no earlier than 2 weeks of age (MGI Ref ID J:31745)
- craniofacial phenotype
- abnormal tongue squamous epithelium morphology
- at 2 weeks of age, first lesions of epithelium are seen; lesions are immediately moderate to severe (MGI Ref ID J:31745)
- integument phenotype
- abnormal coat appearance
- at 3 weeks, affected mice have thinner fur than controls (MGI Ref ID J:31745)
- abnormal dermal layer morphology
- in mice >28 weeks of age, dendritic cells with melanin granules are found in dermis and epidermis; heavily laden melanocytes are present in dermis (MGI Ref ID J:14539)
- mixed cellular infiltration to dermis
- inflammatory cells, predominantly granulocytes and macrophages (MGI Ref ID J:14539)
- fewer neutrophils are observed in dermis and epidermis in aged mice (>28 weeks) (MGI Ref ID J:14539)
- in excess of controls, observed from 1 week of age, and progresses to greater severity at 4 weeks (MGI Ref ID J:31745)
- 24 hours after i.p. injection of tumor necrosis factor into ears, mutant ears show less infiltration by neutrophils and fewer macrophages at 6-12 weeks of age (MGI Ref ID J:53575)
- abnormal epidermal layer morphology
- mild spongiosis (edema) of the epidermis is seen occasionally (MGI Ref ID J:14539)
- abnormal epidermis stratum basale morphology
- basal cell layer shows increased mitosis (MGI Ref ID J:14539)
- thick epidermis stratum basale
- thickness is increased due to cell proliferation at 4 weeks (MGI Ref ID J:31745)
- abnormal epidermis stratum corneum morphology
- some animals display intracorneal microabcesses at 5 weeks (MGI Ref ID J:31745)
- abnormal epidermis stratum granulosum morphology
- acanthosis
- observed at 4 weeks (MGI Ref ID J:31745)
- epidermal hyperplasia (MGI Ref ID J:14539)
- thick epidermis
- abnormal hair follicle morphology
- folliculitis
- folliculitis with some degenerated hair shafts is observed at 3 weeks of age (MGI Ref ID J:31745)
- abnormal hair shaft morphology
- epidermal changes along hair shafts result in hair shaft degeneration (MGI Ref ID J:14539)
- dermatitis
- mice develop dermatitis with associated skin lesions starting at 2-3 weeks of age (MGI Ref ID J:14539)
- increased keratinocyte apoptosis
- single cell death of keratinocytes in epidermis is seen (MGI Ref ID J:14539)
- some apoptosis is observed starting at 3 weeks (MGI Ref ID J:31745)
- 24 hours after i.p. injection of tumor necrosis factor into ears, there is marked apoptosis in epidermis of mutants at 6-12 weeks of age (MGI Ref ID J:53575)
- increased keratinocyte proliferation
- epidermal thickness is increased due to keratinocyte proliferation (MGI Ref ID J:31745)
- increased pruritus
- after 5 weeks of age, mice suffer from severe pruritus (itching) demonstrated by severe scratching (MGI Ref ID J:31745)
- reddish skin
- scaly skin (MGI Ref ID J:14539)
- skin edema
- mild spongiosis (intracellular edema) of the epidermis is seen occasionally (MGI Ref ID J:14539)
- skin lesions
- cellular phenotype
- increased keratinocyte apoptosis
- single cell death of keratinocytes in epidermis is seen (MGI Ref ID J:14539)
- some apoptosis is observed starting at 3 weeks (MGI Ref ID J:31745)
- 24 hours after i.p. injection of tumor necrosis factor into ears, there is marked apoptosis in epidermis of mutants at 6-12 weeks of age (MGI Ref ID J:53575)
- increased keratinocyte proliferation
- epidermal thickness is increased due to keratinocyte proliferation (MGI Ref ID J:31745)
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Sharpincpdm/Sharpincpdm
involves: C57BL/KaLawRij * CAST/EiJ
- integument phenotype
- alopecia
- a CAST/EiJ derived modifier results in incomplete penetrance of the skin phenotype (MGI Ref ID J:68129)
- scaly skin
- a CAST/EiJ derived modifier results in incomplete penetrance of the skin phenotype (MGI Ref ID J:68129)
Sharpincpdm/Sharpincpdm
involves: C57BL/KaLawRij * FVB/NJ
- immune system phenotype
- abnormal spleen B cell follicle morphology
- spleens have no defined follicles and germinal centers are absent (MGI Ref ID J:121810)
- absent spleen germinal center (MGI Ref ID J:121810)
- absent Peyer's patches
- no organized follicular structure are present in the antimesenteric wall of the small intestine (MGI Ref ID J:121810)
- skin inflammation
- the FVB/NJ background modifies the phenotype such that the skin shows mild inflammation and scattered apoptotic keratinocytes with a delayed onset (MGI Ref ID J:121810)
- hematopoietic system phenotype
- abnormal spleen B cell follicle morphology
- spleens have no defined follicles and germinal centers are absent (MGI Ref ID J:121810)
- absent spleen germinal center (MGI Ref ID J:121810)
- integument phenotype
- skin inflammation
- the FVB/NJ background modifies the phenotype such that the skin shows mild inflammation and scattered apoptotic keratinocytes with a delayed onset (MGI Ref ID J:121810)
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:
Dermatology Research
Skin and Hair Texture Defects
Immunology, Inflammation and Autoimmunity Research
Inflammation
Lymphoid Tissue Defects
| Allele Symbol | Sharpincpdm | ||
|---|---|---|---|
| Allele Name | chronic proliferative dermatitis | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | cpd; cpdm; | ||
| Strain of Origin | C57BL/Ka | ||
| Gene Symbol and Name | Sharpin, SHANK-associated RH domain interacting protein | ||
| Chromosome | 15 | ||
| Gene Common Name(s) | 0610041B22Rik; AW121341; Conneck1; RIKEN cDNA 0610041B22 gene; SIPL1; chronic proliferative dermatitis; cpdm; expressed sequence AW121341; | ||
| Molecular Note | A single base pair deletion in the 3' end of exon 1 creates a shift in the open reading frame predicted to cause a premature stop codon at position 624. [MGI Ref ID J:121810] | ||
Genotyping Protocols
Sharpincpdm, Pyrosequencing
Helpful Links
Genotyping resources and troubleshooting
Gijbels MJ; Zurcher C; Kraal G; Elliott GR; HogenEsch H; Schijff G ; Savelkoul HF ; Bruijnzeel PL. 1996. Pathogenesis of skin lesions in mice with chronic proliferative dermatitis (cpdm/cpdm). Am J Pathol 148(3):941-50. [PubMed: 8774148] [MGI Ref ID J:31745]
HogenEsch H; Gijbels MJ; Offerman E; van Hooft J; van Bekkum DW; Zurcher C. 1993. A spontaneous mutation characterized by chronic proliferative dermatitis in C57BL mice. Am J Pathol 143(3):972-82. [PubMed: 8362989] [MGI Ref ID J:14539]
HogenEsch H; Janke S; Boggess D; Sundberg JP. 1999. Absence of Peyer's patches and abnormal lymphoid architecture in chronic proliferative dermatitis (cpdm/cpdm) mice. J Immunol 162(7):3890-6. [PubMed: 10201907] [MGI Ref ID J:53575]
Sharpincpdm relatedDamgaard RB; Nachbur U; Yabal M; Wong WW; Fiil BK; Kastirr M; Rieser E; Rickard JA; Bankovacki A; Peschel C; Ruland J; Bekker-Jensen S; Mailand N; Kaufmann T; Strasser A; Walczak H; Silke J; Jost PJ; Gyrd-Hansen M. 2012. The ubiquitin ligase XIAP recruits LUBAC for NOD2 signaling in inflammation and innate immunity. Mol Cell 46(6):746-58. [PubMed: 22607974] [MGI Ref ID J:188020]
Gallardo Torres HI; Gijbels MJ; HegnEsch H; Kraal G. 1995. Chronic proliferative dermatitis in mice: neutrophil-endothelium interactions and the role of adhesion molecules. Pathobiology 63(6):341-7. [PubMed: 8738473] [MGI Ref ID J:33147]
Gerlach B; Cordier SM; Schmukle AC; Emmerich CH; Rieser E; Haas TL; Webb AI; Rickard JA; Anderton H; Wong WW; Nachbur U; Gangoda L; Warnken U; Purcell AW; Silke J; Walczak H. 2011. Linear ubiquitination prevents inflammation and regulates immune signalling. Nature 471(7340):591-6. [PubMed: 21455173] [MGI Ref ID J:170810]
Gijbels MJ; HogenEsch H; Blauw B; Roholl P; Zurcher C. 1995. Ultrastructure of epidermis of mice with chronic proliferative dermatitis. Ultrastruct Pathol 19(2):107-11. [PubMed: 7792947] [MGI Ref ID J:27806]
Gijbels MJ; HogenEsch H; Bruijnzeel PL; Elliott GR; Zurcher C. 1995. Maintenance of donor phenotype after full-thickness skin transplantation from mice with chronic proliferative dermatitis (cpdm/cpdm) to C57BL/Ka and nude mice and vice versa. J Invest Dermatol 105(6):769-73. [PubMed: 7490470] [MGI Ref ID J:30497]
Gudjonsson JE; Johnston A; Dyson M; Valdimarsson H; Elder JT. 2007. Mouse models of psoriasis. J Invest Dermatol 127(6):1292-308. [PubMed: 17429444] [MGI Ref ID J:121548]
HogenEsch H; Boggess D; Sundberg JP. 1999. Changes in keratin and filaggrin expression in the skin of chronic proliferative dermatitis (cpdm) mutant mice. Pathobiology 67(1):45-50. [PubMed: 9873228] [MGI Ref ID J:52422]
HogenEsch H; Dunham A; Seymour R; Renninger M; Sundberg JP. 2006. Expression of chitinase-like proteins in the skin of chronic proliferative dermatitis (cpdm/cpdm) mice. Exp Dermatol 15(10):808-14. [PubMed: 16984263] [MGI Ref ID J:135844]
HogenEsch H; Torregrosa SE; Boggess D; Sundberg BA; Carroll J; Sundberg JP. 2001. Increased expression of type 2 cytokines in chronic proliferative dermatitis (cpdm) mutant mice and resolution of inflammation following treatment with IL-12. Eur J Immunol 31(3):734-42. [PubMed: 11241277] [MGI Ref ID J:68121]
Ikeda F; Deribe YL; Skanland SS; Stieglitz B; Grabbe C; Franz-Wachtel M; van Wijk SJ; Goswami P; Nagy V; Terzic J; Tokunaga F; Androulidaki A; Nakagawa T; Pasparakis M; Iwai K; Sundberg JP; Schaefer L; Rittinger K; Macek B; Dikic I. 2011. SHARPIN forms a linear ubiquitin ligase complex regulating NF-kappaB activity and apoptosis. Nature 471(7340):637-41. [PubMed: 21455181] [MGI Ref ID J:170302]
Liang Y; Seymour RE; Sundberg JP. 2011. Inhibition of NF-kappaB signaling retards eosinophilic dermatitis in SHARPIN-deficient mice. J Invest Dermatol 131(1):141-9. [PubMed: 20811394] [MGI Ref ID J:182100]
Renninger ML; Seymour R; Lillard JW; Sundberg JP; HogenEsch H. 2005. Increased expression of chemokines in the skin of chronic proliferative dermatitis mutant mice. Exp Dermatol 14(12):906-13. [PubMed: 16274458] [MGI Ref ID J:116833]
Seymour RE; Hasham MG; Cox GA; Schultz LD; Hogenesch H; Roopenian DC; Sundberg JP. 2007. Spontaneous mutations in the mouse Sharpin gene result in multiorgan inflammation, immune system dysregulation and dermatitis Genes Immun 8(5):416-21. [PubMed: 17538631] [MGI Ref ID J:121810]
Sieber S; Lange N; Kollmorgen G; Erhardt A; Quaas A; Gontarewicz A; Sass G; Tiegs G; Kreienkamp HJ. 2012. Sharpin contributes to TNFalpha dependent NFkappaB activation and anti-apoptotic signalling in hepatocytes. PLoS One 7(1):e29993. [PubMed: 22253853] [MGI Ref ID J:184313]
Sundberg JP (ed.). 1994. Handbook of Mouse Mutations with Skin and Hair Abnormalities: Animal Models and Biomedical Tools. In: Handbook of Mouse Mutations with Skin and Hair Abnormalities: Animal Models and Biomedical Tools. CRC Press, Boca Raton. [MGI Ref ID J:30359]
Sundberg JP; Boggess D; Shultz LD; Fijneman RJA; Demant P; Hogenesch H; Cox GA. 2000. The chronic proliferative dermatitis mouse mutation (cpdm): mapping of the mutant gene locus J Exp Anim Sci 41:101-8. [MGI Ref ID J:68129]
Tokunaga F; Nakagawa T; Nakahara M; Saeki Y; Taniguchi M; Sakata S; Tanaka K; Nakano H; Iwai K. 2011. SHARPIN is a component of the NF-kappaB-activating linear ubiquitin chain assembly complex. Nature 471(7340):633-6. [PubMed: 21455180] [MGI Ref ID J:170809]
Wang Z; Sokolovska A; Seymour R; Sundberg JP; Hogenesch H. 2012. SHARPIN is essential for cytokine production, NF-kappaB signaling, and induction of Th1 differentiation by dendritic cells. PLoS One 7(2):e31809. [PubMed: 22348129] [MGI Ref ID J:185326]
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* $2250.00 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 |
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Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2925.00 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).
|
|
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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