Strain Name:

C57BL/KaLawRij-Sharpincpdm/RijSunJ

Stock Number:

007599

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Availability:

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Mice homozygous for this spontaneous mutation develop a severe, chronic, inflammatory skin disease beginning at 3-5 weeks of age. This mutant mouse strain may be useful in studies related to eosinophilic dermatitis, inflammation and secondary lymphoid organ development.

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

Type Coisogenic; Mutant Strain; Spontaneous Mutation;
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Specieslaboratory mouse
H2 Haplotypeb

Appearance
black
Related Genotype: a/a

Description
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 Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls

Phenotype

Phenotype Information

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)
      • decreased IgA level
        • total IgA is significantly lower in serum compared to controls; IgA in feces is greatly reduced at 6-12 weeks of age   (MGI Ref ID J:53575)
      • decreased IgE level
        • serum levels are decreased ~10-fold compared to controls   (MGI Ref ID J:31745)
        • total IgE is significantly lower in serum   (MGI Ref ID J:53575)
      • decreased IgG level
        • total IgG is significantly lower in serum   (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
      • at >28 weeks of age, heavily laden melanocytes are present in draining lymph nodes   (MGI Ref ID J:14539)
      • peripheral lymph nodes draining the skin are swollen, having a thin cortex without clearly defined follicles, and large numbers of eosinophils in the medulla   (MGI Ref ID J:53575)
      • 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)
      • abnormal spleen white pulp morphology   (MGI Ref ID J:31745)
        • white pulp is poorly defined at 6-12 weeks of age   (MGI Ref ID J:53575)
        • abnormal spleen B cell follicle morphology
          • spleens have no defined follicles and germinal centers are absent   (MGI Ref ID J:53575)
          • absent spleen germinal center   (MGI Ref ID J:53575)
        • absent spleen marginal zone
          • no evidence of a marginal zone is found   (MGI Ref ID J:53575)
      • enlarged spleen
        • 3- to 6-fold increase in spleen size is observed   (MGI Ref ID J:14539)
        • spleens in mutants are enlarged 3- to 5-fold due to extramedullary hematopoiesis   (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
    • mutants have increased counts of eosinophilic alveolar macrophages   (MGI Ref ID J:14539)
    • eosinophil infiltration of red and white pulp of spleen is seen starting at 4 weeks of age   (MGI Ref ID J:31745)
  • increased mast cell number
    • numbers are significantly increased in dermis at 6-8 weeks (171/sq. mm) and increase with age (594/sq.mm at 28-30 weeks)   (MGI Ref ID J:14539)
    • 6 week old mice have increased mast cell numbers compared to controls (213/sq.mm vs 82/sq.mm)   (MGI Ref ID J:31745)
  • 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)
    • abnormal spleen white pulp morphology   (MGI Ref ID J:31745)
      • white pulp is poorly defined at 6-12 weeks of age   (MGI Ref ID J:53575)
      • abnormal spleen B cell follicle morphology
        • spleens have no defined follicles and germinal centers are absent   (MGI Ref ID J:53575)
        • absent spleen germinal center   (MGI Ref ID J:53575)
      • absent spleen marginal zone
        • no evidence of a marginal zone is found   (MGI Ref ID J:53575)
    • enlarged spleen
      • 3- to 6-fold increase in spleen size is observed   (MGI Ref ID J:14539)
      • spleens in mutants are enlarged 3- to 5-fold due to extramedullary hematopoiesis   (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)
  • 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)
    • decreased IgA level
      • total IgA is significantly lower in serum compared to controls; IgA in feces is greatly reduced at 6-12 weeks of age   (MGI Ref ID J:53575)
    • decreased IgE level
      • serum levels are decreased ~10-fold compared to controls   (MGI Ref ID J:31745)
      • total IgE is significantly lower in serum   (MGI Ref ID J:53575)
    • decreased IgG level
      • total IgG is significantly lower in serum   (MGI Ref ID J:53575)
  • extramedullary hematopoiesis   (MGI Ref ID J:53575)
    • marked, accounts for splenomegaly   (MGI Ref ID J:14539)
    • at 2 weeks of age, mutants show moderate extramedullary myelopoiesis in liver and spleen   (MGI Ref ID J:31745)
  • increased IgM level
    • levels in feces are significantly increased compared to controls   (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
    • mutants have increased counts of eosinophilic alveolar macrophages   (MGI Ref ID J:14539)
    • eosinophil infiltration of red and white pulp of spleen is seen starting at 4 weeks of age   (MGI Ref ID J:31745)
  • increased mast cell number
    • numbers are significantly increased in dermis at 6-8 weeks (171/sq. mm) and increase with age (594/sq.mm at 28-30 weeks)   (MGI Ref ID J:14539)
    • 6 week old mice have increased mast cell numbers compared to controls (213/sq.mm vs 82/sq.mm)   (MGI Ref ID J:31745)
  • growth/size/body 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
    • at 20 weeks, similar changes to those seen in epidermis are found, with exception of parakeratosis   (MGI Ref ID J:14539)
    • thickness of forestomach epithelium is increased from 34.1 um to 68.9 um in mutants; less severe in aged mice   (MGI Ref ID J:14539)
  • 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
    • portal and perivascular areas in liver are infiltrated by neutrophils and macrophages   (MGI Ref ID J:14539)
    • at 3 weeks, small perivascular infiltrates of eosinophils and macrophages are observed, with progressive severity   (MGI Ref ID J:31745)
  • 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)
    • alopecia
      • clinical alopecia develops by 5 weeks of age and becomes progressively worse   (MGI Ref ID J:68129)
    • premature hair loss
      • beginning at 5 weeks of age, affected mice develop hair loss   (MGI Ref ID J:14539)
      • at 4 weeks, dorsal neck and ventral chest develop hair loss   (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)
      • hyperkeratosis   (MGI Ref ID J:14539)
        • at 4 weeks   (MGI Ref ID J:31745)
        • parakeratosis   (MGI Ref ID J:14539)
          • multifocal, observed at 4 weeks   (MGI Ref ID J:31745)
    • abnormal epidermis stratum granulosum morphology
      • layer is thicker or of normal thickness and absent beneath parakeratotic mounds in mutants   (MGI Ref ID J:14539)
      • some degenerated granulocytes mix with parakeratotic mounds and form microabscesses in keratotic layer   (MGI Ref ID J:14539)
    • acanthosis
      • observed at 4 weeks   (MGI Ref ID J:31745)
    • epidermal hyperplasia   (MGI Ref ID J:14539)
    • thick epidermis
      • interfollicular epidermis is thickened (from 8.8 um to 55.6 um)   (MGI Ref ID J:14539)
      • significantly increased at 4 weeks compared to control, showing increased cellular proliferation   (MGI Ref ID J:31745)
  • abnormal hair follicle morphology
    • epidermal changes along hair shafts result in follicular keratosis   (MGI Ref ID J:14539)
    • increased numbers of proliferating cells are found   (MGI Ref ID J:14539)
    • 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
    • beginning at 5 weeks of age, reddening of skin of dorsal neck and ventral chest is observed, spreading to most skin, except tail, feet, and ear pinnae by 12-15 weeks   (MGI Ref ID J:14539)
    • at 3 weeks, reddening of the axilla is observed, such that mutants can all be identified   (MGI Ref ID J:31745)
  • scaly skin   (MGI Ref ID J:14539)
    • at 4 weeks, dorsal neck and ventral chest develop mild scaling   (MGI Ref ID J:31745)
    • scaling skin is found by 5 weeks of age and becomes progressively worse   (MGI Ref ID J:68129)
  • skin edema
    • mild spongiosis (intracellular edema) of the epidermis is seen occasionally   (MGI Ref ID J:14539)
  • skin lesions
    • lesions are characterized by erythema, severe hair loss, and mild scaling at 20 weeks of age   (MGI Ref ID J:14539)
    • lesions are similar in aged mice (28-30 weeks of age)   (MGI Ref ID J:14539)
    • lesions progress with age, from 2-3 weeks; at 6 weeks, lesions are extensive and severe   (MGI Ref ID J:31745)
  • 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 is associated with a similar, but not exact match to 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

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Sharpincpdm
Allele Name chronic proliferative dermatitis
Allele Type Spontaneous
Common Name(s) cpd; cpdm;
Strain of OriginC57BL/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

Genotyping Information

Genotyping Protocols

Sharpincpdm, Pyrosequencing


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

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]

Additional References

Sharpincpdm related

Damgaard 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]

Pouwels J; De Franceschi N; Rantakari P; Auvinen K; Karikoski M; Mattila E; Potter C; Sundberg JP; Hogg N; Gahmberg CG; Salmi M; Ivaska J. 2013. SHARPIN regulates uropod detachment in migrating lymphocytes. Cell Rep 5(3):619-28. [PubMed: 24210817]  [MGI Ref ID J:205531]

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 R; Shirley BJ; Hogenesch H; Shultz LD; Sundberg JP. 2013. Loss of function of the mouse Sharpin gene results in Peyer's patch regression. PLoS One 8(2):e55224. [PubMed: 23424624]  [MGI Ref ID J:197197]

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]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2450.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 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 View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3185.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 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).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

General Supply Notes

  • View the complete collection of spontaneous mutants in the Mouse Mutant Resource.

Control Information

  Control
   Wild-type from the colony
 
  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
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

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.


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