Strain Name:

B6;129S4-C3tm1Crr/J

Stock Number:

003641

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Availability:

Repository- Live

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Use Restrictions Apply, see Terms of Use
These knock-out mice, susceptible to infection, are useful when studying the role of C3 during immune responses to infection.

Description

Strain Information

Former Names B6.129S4-C3tm1Crr/J    (Changed: 27-APR-11 )
Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHomozygote x Homozygote         (Female x Male)   21-JUN-06
Specieslaboratory mouse
Background Strain C57BL/6
Donor Strain 129S4 via J1 ES cell line
GenerationN7F12 (03-SEP-14)
Generation Definitions
 
Donating Investigator Michael C. Carroll,   The Center for Blood Research

Description
Mice homozygous for the C3 (complement component C3) targeted mutation are viable and fertile. Homozygous mutants exhibit an increased susceptibility to lethal infection by Group B streptococci. Reductions in peritoneal mast cell degranulation, production of tumor necrosis factor alpha, neutrophil infiltration and bacterial clearance have also been reported in these mice. Homozygotes also demonstrate a profound defect in antibody response to T cell dependent antigens. They show a diminished level of peanut agglutin+ germinal centers and a failure in isotype switching despite normal B cell signalling in vitro.

Development
The C3 gene is disrupted by PGK/Neo cassette. Approximately 600 nt of the gene are deleted. A portion of these nts (nt 1850-2214; AA 620-741, pro-C3 numbering) fall within the coding region. The targeting construct was transfected into 129S4/SvJae derived J1 ES cells. Successful transfectants were injected into 3.5 day old C57BL/6 blastocysts which were then implanted into the uterus of pseudopregnant females. Male chimeric mice were bred with C57BL/6 females. The donating investigator reported backcrossing this strain to C57BL/6J for at least five generations prior to sending to The Jackson Laboratory Repository (see SNP notes below).

A 32 SNP (single nucleotide polymorphism) panel analysis, with markers covering all 19 chromosomes and the X chromosome, was performed on the rederived living colony at The Jackson Laboratory Repository. This revealed 3 markers (representing one each on chromosomes 7, 12, and 19) that were not fixed for C57BL/6 allele-type (e.g.: still segregating for 129S4 allele-type markers). The marker on chromosome 12 may be fixed as homozygous for the 129S4 allele-type. These data suggest the mice may have been backcrossed to C57BL/6 for 1-2 fewer generations than reported prior to arrival at The Jackson Laboratory Repository.

Control Information

  Control
   000664 C57BL/6J (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   C3tm1Crr allele
009077   B6;129-C3tm1Crr Man2a1tm1Jxm/J
View Strains carrying   C3tm1Crr     (1 strain)

Strains carrying other alleles of C3
000833   B6.SJL-C3c/J
000944   B6.SJL-H2b C3c/2CyJ
000966   B6.SJL-H2s C3c/1CyJ
022098   B6N(Cg)-C3tm1.1(KOMP)Vlcg/J
012261   CBA.129S4(B6)-C3tm1Hrc/Mmjax
012301   D2.129S4(B6)-C3tm1Hrc/Mmjax
View Strains carrying other alleles of C3     (6 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Complement Component 3 Deficiency, Autosomal Recessive; C3D   (C3)
Hemolytic Uremic Syndrome, Atypical, Susceptibility to, 5; AHUS5   (C3)
Macular Degeneration, Age-Related, 9; ARMD9   (C3)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

C3tm1Crr/C3tm1Crr

        involves: 129S4/SvJae * C57BL/6
  • mortality/aging
  • abnormal induced morbidity/mortality
    • poor survival (20%) after 30 minutes of ischemia while 70% partial hepatectomy performed   (MGI Ref ID J:152533)
    • increased sensitivity to induced morbidity/mortality
      • caecal ligation and puncture (CLP) causes greater mortality in mutants than wild-type in the first 24 hours after CLP (100 vs 20% mortality)   (MGI Ref ID J:44240)
      • reconstitution of mice with ip. injection of purified human C3 (HuC3) reduces mortality from 100% to 40% in the first 24 hours   (MGI Ref ID J:44240)
    • increased susceptibility to bacterial infection induced morbidity/mortality
      • in mice infected with S. pneumoniae   (MGI Ref ID J:205353)
  • immune system phenotype
  • *normal* immune system phenotype
    • secondary immune responses are similar in wild type and mutant mice, so helper T cell function is normal secondary immune responses are similar in wild-type and mutant mice, so helper T cell function is normal   (MGI Ref ID J:64282)
    • B cells from deficient mice show normal proliferative effects in response to surface IgM crosslinking   (MGI Ref ID J:64282)
    • abnormal immune system morphology   (MGI Ref ID J:44240)
      • abnormal spleen germinal center morphology   (MGI Ref ID J:64282)
        • decreased spleen germinal center number
          • after immunization, wild-type mice develop germinal centers (GC) in ~half of splenic follicles while ~10% of splenic follicles in C3-deficient mice contain GCs   (MGI Ref ID J:64282)
        • decreased spleen germinal center size
          • diameter of GCs are less than that observed in wild-type   (MGI Ref ID J:64282)
      • decreased mast cell number
        • after CLP less peritoneal mast cells can be recovered from Cr3-deficient mice compared to controls   (MGI Ref ID J:44240)
      • decreased neutrophil cell number
        • 1 hour after CLP, 50% of peritoneal cells are neutrophils and after 3 hours, 90% are neutrophils while in C3-deficient mice, after 1 hour only 1% and 45% after 3 hours are neutrophils   (MGI Ref ID J:44240)
      • decreased osteoclast cell number
        • bone marrow cells incubated with 1,25(OH)2 vitamin D3 produce fewer osteoclasts than do cells from controls   (MGI Ref ID J:166640)
    • abnormal immune system physiology   (MGI Ref ID J:44240)
      • abnormal cell-mediated immunity
        • in an in vitro assay, opsonization with serum from C3-deficient mice and 1% immune rabbit serum only resulted in a 0.2 log10 reduction in GBS CFU compared to a 1.0 log10 reduction by normal mouse serum   (MGI Ref ID J:30152)
        • abnormal mast cell physiology
          • mast cells from mutants 1 or 3 hours after CLP show reduced degranulation compared to wild-type (75% of wild-type cells vs <50% of C3-deficient cells)   (MGI Ref ID J:44240)
          • treatment with HuC3 results in comparable levels of mast cell degranulation to wild-type   (MGI Ref ID J:44240)
      • abnormal humoral immune response
        • in response to immunization with bacteriophage (phiX174), a T cell dependent antigen, C3-deficient mice mount a weak Ig M response but fail to switch to IgG   (MGI Ref ID J:64282)
        • when immunized with a 10-fold higher amount of bacteriophage, mice show a weak IgG response but response is still 10-fold lower than wild-type   (MGI Ref ID J:64282)
      • abnormal tumor necrosis factor level
        • levels of Tnfa in peritoneal lavage fluids are reduced in C3-deficient mice compared to controls at 1 hour (158 mg/pl vs 400 mg/pl) and 3 hours (218 mg/pl vs 663 pg/ml) after CLP   (MGI Ref ID J:44240)
        • treatment with HuC3 restores levels of Tnfa production in mutants to wild-type levels   (MGI Ref ID J:44240)
        • decreased circulating tumor necrosis factor level
          • reduced TNFalpha levels at 6 and 24 hours after 6 and 24 hours of reperfusion   (MGI Ref ID J:152533)
      • decreased circulating interleukin-6 level
        • reduced levels at 6 and 24 hours after 6 and 24 hours of reperfusion   (MGI Ref ID J:152533)
        • Il-6 production after vitamin D3 stimulation is significantly reduced   (MGI Ref ID J:166640)
      • increased susceptibility to bacterial infection
        • mice challenged with group B Streptococci (GBS) infection become bacteremic within 3 days and die or clear bacteria and survive; C3-deficient mice challenged with GBS infection showed a decreased LD50 dose compared to immunocompetent controls (LD50 dose: control 6.3 x 104 vs. 1.3 x 103 in C3-deficient mice)   (MGI Ref ID J:30152)
        • increased mortality from GBS infection compared to controls is limited to the first 3 days after challenge   (MGI Ref ID J:30152)
        • when pregnant dams are immunized with immune rabbit serum, pups are not protected against lethal challenge on day 2 of life (15/20 pups die within 48 hours)   (MGI Ref ID J:30152)
        • at 1 or 3 hours after CLP, cytocentrifuge preparations or peritoneal fluid from C3-deficient mice have reduced neutrophil counts and large numbers of bacteria, compared to wild-type which have few or no bacteria   (MGI Ref ID J:44240)
        • treatment with HuC3 restore neutrophil numbers and enhance bacterial clearance to wild-type levels   (MGI Ref ID J:44240)
        • increased susceptibility to bacterial infection induced morbidity/mortality
          • in mice infected with S. pneumoniae   (MGI Ref ID J:205353)
      • liver inflammation
        • mild hepatitis is observed in a small number (1/11) of mice surviving systemic challenge with GBS doses of 102 to 105 CFU upon necropsy 15 days post-challenge; there are aggregates of mononuclear or polymorphonuclear leukocytes in hepatic sinusoids; wild-type animals that receive higher doses of GBS showed similar lesions   (MGI Ref ID J:30152)
  • cardiovascular system phenotype
  • decreased vascular permeability
    • upeon reperfusion of ischemic intestine (jejunum), permeability index (PI) of injured C3-deficient mice is reduced compared to control treated wild-type (PI of 2.25 vs 3.26 in controls)   (MGI Ref ID J:78613)
  • digestive/alimentary phenotype
  • abnormal intestine morphology
    • mice show less evidence of infarction compared to controls   (MGI Ref ID J:78613)
  • homeostasis/metabolism phenotype
  • abnormal enzyme/ coenzyme level
    • lower levels of myeloperoxidase in livers at 6 and 24 hours of reperfusion   (MGI Ref ID J:152533)
    • decreased circulating alanine transaminase level
      • levels lower during reperfusion after ischemia than in controls   (MGI Ref ID J:152533)
    • increased circulating alanine transaminase level
      • after 70% partial hepatectomy   (MGI Ref ID J:152533)
  • abnormal tumor necrosis factor level
    • levels of Tnfa in peritoneal lavage fluids are reduced in C3-deficient mice compared to controls at 1 hour (158 mg/pl vs 400 mg/pl) and 3 hours (218 mg/pl vs 663 pg/ml) after CLP   (MGI Ref ID J:44240)
    • treatment with HuC3 restores levels of Tnfa production in mutants to wild-type levels   (MGI Ref ID J:44240)
    • decreased circulating tumor necrosis factor level
      • reduced TNFalpha levels at 6 and 24 hours after 6 and 24 hours of reperfusion   (MGI Ref ID J:152533)
  • decreased circulating interleukin-6 level
    • reduced levels at 6 and 24 hours after 6 and 24 hours of reperfusion   (MGI Ref ID J:152533)
    • Il-6 production after vitamin D3 stimulation is significantly reduced   (MGI Ref ID J:166640)
  • decreased susceptibility to injury
    • mice are resistant to ischemia reperfusion-induced renal injury   (MGI Ref ID J:120567)
    • serum urea nitrogen is reduced 31% to 55% compared to wild-type mice subjected to ischemia reperfusion   (MGI Ref ID J:120567)
    • neutrophil infiltration at the site of injury was reduced   (MGI Ref ID J:120567)
  • increased circulating bilirubin level
    • after 70% partial hepatectomy   (MGI Ref ID J:152533)
  • hematopoietic system phenotype
  • abnormal mast cell physiology
    • mast cells from mutants 1 or 3 hours after CLP show reduced degranulation compared to wild-type (75% of wild-type cells vs <50% of C3-deficient cells)   (MGI Ref ID J:44240)
    • treatment with HuC3 results in comparable levels of mast cell degranulation to wild-type   (MGI Ref ID J:44240)
  • abnormal spleen germinal center morphology   (MGI Ref ID J:64282)
    • decreased spleen germinal center number
      • after immunization, wild-type mice develop germinal centers (GC) in ~half of splenic follicles while ~10% of splenic follicles in C3-deficient mice contain GCs   (MGI Ref ID J:64282)
    • decreased spleen germinal center size
      • diameter of GCs are less than that observed in wild-type   (MGI Ref ID J:64282)
  • decreased mast cell number
    • after CLP less peritoneal mast cells can be recovered from Cr3-deficient mice compared to controls   (MGI Ref ID J:44240)
  • decreased neutrophil cell number
    • 1 hour after CLP, 50% of peritoneal cells are neutrophils and after 3 hours, 90% are neutrophils while in C3-deficient mice, after 1 hour only 1% and 45% after 3 hours are neutrophils   (MGI Ref ID J:44240)
  • decreased osteoclast cell number
    • bone marrow cells incubated with 1,25(OH)2 vitamin D3 produce fewer osteoclasts than do cells from controls   (MGI Ref ID J:166640)
  • liver/biliary system phenotype
  • abnormal liver morphology
    • histological evidence of injury after 6 and 24 hours of reperfusion following ischemia   (MGI Ref ID J:152533)
    • focal hepatic necrosis
      • after 70% partial hepatectomy   (MGI Ref ID J:152533)
    • hepatic steatosis
      • increased steatosis after 70% hepatectomy   (MGI Ref ID J:152533)
  • abnormal liver physiology   (MGI Ref ID J:152533)
    • decreased hepatocyte proliferation
      • impaired hepatocyte proliferation after 30 minutes of ischemia during 70% partial hepatectomy   (MGI Ref ID J:152533)
    • decreased liver regeneration
      • significant hepatic injury after 30 minutes of ischemia during 70% partial hepatectomy   (MGI Ref ID J:152533)
      • impaired regenerative response after 70% hepatectomy   (MGI Ref ID J:152533)
    • liver inflammation
      • mild hepatitis is observed in a small number (1/11) of mice surviving systemic challenge with GBS doses of 102 to 105 CFU upon necropsy 15 days post-challenge; there are aggregates of mononuclear or polymorphonuclear leukocytes in hepatic sinusoids; wild-type animals that receive higher doses of GBS showed similar lesions   (MGI Ref ID J:30152)
  • nervous system phenotype
  • abnormal peripheral nervous system regeneration
    • locomotor recovery from spinal cord injury occurs more rapidly than in controls   (MGI Ref ID J:112353)
    • slight improvement in tissue at 24 hours aftwr injury but considerably improved relative to controls by 72 hours   (MGI Ref ID J:112353)
    • grossly normal at 7 days after injury compared to controls which show marked necrosis and vacuolation in controls at 21 days   (MGI Ref ID J:112353)
  • skeleton phenotype
  • decreased osteoclast cell number
    • bone marrow cells incubated with 1,25(OH)2 vitamin D3 produce fewer osteoclasts than do cells from controls   (MGI Ref ID J:166640)
  • cellular phenotype
  • decreased hepatocyte proliferation
    • impaired hepatocyte proliferation after 30 minutes of ischemia during 70% partial hepatectomy   (MGI Ref ID J:152533)

C3tm1Crr/C3tm1Crr

        B6;129S4-C3tm1Crr/J
  • immune system phenotype
  • *normal* immune system phenotype
    • mice infected with 500 CFU of S. aureus, show higher numbers of bacterial SFU (intraocular growth) at 24 and 48 hours post-infection, levels are indistinguishable from infected wild-type by 72 hours   (MGI Ref ID J:136745)
  • vision/eye phenotype
  • *normal* vision/eye phenotype
    • eyes infected with 500 CFU S. aureus show mild signs of inflammation at 24 and 48 hours but appear normal at 72 hours   (MGI Ref ID J:136745)
    • abnormal eye electrophysiology
      • 24 hours after infection with 500 CFU of S. aureus, mice show a transient loss of b-wave amplitude; this stabilizes at a level of 66% of baseline values, similar to what is seen in eyes of infected wild-type mice   (MGI Ref ID J:136745)

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

C3tm1Crr/C3tm1Crr

        B6.129S4-C3tm1Crr
  • immune system phenotype
  • abnormal inflammatory response
    • following exposure to LPS then challenge with TNF at the same site to initiate a local Shwartman response, mice fail to exhibit hemorrhage and exhibit reduced fibrin deposition compared to the thrombohemorrhagic vasculitis observed in wild-type mice despite normal neutrophil accumulation   (MGI Ref ID J:113463)
    • brain inflammation
      • reduced granulocyte infiltration of infarct sites   (MGI Ref ID J:123658)
  • abnormal neutrophil morphology
    • neutrophils that accumulate at the site of a local Shwartman response are round instead of flattened as in wild-type mice   (MGI Ref ID J:113463)
  • decreased susceptibility to autoimmune hemolytic anemia
    • mice are resistant to hemolytic anemia induced by self-binding IgG2a antibodies   (MGI Ref ID J:145432)
    • no protection is seen with pathogenic IgM or IgA self-antibodies   (MGI Ref ID J:145432)
  • homeostasis/metabolism phenotype
  • abnormal blood homeostasis
    • mouse serum fails to support neutrophil adhesion unlike serum from wild-type mice   (MGI Ref ID J:113463)
  • decreased cerebral infarction size
    • significantly reduced infarct volume but mortality unaffected   (MGI Ref ID J:123658)
  • hematopoietic system phenotype
  • abnormal neutrophil morphology
    • neutrophils that accumulate at the site of a local Shwartman response are round instead of flattened as in wild-type mice   (MGI Ref ID J:113463)
  • decreased susceptibility to autoimmune hemolytic anemia
    • mice are resistant to hemolytic anemia induced by self-binding IgG2a antibodies   (MGI Ref ID J:145432)
    • no protection is seen with pathogenic IgM or IgA self-antibodies   (MGI Ref ID J:145432)
  • nervous system phenotype
  • brain inflammation
    • reduced granulocyte infiltration of infarct sites   (MGI Ref ID J:123658)
  • decreased cerebral infarction size
    • significantly reduced infarct volume but mortality unaffected   (MGI Ref ID J:123658)
  • reproductive system phenotype
  • abnormal female reproductive system physiology   (MGI Ref ID J:150898)
    • impaired embryo implantation
      • insignificantly but consistently reduced level of implantation at day 8   (MGI Ref ID J:150898)
    • prolonged estrous cycle
      • 5.42 days vs 4.41 days in controls   (MGI Ref ID J:150898)
  • embryogenesis phenotype
  • abnormal blastocyst morphology
    • blastocyst count at 4 days is consistently but insignificantly lower than in controls   (MGI Ref ID J:150898)
  • decreased placental labyrinth size
    • labyrinth area significantly reduced at day 15 of pregnancy   (MGI Ref ID J:150898)
  • decreased spongiotrophoblast size
    • significantly reduced spongioblast at day 15 of pregnancy   (MGI Ref ID J:150898)
  • small placenta
    • reduced placenta area at day 15 of pregnancy   (MGI Ref ID J:150898)
  • growth/size/body phenotype
  • decreased fetal weight
    • significantly reduced fetal weight   (MGI Ref ID J:150898)
    • reduced fetus/placenta ratio   (MGI Ref ID J:150898)

C3tm1Crr/C3tm1Crr

        involves: 129S4/SvJae
  • homeostasis/metabolism phenotype
  • abnormal blood coagulation
    • thrombus formation considerably reduced   (MGI Ref ID J:44715)
  • decreased susceptibility to injury
    • following exposure to ethanol, mice do not develop microvesicular or macrovesicular steatosis of the liver and do not accumulate excessive trglycerides as in wild-type mice   (MGI Ref ID J:128218)
    • following exposure to ethanol, mice exhibit a reduced increased in alanine aminotransferase compared to in similarly treated wild-type mice   (MGI Ref ID J:128218)
  • decreased urine albumin level
    • albuminuria 1/50 control levels after 0.5ng dose of anti glomerular basement membrane antiserum and 1/13 of control levels after 1 ng of antiserum   (MGI Ref ID J:44715)
  • liver/biliary system phenotype
  • decreased susceptibility to hepatic steatosis
    • following exposure to ethanol, mice do not develop microvesicular or macrovesicular steatosis of the liver as in wild-type mice   (MGI Ref ID J:128218)
  • renal/urinary system phenotype
  • decreased urine albumin level
    • albuminuria 1/50 control levels after 0.5ng dose of anti glomerular basement membrane antiserum and 1/13 of control levels after 1 ng of antiserum   (MGI Ref ID J:44715)
  • glomerulonephritis
    • reduced neutrophil infiltration of glomerulus relative to controls when injected with 0.5 mg but not with 1.0mg of anti-glomerular basement membrane antiserum   (MGI Ref ID J:44715)
  • immune system phenotype
  • glomerulonephritis
    • reduced neutrophil infiltration of glomerulus relative to controls when injected with 0.5 mg but not with 1.0mg of anti-glomerular basement membrane antiserum   (MGI Ref ID J:44715)
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Research Applications
This mouse can be used to support research in many areas including:

C3tm1Crr related

Developmental Biology Research
Lymphoid Tissue Defects
      hematopoietic defects

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency
      specific complement deficiency
Immunodeficiency Associated with Other Defects
Inflammation

Research Tools
Immunology, Inflammation and Autoimmunity Research
      specific complement deficiency

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol C3tm1Crr
Allele Name targeted mutation 1, Michael C Carroll
Allele Type Targeted (Null/Knockout)
Common Name(s) C3-; C3tm1Crr; mC3-;
Mutation Made By Michael Carroll,   The Center for Blood Research
Strain of Origin129S4/SvJae
ES Cell Line NameJ1
ES Cell Line Strain129S4/SvJae
Gene Symbol and Name C3, complement component 3
Chromosome 17
Gene Common Name(s) AHUS5; AI255234; ARMD9; ASP; C3a; C3b; CPAMD1; HEL-S-62p; Plp; acylation stimulating protein; complement factor 3; expressed sequence AI255234;
Molecular Note Insertion of a PGK-neomycin resistance cassette into an exon of the C3 gene deleted sequences that code for the C-terminal region of the beta chain and the N-terminal region of the alpha chain, including the site for processing the pro-C3 molecule. ELISAtesting did not detect C3 protein in serum of homozygous mutant mice. A C3 hemolytic assay did not detect functional C3 activity. [MGI Ref ID J:30152]

Genotyping

Genotyping Information

Genotyping Protocols

C3tm1Crr, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Hong F; Hansen RD; Yan J; Allendorf DJ; Baran JT; Ostroff GR; Ross GD. 2003. Beta-glucan functions as an adjuvant for monoclonal antibody immunotherapy by recruiting tumoricidal granulocytes as killer cells. Cancer Res 63(24):9023-31. [PubMed: 14695221]  [MGI Ref ID J:87069]

Tuzun E; Scott BG; Goluszko E; Higgs S; Christadoss P. 2003. Genetic evidence for involvement of classical complement pathway in induction of experimental autoimmune myasthenia gravis. J Immunol 171(7):3847-54. [PubMed: 14500686]  [MGI Ref ID J:85645]

Yamada K; Miwa T; Liu J; Nangaku M; Song WC. 2004. Critical protection from renal ischemia reperfusion injury by CD55 and CD59. J Immunol 172(6):3869-75. [PubMed: 15004194]  [MGI Ref ID J:88632]

C3tm1Crr related

Abbate M; Zoja C; Corna D; Rottoli D; Zanchi C; Azzollini N; Tomasoni S; Berlingeri S; Noris M; Morigi M; Remuzzi G. 2008. Complement-mediated dysfunction of glomerular filtration barrier accelerates progressive renal injury. J Am Soc Nephrol 19(6):1158-67. [PubMed: 18354030]  [MGI Ref ID J:150161]

Anderson DR; Tsutsui JM; Xie F; Radio SJ; Porter TR. 2007. The role of complement in the adherence of microbubbles to dysfunctional arterial endothelium and atherosclerotic plaque. Cardiovasc Res 73(3):597-606. [PubMed: 17196951]  [MGI Ref ID J:119533]

Ankeny DP; Guan Z; Popovich PG. 2009. B cells produce pathogenic antibodies and impair recovery after spinal cord injury in mice. J Clin Invest 119(10):2990-9. [PubMed: 19770513]  [MGI Ref ID J:154634]

Atkinson C; Varela JC; Tomlinson S. 2009. Complement-dependent inflammation and injury in a murine model of brain dead donor hearts. Circ Res 105(11):1094-101. [PubMed: 19815824]  [MGI Ref ID J:170147]

Atkinson C; Zhu H; Qiao F; Varela JC; Yu J; Song H; Kindy MS; Tomlinson S. 2006. Complement-dependent P-selectin expression and injury following ischemic stroke. J Immunol 177(10):7266-74. [PubMed: 17082645]  [MGI Ref ID J:140616]

Banda NK; Levitt B; Wood AK; Takahashi K; Stahl GL; Holers VM; Arend WP. 2009. Complement activation pathways in murine immune complex-induced arthritis and in C3a and C5a generation in vitro. Clin Exp Immunol 159(1):100-8. [PubMed: 19843088]  [MGI Ref ID J:155358]

Banda NK; Takahashi K; Wood AK; Holers VM; Arend WP. 2007. Pathogenic complement activation in collagen antibody-induced arthritis in mice requires amplification by the alternative pathway. J Immunol 179(6):4101-9. [PubMed: 17785849]  [MGI Ref ID J:152026]

Baruah P; Simpson E; Dumitriu IE; Derbyshire K; Coe D; Addey C; Dyson J; Chai JG; Cook T; Scott D; Botto M. 2010. Mice lacking C1q or C3 show accelerated rejection of minor H disparate skin grafts and resistance to induction of tolerance. Eur J Immunol 40(6):1758-67. [PubMed: 20213737]  [MGI Ref ID J:160952]

Baudino L; Fossati-Jimack L; Chevalley C; Martinez-Soria E; Shulman MJ; Izui S. 2007. IgM and IgA anti-erythrocyte autoantibodies induce anemia in a mouse model through multivalency-dependent hemagglutination but not through complement activation. Blood 109(12):5355-62. [PubMed: 17317854]  [MGI Ref ID J:145432]

Baudino L; Nimmerjahn F; Azeredo da Silveira S; Martinez-Soria E; Saito T; Carroll M; Ravetch JV; Verbeek JS; Izui S. 2008. Differential contribution of three activating IgG Fc receptors (FcgammaRI, FcgammaRIII, and FcgammaRIV) to IgG2a- and IgG2b-induced autoimmune hemolytic anemia in mice. J Immunol 180(3):1948-53. [PubMed: 18209093]  [MGI Ref ID J:131620]

Baudino L; Sardini A; Ruseva MM; Fossati-Jimack L; Cook HT; Scott D; Simpson E; Botto M. 2014. C3 opsonization regulates endocytic handling of apoptotic cells resulting in enhanced T-cell responses to cargo-derived antigens. Proc Natl Acad Sci U S A 111(4):1503-8. [PubMed: 24474777]  [MGI Ref ID J:206648]

Bauer EM; Zheng H; Comhair S; Erzurum S; Billiar TR; Bauer PM. 2011. Complement C3 deficiency attenuates chronic hypoxia-induced pulmonary hypertension in mice. PLoS One 6(12):e28578. [PubMed: 22194859]  [MGI Ref ID J:182250]

Baumann U; Chouchakova N; Gewecke B; Kohl J; Carroll MC; Schmidt RE; Gessner JE. 2001. Distinct tissue site-specific requirements of mast cells and complement components C3/C5a receptor in IgG immune complex-induced injury of skin and lung. J Immunol 167(2):1022-7. [PubMed: 11441111]  [MGI Ref ID J:120524]

Bergthaler A; Flatz L; Verschoor A; Hegazy AN; Holdener M; Fink K; Eschli B; Merkler D; Sommerstein R; Horvath E; Fernandez M; Fitsche A; Senn BM; Verbeek JS; Odermatt B; Siegrist CA; Pinschewer DD. 2009. Impaired antibody response causes persistence of prototypic T cell-contained virus. PLoS Biol 7(4):e1000080. [PubMed: 19355789]  [MGI Ref ID J:150498]

Bergtold A; Desai DD; Gavhane A; Clynes R. 2005. Cell surface recycling of internalized antigen permits dendritic cell priming of B cells. Immunity 23(5):503-14. [PubMed: 16286018]  [MGI Ref ID J:113283]

Binstadt BA; Patel PR; Alencar H; Nigrovic PA; Lee DM; Mahmood U; Weissleder R; Mathis D; Benoist C. 2006. Particularities of the vasculature can promote the organ specificity of autoimmune attack. Nat Immunol 7(3):284-92. [PubMed: 16444258]  [MGI Ref ID J:112604]

Bode J; Dutow P; Sommer K; Janik K; Glage S; Tummler B; Munder A; Laudeley R; Sachse KW; Klos A. 2012. A new role of the complement system: C3 provides protection in a mouse model of lung infection with intracellular Chlamydia psittaci. PLoS One 7(11):e50327. [PubMed: 23189195]  [MGI Ref ID J:194784]

Borkowska S; Suszynska M; Wysoczynski M; Ratajczak MZ. 2013. Mobilization studies in C3-deficient mice unravel the involvement of a novel crosstalk between the coagulation and complement cascades in mobilization of hematopoietic stem/progenitor cells. Leukemia 27(9):1928-30. [PubMed: 23511127]  [MGI Ref ID J:200120]

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Nguyen CQ; Kim H; Cornelius JG; Peck AB. 2007. Development of Sjogren's syndrome in nonobese diabetic-derived autoimmune-prone C57BL/6.NOD-Aec1Aec2 mice is dependent on complement component-3. J Immunol 179(4):2318-29. [PubMed: 17675493]  [MGI Ref ID J:151221]

Nimmerjahn F; Anthony RM; Ravetch JV. 2007. Agalactosylated IgG antibodies depend on cellular Fc receptors for in vivo activity. Proc Natl Acad Sci U S A 104(20):8433-7. [PubMed: 17485663]  [MGI Ref ID J:121840]

Nimmerjahn F; Ravetch JV. 2005. Divergent immunoglobulin g subclass activity through selective Fc receptor binding. Science 310(5753):1510-2. [PubMed: 16322460]  [MGI Ref ID J:103229]

Nishiguchi KM; Yasuma TR; Tomida D; Nakamura M; Ishikawa K; Kikuchi M; Ohmi Y; Niwa T; Hamajima N; Furukawa K; Terasaki H. 2012. C9-R95X polymorphism in patients with neovascular age-related macular degeneration. Invest Ophthalmol Vis Sci 53(1):508-12. [PubMed: 22190594]  [MGI Ref ID J:191511]

Nunez-Cruz S; Gimotty PA; Guerra MW; Connolly DC; Wu YQ; DeAngelis RA; Lambris JD; Coukos G; Scholler N. 2012. Genetic and pharmacologic inhibition of complement impairs endothelial cell function and ablates ovarian cancer neovascularization. Neoplasia 14(11):994-1004. [PubMed: 23226093]  [MGI Ref ID J:194414]

O'Brien KB; Morrison TE; Dundore DY; Heise MT; Schultz-Cherry S. 2011. A protective role for complement C3 protein during pandemic 2009 H1N1 and H5N1 influenza A virus infection. PLoS One 6(3):e17377. [PubMed: 21408070]  [MGI Ref ID J:171714]

O'Connell AE; Hess JA; Santiago GA; Nolan TJ; Lok JB; Lee JJ; Abraham D. 2011. Major Basic Protein from Eosinophils and Myeloperoxidase from Neutrophils Are Required for Protective Immunity to Strongyloides stercoralis in Mice. Infect Immun 79(7):2770-8. [PubMed: 21482685]  [MGI Ref ID J:173497]

Ochsenbein AF; Pinschewer DD; Odermatt B; Carroll MC; Hengartner H; Zinkernagel RM. 1999. Protective T cell-independent antiviral antibody responses are dependent on complement. J Exp Med 190(8):1165-74. [PubMed: 10523614]  [MGI Ref ID J:115126]

Ohmi Y; Tajima O; Ohkawa Y; Mori A; Sugiura Y; Furukawa K; Furukawa K. 2009. Gangliosides play pivotal roles in the regulation of complement systems and in the maintenance of integrity in nerve tissues. Proc Natl Acad Sci U S A 106(52):22405-10. [PubMed: 20018737]  [MGI Ref ID J:156459]

Otten MA; Groeneveld TW; Flierman R; Rastaldi MP; Trouw LA; Faber-Krol MC; Visser A; Essers MC; Claassens J; Verbeek JS; van Kooten C; Roos A; Daha MR. 2009. Both complement and IgG fc receptors are required for development of attenuated antiglomerular basement membrane nephritis in mice. J Immunol 183(6):3980-8. [PubMed: 19710463]  [MGI Ref ID J:152300]

Peng Q; Li K; Anderson K; Farrar CA; Lu B; Smith RA; Sacks SH; Zhou W. 2008. Local production and activation of complement up-regulates the allostimulatory function of dendritic cells through C3a-C3aR interaction. Blood 111(4):2452-61. [PubMed: 18056835]  [MGI Ref ID J:131316]

Peng Q; Li K; Patel H; Sacks SH; Zhou W. 2006. Dendritic cell synthesis of C3 is required for full T cell activation and development of a Th1 phenotype. J Immunol 176(6):3330-41. [PubMed: 16517700]  [MGI Ref ID J:129540]

Pozdnyakova O; Guttormsen HK; Lalani FN; Carroll MC; Kasper DL. 2003. Impaired antibody response to group B streptococcal type III capsular polysaccharide in C3- and complement receptor 2-deficient mice. J Immunol 170(1):84-90. [PubMed: 12496386]  [MGI Ref ID J:127041]

Pritchard MT; McMullen MR; Stavitsky AB; Cohen JI; Lin F; Medof ME; Nagy LE. 2007. Differential contributions of C3, C5, and decay-accelerating factor to ethanol-induced fatty liver in mice. Gastroenterology 132(3):1117-26. [PubMed: 17383432]  [MGI Ref ID J:128218]

Prodeus AP; Zhou X; Maurer M; Galli SJ; Carroll MC. 1997. Impaired mast cell-dependent natural immunity in complement C3-deficient mice. Nature 390(6656):172-5. [PubMed: 9367154]  [MGI Ref ID J:44240]

Qiao F; Atkinson C; Song H; Pannu R; Singh I; Tomlinson S. 2006. Complement plays an important role in spinal cord injury and represents a therapeutic target for improving recovery following trauma. Am J Pathol 169(3):1039-47. [PubMed: 16936276]  [MGI Ref ID J:112353]

Qin D; Wu J; Carroll MC; Burton GF; Szakal AK; Tew JG. 1998. Evidence for an important interaction between a complement-derived CD21 ligand on follicular dendritic cells and CD21 on B cells in the initiation of IgG responses. J Immunol 161(9):4549-54. [PubMed: 9794381]  [MGI Ref ID J:112151]

Qin X; Dobarro M; Bedford SJ; Ferris S; Miranda PV; Song W; Bronson RT; Visconti PE; Halperin JA. 2005. Further characterization of reproductive abnormalities in mCd59b knockout mice: a potential new function of mCd59 in male reproduction. J Immunol 175(10):6294-302. [PubMed: 16272280]  [MGI Ref ID J:108100]

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Rodriguez W; Mold C; Kataranovski M; Hutt JA; Marnell LL; Verbeek JS; Du Clos TW. 2007. C-reactive protein-mediated suppression of nephrotoxic nephritis: role of macrophages, complement, and Fcgamma receptors. J Immunol 178(1):530-8. [PubMed: 17182593]  [MGI Ref ID J:141920]

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Rupprecht TA; Angele B; Klein M; Heesemann J; Pfister HW; Botto M; Koedel U. 2007. Complement C1q and C3 are critical for the innate immune response to Streptococcus pneumoniae in the central nervous system. J Immunol 178(3):1861-9. [PubMed: 17237437]  [MGI Ref ID J:143634]

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Sun K; Metzger DW. 2008. Inhibition of pulmonary antibacterial defense by interferon-gamma during recovery from influenza infection. Nat Med 14(5):558-64. [PubMed: 18438414]  [MGI Ref ID J:136669]

Sun S; Guo Y; Zhao G; Zhou X; Li J; Hu J; Yu H; Chen Y; Song H; Qiao F; Xu G; Yang F; Wu Y; Tomlinson S; Duan Z; Zhou Y. 2011. Complement and the alternative pathway play an important role in LPS/D-GalN-induced fulminant hepatic failure. PLoS One 6(11):e26838. [PubMed: 22069473]  [MGI Ref ID J:181002]

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Trcka J; Moroi Y; Clynes RA; Goldberg SM; Bergtold A; Perales MA; Ma M; Ferrone CR; Carroll MC; Ravetch JV; Houghton AN. 2002. Redundant and alternative roles for activating Fc receptors and complement in an antibody-dependent model of autoimmune vitiligo. Immunity 16(6):861-8. [PubMed: 12121667]  [MGI Ref ID J:113538]

Trendelenburg M; Fossati-Jimack L; Cortes-Hernandez J; Turnberg D; Lewis M; Izui S; Cook HT; Botto M. 2005. The role of complement in cryoglobulin-induced immune complex glomerulonephritis. J Immunol 175(10):6909-14. [PubMed: 16272350]  [MGI Ref ID J:119691]

Tsoni SV; Kerrigan AM; Marakalala MJ; Srinivasan N; Duffield M; Taylor PR; Botto M; Steele C; Brown GD. 2009. Complement C3 plays an essential role in the control of opportunistic fungal infections. Infect Immun 77(9):3679-85. [PubMed: 19581397]  [MGI Ref ID J:152233]

Tu Z; Bu H; Dennis JE; Lin F. 2010. Efficient osteoclast differentiation requires local complement activation. Blood 116(22):4456-63. [PubMed: 20709903]  [MGI Ref ID J:166640]

Turnberg D; Lewis M; Moss J; Xu Y; Botto M; Cook HT. 2006. Complement activation contributes to both glomerular and tubulointerstitial damage in adriamycin nephropathy in mice. J Immunol 177(6):4094-102. [PubMed: 16951374]  [MGI Ref ID J:138043]

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Twohig J; Kulik L; Haluszczak C; Reuter J; Rossbach A; Bull M; Holers VM; Marchbank KJ. 2007. Defective B cell ontogeny and immune response in human complement receptor 2 (CR2, CD21) transgenic mice is partially recovered in the absence of C3. Mol Immunol 44(13):3434-44. [PubMed: 17379312]  [MGI Ref ID J:123562]

Veninga H; de Groot DM; McCloskey N; Owens BM; Dessing MC; Verbeek JS; Nourshargh S; van Eenennaam H; Boots AM; Hamann J. 2011. CD97 antibody depletes granulocytes in mice under conditions of acute inflammation via a Fc receptor-dependent mechanism. J Leukoc Biol 89(3):413-21. [PubMed: 21169517]  [MGI Ref ID J:170387]

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Wysoczynski M; Kucia M; Ratajczak J; Ratajczak MZ. 2007. Cleavage fragments of the third complement component (C3) enhance stromal derived factor-1 (SDF-1)-mediated platelet production during reactive postbleeding thrombocytosis. Leukemia 21(5):973-82. [PubMed: 17330096]  [MGI Ref ID J:121386]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, homozygous mice may be bred together. The expected coat color from breeding is black.
Mating SystemHomozygote x Homozygote         (Female x Male)   21-JUN-06
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $199.90Female or MaleHomozygous for C3tm1Crr  
Price per Pair (US dollars $)Pair Genotype
$399.80Homozygous for C3tm1Crr x Homozygous for C3tm1Crr  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Cryopreserved

Frozen Products

Price (US dollars $)
Frozen Embryo $1650.00

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $259.90Female or MaleHomozygous for C3tm1Crr  
Price per Pair (US dollars $)Pair Genotype
$519.80Homozygous for C3tm1Crr x Homozygous for C3tm1Crr  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Cryopreserved

Frozen Products

Price (US dollars $)
Frozen Embryo $2145.00

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   000664 C57BL/6J (approximate)
 
  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.
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JAX® Mice
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JAX® Services
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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:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

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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