Overview

A C57BL/6J-congenic version of this strain is available as Stock No. 029661.

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

Donating Investigator

Michael C. Carroll, The Center for Blood Research

Genetic overview

Genetic Background	Generation
	N?+pN7F27 (2021-01-01 00:00:00)

C3^tm1Crr

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	C3	complement component 3

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Research Applications

Immunology, Inflammation and Autoimmunity Research
Developmental Biology Research
Research Tools

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Base Price

Starting at:

$247.50 Domestic price for female 4-week

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Details

Detailed 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 agglutinin+ germinal centers and a failure in isotype switching despite normal B cell signaling 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 Suggestions

Approximate Controls

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Wessels MR; Butko P; Ma M; Warren HB; Lage AL; Carroll MC. 1995. Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity. Proc Natl Acad Sci U S A 92(25):11490-4PubMed: 8524789 MGI: J:30152

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Genetics

C3^tm1Crr

Allele Symbol: C3^tm1Crr

Allele Name	targeted mutation 1, Michael C Carroll
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	C^3tm1Crr; C3-; mC3^-
Gene Symbol and Name	C3, complement component 3
Gene Synonym(s)
Strain of Origin	129S4/SvJae
Chromosome	17
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. ELISA testing did not detect C3 protein in serum of homozygous mutant mice. A C3 hemolytic assay did not detect functional C3 activity.
Mutations Made By	Michael Carroll, The Center for Blood Research

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

complement component 3 deficiency

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: C3^tm1Crr related

Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency Associated with Other Defects
- Inflammation
- Immunodeficiency
  - specific complement deficiency
Developmental Biology Research
- Lymphoid Tissue Defects
  - hematopoietic defects
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - specific complement deficiency

Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - specific complement deficiency
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - specific complement deficiency

Mammalian Phenotype Terms by Genotype

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

Genotype: C3^tm1Crr/C3^tm1Crr
involves: 129S4/SvJae

homeostasis/metabolism phenotype

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
- following exposure to ethanol, mice exhibit a reduced increased in alanine aminotransferase compared to in similarly treated wild-type mice

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

abnormal blood coagulation
- thrombus formation considerably reduced

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

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

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

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

Genotype: C3^tm1Crr/C3^tm1Crr
B6.129S4-C3

embryo phenotype

decreased spongiotrophoblast size
- significantly reduced spongioblast at day 15 of pregnancy

small placenta
- reduced placenta area at day 15 of pregnancy

abnormal blastocyst morphology
- blastocyst count at 4 days is consistently but insignificantly lower than in controls

decreased placental labyrinth size
- labyrinth area significantly reduced at day 15 of pregnancy

growth/size/body region phenotype

decreased fetal weight
- significantly reduced fetal weight
- reduced fetus/placenta ratio

hematopoietic system phenotype

decreased susceptibility to autoimmune hemolytic anemia
- mice are resistant to hemolytic anemia induced by self-binding IgG2a antibodies
- no protection is seen with pathogenic IgM or IgA self-antibodies

abnormal neutrophil morphology
- neutrophils that accumulate at the site of a local Shwartman response are round instead of flattened as in wild-type mice

homeostasis/metabolism phenotype

decreased cerebral infarction size
- significantly reduced infarct volume but mortality unaffected

abnormal blood homeostasis
- mouse serum fails to support neutrophil adhesion unlike serum from wild-type mice

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
- te normal neutrophil accumulation

abnormal neutrophil morphology
- neutrophils that accumulate at the site of a local Shwartman response are round instead of flattened as in wild-type mice

decreased susceptibility to autoimmune hemolytic anemia
- mice are resistant to hemolytic anemia induced by self-binding IgG2a antibodies
- no protection is seen with pathogenic IgM or IgA self-antibodies

brain inflammation
- reduced granulocyte infiltration of infarct sites

nervous system phenotype

abnormal hippocampus CA3 region morphology
- mutant mice do not exhibit age-dependent neuron loss in the hippocampal CA3 region from P30 to 16 months

brain inflammation
- reduced granulocyte infiltration of infarct sites

abnormal synaptic vesicle number
- synaptic puncta density in the hippocampal CA3 region is higher in mutant males than in wild-type males at 4 months of age; density is similar to wild-type at P30
- protective effects (to a lesser extent) against synapse loss are also observed in hippocampal DG and V1 regions, but not in the CA1 region, at 16 months of age

enhanced paired-pulse facilitation
- observed in 12 month old mice as compared to age-matched wild-type

abnormal synaptic plasticity
- synaptic plasticity is improved as compared to age matched 12 month old wild-type mice

enhanced long term potentiation
- observed in 12 month old mice as compared to age-matched wild-type

decreased cerebral infarction size
- significantly reduced infarct volume but mortality unaffected

increased neuron number
- neuron numbers in CA1, V1 cortex and cerebellum are similar to wild-type
- mutant mice do not exhibit age-dependent neuron loss in the hippocampal CA3 region from P30 to 16 months

abnormal dendritic spine morphology
- increased dendritic spine density is observed in the hippocampal CA3 region of 16 month old mice as compared to wild-type

reproductive system phenotype

abnormal female reproductive system physiology

impaired embryo implantation
- insignificantly but consistently reduced level of implantation at day 8

prolonged estrous cycle
- 5.42 days vs 4.41 days in controls

behavior/neurological phenotype

enhanced contextual conditioning behavior
- 16 month old mutant mice exhibit increased freezing time during initial testing and 24 hours later as compared to age-matched wild-type mice
- 4 month old mutant mice exhibit increased freezing time during training, but not retention

decreased anxiety-related response
- 16 month old mutant mice make more contacts with novel objects in first minute of test than age-matched wild-type mice
- 16 month old mutant mice spend more ambulatory time in the center of the field than age-matched wild-type mice
- 16 month old mutant mice make more total open arm entries than age-matched wild-type mice

abnormal spatial working memory
- age-matched 16 month old mutant mice more quickly relearn and retain new platform location than wild-type mice is reversal trial of water T maze

enhanced spatial learning
- age-matched 16 month old mutant mice more quickly relearn and retain new platform location than wild-type mice is reversal trial of water T maze

The following phenotype relates to a compound genotype created using this strain

Genotype: C3^tm1Crr/C3^tm1Crr
involves: 129S4/SvJae * C57BL/6

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)

hematopoietic system phenotype

decreased osteoclast cell number
- bone marrow cells incubated with 1,25(OH)2 vitamin D3 produce fewer osteoclasts than do cells from controls

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

decreased mast cell number
- after CLP less peritoneal mast cells can be recovered from Cr3-deficient mice compared to controls

decreased spleen germinal center size
- diameter of GCs are less than that observed in wild-type

abnormal mast cell physiology
- treatment with HuC3 results in comparable levels of mast cell degranulation to wild-type
- 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)

abnormal spleen germinal center morphology

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

homeostasis/metabolism phenotype

decreased circulating interleukin-6 level
- Il-6 production after vitamin D3 stimulation is significantly reduced
- reduced levels at 6 and 24 hours after 6 and 24 hours of reperfusion

decreased susceptibility to injury
- serum urea nitrogen is reduced 31% to 55% compared to wild-type mice subjected to ischemia reperfusion
- mice are resistant to ischemia reperfusion-induced renal injury
- neutrophil infiltration at the site of injury was reduced

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
- treatment with HuC3 restores levels of Tnfa production in mutants to wild-type levels

increased circulating alanine transaminase level
- after 70% partial hepatectomy

increased circulating bilirubin level
- after 70% partial hepatectomy

abnormal enzyme/coenzyme level
- lower levels of myeloperoxidase in livers at 6 and 24 hours of reperfusion

decreased circulating tumor necrosis factor level
- reduced TNFalpha levels at 6 and 24 hours after 6 and 24 hours of reperfusion

decreased circulating alanine transaminase level
- levels lower during reperfusion after ischemia than in controls

cellular phenotype

focal hepatic necrosis
- after 70% partial hepatectomy

decreased hepatocyte proliferation
- impaired hepatocyte proliferation after 30 minutes of ischemia during 70% partial hepatectomy

immune system phenotype

abnormal mast cell physiology
- treatment with HuC3 results in comparable levels of mast cell degranulation to wild-type
- 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)

increased susceptibility to bacterial infection
- increased mortality from GBS infection compared to controls is limited to the first 3 days after challenge
- LD₅₀ dose: control 6.3 x 10⁴ vs. 1.3 x 10³ in C3-deficient mice)
- 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)
- 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)
- treatment with HuC3 restore neutrophil numbers and enhance bacterial clearance to wild-type levels
- 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

liver inflammation
- patic sinusoids; wild-type animals that receive higher doses of GBS showed similar lesions
- 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

decreased circulating tumor necrosis factor level
- reduced TNFalpha levels at 6 and 24 hours after 6 and 24 hours of reperfusion

decreased spleen germinal center size
- diameter of GCs are less than that observed in wild-type

decreased circulating interleukin-6 level
- Il-6 production after vitamin D3 stimulation is significantly reduced
- reduced levels at 6 and 24 hours after 6 and 24 hours of reperfusion

decreased mast cell number
- after CLP less peritoneal mast cells can be recovered from Cr3-deficient mice compared to controls

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
- 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

abnormal immune system physiology

abnormal spleen germinal center morphology

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

abnormal immune system morphology

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

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

increased susceptibility to bacterial infection induced morbidity/mortality
- in mice infected with S. pneumoniae

decreased osteoclast cell number
- bone marrow cells incubated with 1,25(OH)2 vitamin D3 produce fewer osteoclasts than do cells from controls

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
- treatment with HuC3 restores levels of Tnfa production in mutants to wild-type levels

digestive/alimentary phenotype

abnormal intestine morphology
- mice show less evidence of infarction compared to controls

liver/biliary system phenotype

decreased liver regeneration
- impaired regenerative response after 70% hepatectomy
- significant hepatic injury after 30 minutes of ischemia during 70% partial hepatectomy

decreased hepatocyte proliferation
- impaired hepatocyte proliferation after 30 minutes of ischemia during 70% partial hepatectomy

hepatic steatosis
- increased steatosis after 70% hepatectomy

liver inflammation
- patic sinusoids; wild-type animals that receive higher doses of GBS showed similar lesions
- 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

focal hepatic necrosis
- after 70% partial hepatectomy

abnormal liver physiology

abnormal liver morphology
- histological evidence of injury after 6 and 24 hours of reperfusion following ischemia

mammalian phenotype

immune system phenotype
- secondary immune responses are similar in wild type and mutant mice, so helper T cell function is normal
- Normal - secondary immune responses are similar in wild-type and mutant mice, so helper T cell function is normal
- Normal - B cells from deficient mice show normal proliferative effects in response to surface IgM crosslinking

mortality/aging

abnormal induced morbidity/mortality
- poor survival (20%) after 30 minutes of ischemia while 70% partial hepatectomy performed

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)
- reconstitution of mice with ip. injection of purified human C3 (HuC3) reduces mortality from 100% to 40% in the first 24 hours

increased susceptibility to bacterial infection induced morbidity/mortality
- in mice infected with S. pneumoniae

nervous system phenotype

abnormal peripheral nervous system regeneration
- locomotor recovery from spinal cord injury occurs more rapidly than in controls
- grossly normal at 7 days after injury compared to controls which show marked necrosis and vacuolation in controls at 21 days
- slight improvement in tissue at 24 hours aftwr injury but considerably improved relative to controls by 72 hours

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

Genotype: C3^tm1Crr/C3^tm1Crr
B6;129S4-C3/J

homeostasis/metabolism phenotype

decreased circulating free fatty acids level
- plasma free polyunsaturdated fatty acid (linoleic acid and arachidonic acid) levels are decreased at 14 months of age

vision/eye phenotype

abnormal c-wave shape
- the amplitude of the c-wave is reduced at 12 months of age, but not at 8 weeks of age
- Normal - however, no other component of the dc-ERG is different

decreased b-wave amplitude
- ERG b-waves are decreased at 12 months of age but not at younger ages

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

abnormal retinal rod bipolar cell morphology
- the number of rod bipolar cells is decreased at 14 months of age

abnormal retinal horizontal cell morphology
- density of horizontal cells is decreased

immune system phenotype

decreased susceptibility to Coronaviridae infection
- mice show partial protection from intranasal infection with the mouse-adapted SARS-CoV MA15 compared to wild-type controls, showing no significant weight loss, decreased airway resistance associated with airway debris and exhalation force indicating improved respiratory function, reduced lung pathology, reductions in inflammatory monocytes and neutrophils and increases in dendritic cells and alveolar macrophages in the lungs by day 4 postinfection, and reduction in cytokine and chemokine responses in the lungs
- SARS-CoV MA15-infected mice exhibit more airspace inflammation at day 2 postinfection than controls but his is reversed later in infection
- Normal - however, SARS-CoV MA15-infected mice show similar levels of viral titers in the lung and ratio of peak expiratory flow as in controls

increased susceptibility to bacterial infection
- Normal - 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

mammalian phenotype

vision/eye phenotype
- Normal - eyes infected with 500 CFU S. aureus show mild signs of inflammation at 24 and 48 hours but appear normal at 72 hours

nervous system phenotype

abnormal retinal rod bipolar cell morphology
- the number of rod bipolar cells is decreased at 14 months of age

abnormal retinal horizontal cell morphology
- density of horizontal cells is decreased

References

Wessels MR; Butko P; Ma M; Warren HB; Lage AL; Carroll MC. 1995. Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity. Proc Natl Acad Sci U S A 92(25):11490-4PubMed: 8524789 MGI: J:30152

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):9023-31PubMed: 14695221 MGI: J:87069
Shi Q; Colodner KJ; Matousek SB; Merry K; Hong S; Kenison JE; Frost JL; Le KX; Li S; Dodart JC; Caldarone BJ; Stevens B; Lemere CA. 2015. Complement C3-Deficient Mice Fail to Display Age-Related Hippocampal Decline. J Neurosci 35(38):13029-42PubMed: 26400934 MGI: J:224676
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):3847-54PubMed: 14500686 MGI: 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):3869-75PubMed: 15004194 MGI: J:88632

Additional - C3^tm1Crr related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:C3
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, homozygous mice may be bred together. The expected coat color from breeding is black.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Citation
When using the B6;129S4-C3^tm1Crr/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #003641 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX11 (Maximum)

Pricing & Availability

Available

Domestic
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Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or Wild-type for C3<tm1Crr>

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Frozen Mouse Embryo	B6;129S4-C3<tm1Crr>/J Frozen Embryos	$2595.00
Frozen Mouse Embryo	B6;129S4-C3<tm1Crr>/J Frozen Embryos	$2595.00
Frozen Mouse Embryo	B6;129S4-C3<tm1Crr>/J Frozen Embryos	$3373.50
Frozen Mouse Embryo	B6;129S4-C3<tm1Crr>/J Frozen Embryos	$3373.50

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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Use of MICE by companies or for-profit entities requires a license prior to shipping.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

C3tm1Crr

Allele Symbol: C3tm1Crr

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: C3tm1Crr related

Mammalian Phenotype Terms by Genotype

Genotype: C3tm1Crr/C3tm1Crrinvolves: 129S4/SvJae

homeostasis/metabolism phenotype

immune system phenotype

liver/biliary system phenotype

renal/urinary system phenotype

Genotype: C3tm1Crr/C3tm1CrrB6.129S4-C3

embryo phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

nervous system phenotype

reproductive system phenotype

behavior/neurological phenotype

Genotype: C3tm1Crr/C3tm1Crrinvolves: 129S4/SvJae * C57BL/6

cardiovascular system phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

cellular phenotype

immune system phenotype

digestive/alimentary phenotype

liver/biliary system phenotype

mammalian phenotype

mortality/aging

nervous system phenotype

skeleton phenotype

Genotype: C3tm1Crr/C3tm1CrrB6;129S4-C3/J

homeostasis/metabolism phenotype

vision/eye phenotype

immune system phenotype

mammalian phenotype

nervous system phenotype

References

Additional References

Additional - C3tm1Crr related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Additional Use Restrictions Apply

Licensing Information

C3^tm1Crr

Allele Symbol: C3^tm1Crr

Genotype: C3^tm1Crr related

Genotype: C3^tm1Crr/C3^tm1Crr
involves: 129S4/SvJae

Genotype: C3^tm1Crr/C3^tm1Crr
B6.129S4-C3

Genotype: C3^tm1Crr/C3^tm1Crr
involves: 129S4/SvJae * C57BL/6

Genotype: C3^tm1Crr/C3^tm1Crr
B6;129S4-C3/J

Additional - C3^tm1Crr related