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Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse Generation N8F?+5pN1 Description
Mice that are homozygous null for the Alox12 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Alox12 protein product or enzyme activity is detected in platelets derived from homozygous null animals. Platelets exhibit a hyperresponsiveness to ADP-induced aggregation. Studies examining basal transepidermal water loss indicate that null animals exhibit greater water loss through the skin when compared to control animals.Development
A targeting vector containing a neomycin cassette was used to disrupt exon 8. The construct was electroporated into 129S2/SvPas-derived D3H embryonic stem cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts and chimeric animals were obtained.
| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
Congenic Nomenclature
View Mammalian Phenotype Terms
Mammalian Phenotype Terms
assigned by genotype
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Alox12tm1Fun/Alox12tm1Fun
involves: 129S2/SvPas * C57BL/6
- homeostasis/metabolism phenotype
- abnormal platelet physiology (MGI Ref ID J:46896)
- homozygotes display normal platelet adhesion to various extracellular matrix proteins including fibrinogen, collagen, and fibronectin; in addition, thrombin, collagen, U46619, and arachidonic acid-induced aggregation responses are largely unaffected
- however, mutant platelets exhibit increased sensitivity to ADP, manifested as a significant increase in slope and percent aggregation in ex vivo assays
- notably, platelet hyperresponsiveness to ADP is not secondary to thromboxane synthesis, PKC activity, or dense granule release and can be attenuated by the addition of 12-(S)-hydroperoxyeicosatetraenoic acid to platelet-rich plasma
- impaired skin barrier function (MGI Ref ID J:55741)
- homozygotes exhibit increased transepidermal water loss, without increased basal mitotic activity of epidermal cells, and normal recovery of the epidermal barrier after acetone disruption
- notably, the mutant epidermis appears structurally normal, with no detectable differences in number or appearance of lamellar bodies and no changes in the content of major fatty acids
- thrombosis (MGI Ref ID J:46896)
- homozygotes are more sensitive to thrombosis elicited by i.v. ADP injection: 87.5% of mutants (vs only 20% of wild-type) exhibit thrombolytic death at an ADP dose of 0.035 mg/g (body weight)
- in contrast, no differences in mortality with arachidonic acid-induced thrombosis are observed at 30 mg/kg and 100 mg/kg
- hematopoietic system phenotype
- abnormal platelet physiology (MGI Ref ID J:46896)
- homozygotes display normal platelet adhesion to various extracellular matrix proteins including fibrinogen, collagen, and fibronectin; in addition, thrombin, collagen, U46619, and arachidonic acid-induced aggregation responses are largely unaffected
- however, mutant platelets exhibit increased sensitivity to ADP, manifested as a significant increase in slope and percent aggregation in ex vivo assays
- notably, platelet hyperresponsiveness to ADP is not secondary to thromboxane synthesis, PKC activity, or dense granule release and can be attenuated by the addition of 12-(S)-hydroperoxyeicosatetraenoic acid to platelet-rich plasma
- skin/coat/nails phenotype
- impaired skin barrier function (MGI Ref ID J:55741)
- homozygotes exhibit increased transepidermal water loss, without increased basal mitotic activity of epidermal cells, and normal recovery of the epidermal barrier after acetone disruption
- notably, the mutant epidermis appears structurally normal, with no detectable differences in number or appearance of lamellar bodies and no changes in the content of major fatty acids
- immune system phenotype
- *normal* immune system phenotype (MGI Ref ID J:55741)
- homozygotes exhibit a normal arachidonic acid-induced ear inflammatory response, as measured by plasma leakage and edema formation
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:Alox12tm1Fun related
Cardiovascular Research
Vascular Defects (Thrombosis)
Dermatology Research
Other (Studies of transepidermal water loss)
Hematological Research
Platelet Defects (Alterations in platelet aggregation)
Research Tools
Hematological Research
| Allele Symbol | Alox12tm1Fun | ||
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| Allele Name | targeted mutation 1, Colin Funk | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | P-12LO-; | ||
| Strain of Origin | 129S2/SvPas | ||
| ES Cell Line Name | D3H | ||
| ES Cell Line Strain | 129S2/SvPas | ||
| Gene Symbol and Name | Alox12, arachidonate 12-lipoxygenase | ||
| Chromosome | 11 | ||
| Gene Common Name(s) | 12-LOX; 12S-LOX; 9930022G08Rik; Alox12p; LOG12; MGC187960; P-12LO; RIKEN cDNA 9930022G08 gene; arachidonate 12-lipoxygenase, platelet; | ||
| Molecular Note | Insertion of a neomycin resistance cassette deleted exon 8 of the Alox12 gene. Western blot analysis did not detect protein in homozygous mutant platelets. [MGI Ref ID J:46896] | ||
Genotyping Protocols
Alox12tm1Fun, SEP PCR, vers. 1
Helpful Links
Optimizing PCR Protocols
Virmani J; Johnson EN; Klein-Szanto AJ; Funk CD. 2001. Role of 'platelet-type' 12-lipoxygenase in skin carcinogenesis. Cancer Lett 162(2):161-5. [PubMed: 11146221] [MGI Ref ID J:67133]
Alox12tm1Fun relatedBleich D; Chen S; Zipser B; Sun D; Funk CD; Nadler JL. 1999. Resistance to type 1 diabetes induction in 12-lipoxygenase knockout mice. J Clin Invest 103(10):1431-6. [PubMed: 10330425] [MGI Ref ID J:55050]
Gabel SA; London RE; Funk CD; Steenbergen C; Murphy E. 2001. Leukocyte-type 12-lipoxygenase-deficient mice show impaired ischemic preconditioning-induced cardioprotection. Am J Physiol Heart Circ Physiol 280(5):H1963-9. [PubMed: 11299195] [MGI Ref ID J:69296]
Gubitosi-Klug RA; Talahalli R; Du Y; Nadler JL; Kern TS. 2008. 5-Lipoxygenase, but not 12/15-lipoxygenase, contributes to degeneration of retinal capillaries in a mouse model of diabetic retinopathy. Diabetes 57(5):1387-93. [PubMed: 18346986] [MGI Ref ID J:136092]
Johnson EN; Brass LF; Funk CD. 1998. Increased platelet sensitivity to ADP in mice lacking platelet-type 12-lipoxygenase. Proc Natl Acad Sci U S A 95(6):3100-5. [PubMed: 9501222] [MGI Ref ID J:46896]
Johnson EN; Nanney LB; Virmani J; Lawson JA; Funk CD. 1999. Basal transepidermal water loss is increased in platelet-type 12-lipoxygenase deficient mice. J Invest Dermatol 112(6):861-5. [PubMed: 10383730] [MGI Ref ID J:55741]
Colony Maintenance
Breeding & Husbandry This strain originated on a B6;129S2 background and has been backcrossed to C57BL/6J for eight generations before being made homozygous.Coat color expected from breeding:Black Diet Information LabDiet® 5K52/5K67
| Pricing for USA, Canada and Mexico shipping destinations |
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*Price(s) in US dollars ($)
Weeks of Age Price* Gender Cryorecovery Fee $1900.00
| Pricing for International shipping destinations |
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*Price(s) in US dollars ($)
Weeks of Age Price* Gender Cryorecovery Fee $2470.00
| Standard Supply | Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information. |
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| Supply Notes |
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| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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