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- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
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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 Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Generation N17p (11-DEC-05)
Generation DefinitionsDonating Investigator Bruce Aronow, Cincinnati Children's Hospital Med Cntr Description
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size, and do not display any behavioral abnormalities. No protein is detected in serum, liver, or brain and in situ hybridization shows no mRNA in heart. This mutant has been studied for different functions on different backgrounds. On the Swiss Black outbred background, aging homozygous mutant mice develop a progressive glomerulopathy characterized by deposition of tubulo-fibrillary immune complexes devoid of inflammation or necrosis. On the FVB/N background, homozygous null mice with chemically induced autoimmune myocarditis show severe and diffuse lesions with postinflammatory functional impairment. Induced skin carcinogenesis is more severe than wildtype. On the C57BL/6 background, homozygotes given a hypoxia-ischemia brain injury (modeling cerebral palsy) had 50% less brain injury compared to wild type. Conversely, mutants have less neuroprotective properties after permanent focal cerebral ischemia, a mouse model of human stroke. Mutant mice have altered heat-induced apoptosis in the testis. This mutant confers less fibrillar amyloid-beta damage and less neuritic dystrophy when bred with Alzheimer's disease model mice compared to control. This mutant mouse strain contains a targeted mutation of a widely expressed circulating glycoprotein associated with Alzheimer's disease, cerebral palsy, stroke, apoptosis, autoimmune myocarditis, kidney disease, and skin carcinogenesis.Development
A targeting vector was constructed in which exon 1 and 2 of the endogenous gene were replaced with a mouse phosphoglycerol kinase promoter driven hypoxanthine phosphoribosyl-transferase gene. The construct was electroporated into 129S2/SvPas-derived D3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts which were then implanted into pseudopregnant (C3H/HeN x C57BL/6J)F1 females. The resulting chimeric males were backcrossed for germ-line transmission to CF1 females. Heterozygotes were backcrossed to the Black Swiss outbred strain for one generation and then to C57BL/6J for more than 7 generations.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| Considerations for Choosing Controls | ||
Related Strains
Alzheimer's Disease Models
View Alzheimer's Disease Models (87 strains)
Additional Web Information
Genetic Quality Control Annual Report
Visit the Alzheimer's Disease Mouse Model Resource site for helpful information on Alzheimer's Disease and research resources.
Phenotype
Phenotype Information
assigned by genotype
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Clutm1Jakh/Clutm1Jakh
involves: Black Swiss * FVB/N
- cardiovascular system phenotype
- abnormal heart morphology (MGI Ref ID J:65660)
- after immunization with cardiac myosin, mutant hearts become pale and enlarged, mutants exhibit 3-fold greater heart tissue injury than wild-type
- abnormal cardiac muscle morphology (MGI Ref ID J:65660)
- 21 days after myocarditis initiation, mice show significant cardiac tissue injury than wild-type mice
- abnormal myocardial fiber morphology (MGI Ref ID J:65660)
- after immunization, myocyte necrosis is observed in some animals
- decreased myocardial fiber number (MGI Ref ID J:65660)
- 7 weeks following myocarditis, widespread loss of myocardial fibers is found in mutant hearts, whereas none is seen in wild-type controls
- abnormal heart ventricle morphology (MGI Ref ID J:65660)
- ventricular damage in females is 6-fold greater than in wild-type females; males do not show as severe cardiac damage
- decreased cardiac muscle contractility (MGI Ref ID J:65660)
- postmyocarditis heart function is impaired with decreased shortening fraction measured in mutants;
- heart inflammation (MGI Ref ID J:65660)
- severe, diffuse inflammation with large inflammatory aggregates occurs after immunization with cardiac myosin
- myocarditis (MGI Ref ID J:65660)
- severe myocarditis after immunization with cardiac myosin, more severe than in wild-type
- muscle phenotype
- abnormal cardiac muscle morphology (MGI Ref ID J:65660)
- 21 days after myocarditis initiation, mice show significant cardiac tissue injury than wild-type mice
- abnormal myocardial fiber morphology (MGI Ref ID J:65660)
- after immunization, myocyte necrosis is observed in some animals
- decreased myocardial fiber number (MGI Ref ID J:65660)
- 7 weeks following myocarditis, widespread loss of myocardial fibers is found in mutant hearts, whereas none is seen in wild-type controls
- decreased cardiac muscle contractility (MGI Ref ID J:65660)
- postmyocarditis heart function is impaired with decreased shortening fraction measured in mutants;
- immune system phenotype
- heart inflammation (MGI Ref ID J:65660)
- severe, diffuse inflammation with large inflammatory aggregates occurs after immunization with cardiac myosin
- myocarditis (MGI Ref ID J:65660)
- severe myocarditis after immunization with cardiac myosin, more severe than in wild-type
- homeostasis/metabolism phenotype
- edema (MGI Ref ID J:65660)
- immunized mice show cardiac edema
Clutm1Jakh/Clutm1Jakh
involves: 129S2/SvPas
- nervous system phenotype
- *normal* nervous system phenotype (MGI Ref ID J:58019)
- astrocytes secrete a normal composition of lipid particles
This mouse can be used to support research in many areas including:
Cardiovascular Research
Ischemia studies
Developmental Biology Research
Internal/Organ Defects
brain
Neurobiology Research
Alzheimer's Disease
Research Tools
Apoptosis Research
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Clutm1Jakh | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Judith A K Harmony | ||
| Allele Type | Targeted (knock-out) | ||
| Mutation Made By | Bruce Aronow, Cincinnati Children's Hospital Med Cntr | ||
| Strain of Origin | 129S2/SvPas | ||
| ES Cell Line Name | D3 | ||
| ES Cell Line Strain | 129S2/SvPas | ||
| Gene Symbol and Name | Clu, clusterin | ||
| Chromosome | 14 | ||
| Gene Common Name(s) | AAG4; AI893575; APOJ; Apolipoprotein J; CLI; Cli; D14Ucla3; DNA segment, Chr 14, University of California at Los Angeles 3; KUB1; MGC24903; RATTRPM2B; SGP-2; SGP2; SP-40; Sugp-2; TRPM-2; TRPM2; TRPM2B; Trpmb; complement lysis inhibitor; expressed sequence AI893575; sulfated glycoprotein 2; testosterone repressed prostate message-2; | ||
| Molecular Note | An HPRT cassette replaced exons 1 and 2. Normal transcript was undetectable in homozygous mutant tissue. Western blot analysis of plasma and liver extracts showed an absence of protein in homozygous mutant mice. [MGI Ref ID J:2892] [MGI Ref ID J:65660] [MGI Ref ID J:67960] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Clutm1Jakh, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References
Selected Reference(s)
McLaughlin L; Zhu G; Mistry M; Ley-Ebert C; Stuart WD; Florio CJ; Groen PA; Witt SA; Kimball TR; Witte DP; Harmony JA; Aronow BJ. 2000. Apolipoprotein J/clusterin limits the severity of murine autoimmune myocarditis J Clin Invest 106(9):1105-13. [PubMed: 11067863] [MGI Ref ID J:65660]
Additional References
Clutm1Jakh relatedBailey RW; Aronow B; Harmony JA; Griswold MD. 2002. Heat Shock-Initiated Apoptosis Is Accelerated and Removal of Damaged Cells Is Delayed in the Testis of Clusterin/ApoJ Knock-Out Mice. Biol Reprod 66(4):1042-53. [PubMed: 11906924] [MGI Ref ID J:75670]
Charnay Y; Imhof A; Vallet PG; Hakkoum D; Lathuiliere A; Poku N; Aronow B; Kovari E; Bouras C; Giannakopoulos P. 2008. Clusterin expression during fetal and postnatal CNS development in mouse. Neuroscience 155(3):714-24. [PubMed: 18620027] [MGI Ref ID J:140877]
Chayka O; Corvetta D; Dews M; Caccamo AE; Piotrowska I; Santilli G; Gibson S; Sebire NJ; Himoudi N; Hogarty MD; Anderson J; Bettuzzi S; Thomas-Tikhonenko A; Sala A. 2009. Clusterin, a haploinsufficient tumor suppressor gene in neuroblastomas. J Natl Cancer Inst 101(9):663-77. [PubMed: 19401549] [MGI Ref ID J:148260]
DeMattos RB; Cirrito JR; Parsadanian M; May PC; O'Dell MA; Taylor JW; Harmony JA; Aronow BJ; Bales KR; Paul SM; Holtzman DM. 2004. ApoE and clusterin cooperatively suppress Abeta levels and deposition: evidence that ApoE regulates extracellular Abeta metabolism in vivo. Neuron 41(2):193-202. [PubMed: 14741101] [MGI Ref ID J:107702]
DeMattos RB; O'dell MA; Parsadanian M; Taylor JW; Harmony JA; Bales KR; Paul SM; Aronow BJ; Holtzman DM. 2002. Clusterin promotes amyloid plaque formation and is critical for neuritic toxicity in a mouse model of Alzheimer's disease. Proc Natl Acad Sci U S A 99(16):10843-8. [PubMed: 12145324] [MGI Ref ID J:78357]
Fagan AM; Holtzman DM; Munson G; Mathur T; Schneider D; Chang LK; Getz GS; Reardon CA; Lukens J; Shah JA; LaDu MJ. 1999. Unique lipoproteins secreted by primary astrocytes from wild type, apoE (-/-), and human apoE transgenic mice. J Biol Chem 274(42):30001-7. [PubMed: 10514484] [MGI Ref ID J:58019]
Han BH; DeMattos RB; Dugan LL; Kim-Han JS; Brendza RP; Fryer JD; Kierson M; Cirrito J; Quick K; Harmony JA; Aronow BJ; Holtzman DM. 2001. Clusterin contributes to caspase-3-independent brain injury following neonatal hypoxia-ischemia. Nat Med 7(3):338-43. [PubMed: 11231633] [MGI Ref ID J:67960]
Hughes AT; Guilding C; Lennox L; Samuels RE; McMahon DG; Piggins HD. 2008. Live imaging of altered period1 expression in the suprachiasmatic nuclei of Vipr2-/- mice. J Neurochem 106(4):1646-57. [PubMed: 18554318] [MGI Ref ID J:138727]
Imhof A; Charnay Y; Vallet PG; Aronow B; Kovari E; French LE; Bouras C; Giannakopoulos P. 2006. Sustained astrocytic clusterin expression improves remodeling after brain ischemia. Neurobiol Dis 22(2):274-83. [PubMed: 16473512] [MGI Ref ID J:111243]
Kempster S; Collins ME; Aronow BJ; Simmons M; Green RB; Edington N. 2004. Clusterin shortens the incubation and alters the histopathology of bovine spongiform encephalopathy in mice. Neuroreport 15(11):1735-8. [PubMed: 15257138] [MGI Ref ID J:103644]
Rosenberg ME; Girton R; Finkel D; Chmielewski D; Barrie A rd; Witte DP; Zhu G; Bissler JJ; Harmony JA; Aronow BJ. 2002. Apolipoprotein J/clusterin prevents a progressive glomerulopathy of aging. Mol Cell Biol 22(6):1893-902. [PubMed: 11865066] [MGI Ref ID J:74983]
Savkovic V; Gantzer H; Reiser U; Selig L; Gaiser S; Sack U; Kloppel G; Mossner J; Keim V; Horn F; Bodeker H. 2007. Clusterin is protective in pancreatitis through anti-apoptotic and anti-inflammatory properties. Biochem Biophys Res Commun 356(2):431-7. [PubMed: 17359935] [MGI Ref ID J:121479]
Shull MM; Ormsby I; Kier AB; Pawlowski S; Diebold RJ; Yin M; Allen R; Sidman C; Proetzel G; Calvin D; Annunziata N; Doetschman T. 1992. Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease. Nature 359(6397):693-9. [PubMed: 1436033] [MGI Ref ID J:2892]
Tesseur I; Wyss-Coray T. 2006. A role for TGF-beta signaling in neurodegeneration: evidence from genetically engineered models. Curr Alzheimer Res 3(5):505-13. [PubMed: 17168649] [MGI Ref ID J:125213]
Thomas-Tikhonenko A; Viard-Leveugle I; Dews M; Wehrli P; Sevignani C; Yu D; Ricci S; el-Deiry W; Aronow B; Kaya G; Saurat JH; French LE. 2004. Myc-transformed epithelial cells down-regulate clusterin, which inhibits their growth in vitro and carcinogenesis in vivo. Cancer Res 64(9):3126-36. [PubMed: 15126350] [MGI Ref ID J:89749]
Wehrli P; Charnay Y; Vallet P; Zhu G; Harmony J; Aronow B; Tschopp J; Bouras C; Viard-Leveugle I; French LE; Giannakopoulos P. 2001. Inhibition of post-ischemic brain injury by clusterin overexpression. Nat Med 7(9):977-9. [PubMed: 11533682] [MGI Ref ID J:99683]
Wicher GK; Aldskogius H. 2005. Adult motor neurons show increased susceptibility to axotomy-induced death in mice lacking clusterin. Eur J Neurosci 21(7):2024-8. [PubMed: 15869496] [MGI Ref ID J:101072]
Health & husbandry
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.
Health & Colony Maintenance Information
Colony Maintenance
Breeding & Husbandry Homozygotes are viable and fertile. The donating investigator indicates that these mice can be maintained on a high fat diet to increase viability and fecundity, but it is not required.
Purchasing information
Pricing, Supply Level & Notes, Controls, General Terms & Conditions
Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
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Animals Provided
Price (US dollars $) Cryorecovery Fee $1900.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Additional Supply Details
| Pricing for International shipping destinations |
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|
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Animals Provided
Price (US dollars $) Cryorecovery Fee $2470.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Additional Supply Details
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Supply Details
| Standard Supply | Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information. |
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| Supply Notes |
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Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 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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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 and Purchasing Information
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