Strain Name:

B6.129S4-Park2tm1Shn/J

Stock Number:

006582

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Availability:

Repository- Live

Use Restrictions Apply, see Terms of Use
Homozygous Parkinson disease (autosomal recessive, juvenile) 2, parkin (Park2tm1Shn) knock-out mice have increased extracellular dopamine concentration in the striatum, dysfunctional nigrostriatal pathways, and dysfunctional mitochondria. These mice model the exon 3 deletion mutation most common in human autosomal recessive juvenile parkinsonism patients and may be useful in studies of Parkinson's disease, dopamine regulation, nigrostriatal function, mitochondrial function, and other neurobiological research.

Description

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.
Mating SystemHomozygote x Homozygote         (Female x Male)   01-JUL-08
Specieslaboratory mouse
GenerationN22+F12 (18-JUN-12)
Generation Definitions
 
Donating Investigator Jie Shen,   Harvard Med Sch/Brigham Women's Hosp

Description
Homozygous mice are viable and fertile, and exhibit grossly normal brain morphology. Western blot analysis using antibody specific to C-terminal sequences indicates the absence of full length gene product. RT-PCR shows that exon 2 splices to exon 4, skipping exon 3 entirely, resulting in a frame shift and a premature stop codon in exon 5. While EGFP transcripts are present, little parkin-EGFP fusion protein is detectable by Western analysis. Homozygous mice have increased extracellular dopamine concentration in the striatum. Further, medium-sized striatal spiny neurons require greater currents to induce synaptic responses, suggesting a reduction in synaptic excitability in the absence of the endogenous gene. Homozygotes also exhibit deficits in behavioral paradigms sensitive to dysfunction of the nigrostriatal pathway. The numbers of dopaminergic neurons in the substantia nigra, however, are normal up to the age of 24 months, in contrast to the substantial loss of nigral neurons characteristic of Parkinson's disease. Homozygous mice and their isolated cells exhibit mitochondrial dysfunction and impaired protection from oxidative stress. Muscle cells isolated from homozygous mice have defective skeletal muscle mitochondrial homeostasis and increased sensitivity to amyloid-beta toxicity. These mice model the exon 3 deleti on mutation most common in human autosomal recessive juvenile parkinsonism (AR-JP) patients and may be useful in studies of Parkinson's disease, dopamine regulation, nigrostriatal function, mitochondrial function, and other neurobiological research.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. Mice with this mutation were originally published on a mixed B6;129S4 genetic background. It should be noted that the phenotype could vary from that originally described. The strain description will be modified as published results become available.

Development
A targeting vector was designed to replace most of exon 3 of the endogenous gene with the in-frame EGFP coding sequence (followed by translation and transcription termination sequences and a PGK-neomycin cassette). The construct was electroporated into the 129S4/SvJae-derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts. The donating investigator reported that the resulting mutant mice were backcrossed to C57BL/6 (see SNP note below) inbred mice for more than 20 generations before arriving at The Jackson Laboratory.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, 2 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6J ; C57BL/6N genetic background.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

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View Parkinson's Disease Models     (112 strains)

Strains carrying   Park2tm1Shn allele
023968   B6.Cg-Park7tm1Shn Gpx1tm1Ysh Park2tm1Shn/MgoldJ
View Strains carrying   Park2tm1Shn     (1 strain)

Strains carrying other alleles of Park2
007587   129S-Park2tm1Rpa/J
View Strains carrying other alleles of Park2     (1 strain)

Additional Web Information

Visit the Parkinson's Disease Resource site for helpful information on Parkinson's and research resources.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- 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).
Parkinson Disease 2, Autosomal Recessive Juvenile; PARK2
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Leprosy, Susceptibility to, 2; LPRS2   (PARK2)
Lung Cancer   (PARK2)
Ovarian Cancer   (PARK2)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Park2tm1Shn/Park2tm1Shn

        B6.129S4-Park2tm1Shn/J
  • cellular phenotype
  • abnormal autophagy
    • following myocardial infarction, mitophagy is impaired in the border zone of the infarct, but not in remote zones   (MGI Ref ID J:193741)
    • myocytes treated with rotenone, a mitochondrial complex I inhibitor, do not show an increase in mitophagy or autophagy as in wild-type myocytes   (MGI Ref ID J:193741)
  • abnormal mitochondrial physiology
    • mitochondria isolated from the border zones and subjected to 4 hours of myocardial infarction, have lower oxygen consumption rates than mitochondria from remote zones   (MGI Ref ID J:193741)
  • abnormal mitochondrion morphology
    • mitochondria in 12 week old mutant hearts are more disorganized and often found in large clusters with many small, round mitochondria   (MGI Ref ID J:193741)
    • following myocardial infarction, mitochondria in myocytes in the border zone are swollen and show severe cristae remodeling   (MGI Ref ID J:193741)
    • decreased mitochondria size
      • mitochondria in the heart are smaller but have normal respiratory capacity   (MGI Ref ID J:193741)
  • increased sensitivity to induced cell death
    • in MPP+ treated mouse embryonic fibroblasts   (MGI Ref ID J:194987)
    • isolated myocytes are more susceptible to hypoxia-induced cell death   (MGI Ref ID J:193741)
  • cardiovascular system phenotype
  • altered response to myocardial infarction
    • mutants exhibit increased sensitivity to myocardial infarction, with about 60% mortality within the first week compared to about 20% for wild-type mice and show severe thinning of left ventricular wall, enlarged left ventricle interior dimensions, and increased remodeling compared to wild-type   (MGI Ref ID J:193741)
    • 7 days following myocardial infarction, surviving mutants exhibit lower fractional shortening and ejection fractions, increased left ventricular end diastolic and systolic dimensions, and increased left ventricular volume, indicating impaired recovery after infarction   (MGI Ref ID J:193741)
  • growth/size/body phenotype
  • decreased body size   (MGI Ref ID J:193741)
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction
    • mutants exhibit increased sensitivity to myocardial infarction, with about 60% mortality within the first week compared to about 20% for wild-type mice and show severe thinning of left ventricular wall, enlarged left ventricle interior dimensions, and increased remodeling compared to wild-type   (MGI Ref ID J:193741)
    • 7 days following myocardial infarction, surviving mutants exhibit lower fractional shortening and ejection fractions, increased left ventricular end diastolic and systolic dimensions, and increased left ventricular volume, indicating impaired recovery after infarction   (MGI Ref ID J:193741)
  • mortality/aging
  • increased sensitivity to induced morbidity/mortality
    • mutants exhibit increased sensitivity to myocardial infarction, with about 60% mortality within the first week compared to about 20% for wild-type mice   (MGI Ref ID J:193741)
  • behavior/neurological phenotype
  • impaired coordination
    • trained mutant mice remain on rotarod longer than trained wild type at 5, 10, and 15 rpm, but 20 rpm and spend less time "distracted" while on the rod   (MGI Ref ID J:202221)

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Park2tm1Shn/Park2tm1Shn

        involves: 129S4/SvJae
  • behavior/neurological phenotype
  • impaired coordination
    • poorer performance in various measures of motor performance   (MGI Ref ID J:86377)
    • rotarod performance was normal   (MGI Ref ID J:86377)
  • nervous system phenotype
  • abnormal nervous system electrophysiology
    • higher currents are required in striatal neurons to trigger synaptic response   (MGI Ref ID J:86377)
  • increased dopamine level
    • higher than normal levels of dopamine in the striatum   (MGI Ref ID J:86377)
  • homeostasis/metabolism phenotype
  • increased dopamine level
    • higher than normal levels of dopamine in the striatum   (MGI Ref ID J:86377)
View Research Applications

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

Neurobiology Research
Parkinson's Disease
      Park2 (parkin) mutants

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Park2tm1Shn
Allele Name targeted mutation 1, Jie Shen
Allele Type Targeted (knock-out)
Common Name(s) parkin -;
Mutation Made By Jie Shen,   Harvard Med Sch/Brigham Women's Hosp
Strain of Origin129S4/SvJae
ES Cell Line NameJ1
ES Cell Line Strain129S4/SvJae
Gene Symbol and Name Park2, Parkinson disease (autosomal recessive, juvenile) 2, parkin
Chromosome 17
Gene Common Name(s) AR-JP; LPRS2; PDJ; PRKN; Park;
Molecular Note Exon 3 was replaced in-frame by the coding sequence for EGFP followed by a PGK-neomycin cassette. RT-PCR analysis indicated that exon 2 spliced to exon 4 in transcripts thus skipping exon 3 entirely. This results in a frame shift and a premature stop codon in exon 5. Western blot analysis using antibody specific to C-terminal sequences indicated the absence of gene product. [MGI Ref ID J:86377]

Genotyping

Genotyping Information

Genotyping Protocols

Park2tm1Shn, Melt Curve Analysis
Park2tm1Shn, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Goldberg MS; Fleming SM; Palacino JJ; Cepeda C; Lam HA; Bhatnagar A; Meloni EG; Wu N; Ackerson LC; Klapstein GJ; Gajendiran M; Roth BL; Chesselet MF; Maidment NT; Levine MS; Shen J. 2003. Parkin-deficient mice exhibit nigrostriatal deficits but not loss of dopaminergic neurons. J Biol Chem 278(44):43628-35. [PubMed: 12930822]  [MGI Ref ID J:86377]

Additional References

Park2tm1Shn related

Berthet A; Bezard E; Porras G; Fasano S; Barroso-Chinea P; Dehay B; Martinez A; Thiolat ML; Nosten-Bertrand M; Giros B; Baufreton J; Li Q; Bloch B; Martin-Negrier ML. 2012. L-DOPA Impairs Proteasome Activity in Parkinsonism through D1 Dopamine Receptor. J Neurosci 32(2):681-91. [PubMed: 22238104]  [MGI Ref ID J:179902]

Chen Y; Sawada O; Kohno H; Le YZ; Subauste C; Maeda T; Maeda A. 2013. Autophagy protects the retina from light-induced degeneration. J Biol Chem 288(11):7506-18. [PubMed: 23341467]  [MGI Ref ID J:196891]

Ekholm-Reed S; Goldberg MS; Schlossmacher MG; Reed SI. 2013. Parkin-dependent degradation of the F-box protein Fbw7beta promotes neuronal survival in response to oxidative stress by stabilizing Mcl-1. Mol Cell Biol 33(18):3627-43. [PubMed: 23858059]  [MGI Ref ID J:204747]

Frank-Cannon TC; Tran T; Ruhn KA; Martinez TN; Hong J; Marvin M; Hartley M; Trevino I; O'Brien DE; Casey B; Goldberg MS; Tansey MG. 2008. Parkin deficiency increases vulnerability to inflammation-related nigral degeneration. J Neurosci 28(43):10825-34. [PubMed: 18945890]  [MGI Ref ID J:140159]

Hennis MR; Marvin MA; Taylor CM 2nd; Goldberg MS. 2013. Surprising behavioral and neurochemical enhancements in mice with combined mutations linked to Parkinson's disease. Neurobiol Dis 62C:113-123. [PubMed: 24075852]  [MGI Ref ID J:202221]

Hoshino A; Ariyoshi M; Okawa Y; Kaimoto S; Uchihashi M; Fukai K; Iwai-Kanai E; Ikeda K; Ueyama T; Ogata T; Matoba S. 2014. Inhibition of p53 preserves Parkin-mediated mitophagy and pancreatic beta-cell function in diabetes. Proc Natl Acad Sci U S A 111(8):3116-21. [PubMed: 24516131]  [MGI Ref ID J:206823]

Kao SY. 2009. Regulation of DNA repair by parkin. Biochem Biophys Res Commun 382(2):321-5. [PubMed: 19285961]  [MGI Ref ID J:147872]

Kim KY; Stevens MV; Akter MH; Rusk SE; Huang RJ; Cohen A; Noguchi A; Springer D; Bocharov AV; Eggerman TL; Suen DF; Youle RJ; Amar M; Remaley AT; Sack MN. 2011. Parkin is a lipid-responsive regulator of fat uptake in mice and mutant human cells. J Clin Invest 121(9):3701-12. [PubMed: 21865652]  [MGI Ref ID J:178238]

Kitada T; Pisani A; Karouani M; Haburcak M; Martella G; Tscherter A; Platania P; Wu B; Pothos EN; Shen J. 2009. Impaired dopamine release and synaptic plasticity in the striatum of parkin-/- mice. J Neurochem 110(2):613-21. [PubMed: 19457102]  [MGI Ref ID J:150857]

Kubli DA; Zhang X; Lee Y; Hanna RA; Quinsay MN; Nguyen CK; Jimenez R; Petrosyan S; Murphy AN; Gustafsson AB. 2013. Parkin protein deficiency exacerbates cardiac injury and reduces survival following myocardial infarction. J Biol Chem 288(2):915-26. [PubMed: 23152496]  [MGI Ref ID J:193741]

Lee Y; Lee HY; Hanna RA; Gustafsson AB. 2011. Mitochondrial autophagy by Bnip3 involves Drp1-mediated mitochondrial fission and recruitment of Parkin in cardiac myocytes. Am J Physiol Heart Circ Physiol 301(5):H1924-31. [PubMed: 21890690]  [MGI Ref ID J:178330]

Madeo G; Martella G; Schirinzi T; Ponterio G; Shen J; Bonsi P; Pisani A. 2012. Aberrant striatal synaptic plasticity in monogenic parkinsonisms. Neuroscience 211:126-35. [PubMed: 21839811]  [MGI Ref ID J:184659]

Martella G; Platania P; Vita D; Sciamanna G; Cuomo D; Tassone A; Tscherter A; Kitada T; Bonsi P; Shen J; Pisani A. 2009. Enhanced sensitivity to group II mGlu receptor activation at corticostriatal synapses in mice lacking the familial parkinsonism-linked genes PINK1 or Parkin. Exp Neurol 215(2):388-96. [PubMed: 19071114]  [MGI Ref ID J:144364]

Palacino JJ; Sagi D; Goldberg MS; Krauss S; Motz C; Wacker M; Klose J; Shen J. 2004. Mitochondrial dysfunction and oxidative damage in parkin-deficient mice. J Biol Chem 279(18):18614-22. [PubMed: 14985362]  [MGI Ref ID J:89508]

Pickrell AM; Pinto M; Moraes CT. 2013. Mouse models of Parkinson's disease associated with mitochondrial dysfunction. Mol Cell Neurosci 55:87-94. [PubMed: 22954895]  [MGI Ref ID J:203680]

Rosen KM; Veereshwarayya V; Moussa CE; Fu Q; Goldberg MS; Schlossmacher MG; Shen J; Querfurth HW. 2006. Parkin protects against mitochondrial toxins and beta-amyloid accumulation in skeletal muscle cells. J Biol Chem 281(18):12809-16. [PubMed: 16517603]  [MGI Ref ID J:112711]

Sul JW; Park MY; Shin J; Kim YR; Yoo SE; Kong YY; Kwon KS; Lee YH; Kim E. 2013. Accumulation of the parkin substrate, FAF1, plays a key role in the dopaminergic neurodegeneration. Hum Mol Genet 22(8):1558-73. [PubMed: 23307929]  [MGI Ref ID J:194987]

Zhang C; Lin M; Wu R; Wang X; Yang B; Levine AJ; Hu W; Feng Z. 2011. Parkin, a p53 target gene, mediates the role of p53 in glucose metabolism and the Warburg effect. Proc Natl Acad Sci U S A 108(39):16259-64. [PubMed: 21930938]  [MGI Ref ID J:177137]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, homozygous mice may be bred together.
Mating SystemHomozygote x Homozygote         (Female x Male)   01-JUL-08
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 $195.00Female or MaleHomozygous for Park2tm1Shn  
Price per Pair (US dollars $)Pair Genotype
$390.00Homozygous for Park2tm1Shn x Homozygous for Park2tm1Shn  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $253.50Female or MaleHomozygous for Park2tm1Shn  
Price per Pair (US dollars $)Pair Genotype
$507.00Homozygous for Park2tm1Shn x Homozygous for Park2tm1Shn  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
Ordering Information
JAX® Mice
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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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