| ||||||||||||||||||||||
| These double transgenic homozygous mice (dbl-PAC-Tg(SNCAA53T);Snca-/- mice) harbor a Snca knockout allele and two independently inserted transgenes encoding the human A53T-mutant α-synuclein associated with autosomal dominant Parkinson's disease. The very early gastrointestinal dysfunction in the absence of major central nervous system pathology in dbl-PAC-Tg(SNCAA53T);Snca-/- mice mimics what is seen early in human Parkinson's disease, when enteric nervous system dysfunction may precede the more classical motor symptoms by years to decades. | ||||||||||||||||||||||
- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
Description
Strain Information
Type Mutant Stock; Targeted Mutation; Transgenic; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Mating System See Colony Maintenance under the Health & husbandry tab (Female x Male) 30-MAR-10 Species laboratory mouse Generation F?+F4 (30-SEP-11)
Generation DefinitionsDonating Investigator Robert Nussbaum, University of California San Francisco Description
These double transgenic homozygous mice (dbl-PAC-Tg(SNCAA53T);Snca-/- mice) are viable and fertile, harboring a Snca knockout allele and two independently inserted transgenes encoding the human A53T-mutant α-synuclein associated with autosomal dominant Parkinson's disease. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by α-synuclein*A53T from the four total insertions of the PAC-Tg(SNCAA53T). While brain RNA expression of SNCAA53T is ~10-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAA53T are ~80-fold greater than normal endogenous mouse α-synuclein. By three months of age, dbl-PAC-Tg(SNCAA53T);Snca-/- mice show robust abnormalities in enteric nervous system function (impaired colonic motility [males only] and prolonged gut transit time). Significant α-synuclein*A53T aggregation is observed in colonic myenteric plexus, while no widespread aggregation in brain is reported. Subtle motor behavior abnormalities develop between 6-12 months. No detectable autonomic abnormalities, olfactory dysfunction, dopaminergic deficits, Lewy body inclusions or neurodegeneration are associated with α-synuclein*A53T expression in these double transgenic mice. The very early gastrointestinal dysfunction in the absence of major central nervous system pathology in dbl-PAC-Tg(SNCAA53T);Snca-/- mice mimics what is seen early in human Parkinson's disease, when enteric nervous system dysfunction may precede the more classical motor symptoms by years to decades.Development
To generate the PAC-Tg(SNCAA53T) transgene, the 146 kb RPCI-1 human male P1 artificial chromosome (PAC) clone 27M07, containing the entire human SNCA (synuclein, alpha (non A4 component of amyloid precursor)) gene and 34 kb of its upstream region, was modified to have the A53T human mutation associated with autosomal dominant Parkinson's disease (G>A substitution at base 420 of the cDNA sequence). This transgene was microinjected into the pronuclei of fertilized FVB/N ova. Each transgenic founder mouse was bred to FVB/N wildtype mice to generate the individual founder lines (1 and 2). Each PAC-Tg(SNCAA53T) transgenic line was independently maintained as coisogenic on the FVB/N genetic background by breeding together as homozygotes.To generate the Snca knockout allele, a targeting vector was designed to replace exons 4 and 5 with a reverse-oriented neomycin resistance cassette (PGK-neo from the vector pPNT). The construct was electroporated into 129S6/SvEvTac-derived TC-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts and the resulting mutant mice were generated and maintained as coisogenic on the 129S6/SvEvTac genetic background.
To generate the dbl-PAC-Tg(SNCAA53T);Snca-/- strain, homozygous PAC-Tg(SNCAA53T) line 1 mice (FVB/N genetic background) were bred with mice homozygous for the Snca knockout allele (129S6/SvEvTac genetic background). Similarly, PAC-Tg(SNCAA53T) line 2 homozygotes were bred with Snca knockout mice. These two mutant strains were then intercrossed and bred to homozygosity to create the double transgenic strain. As homozygotes, dbl-PAC-Tg(SNCAA53T);Snca-/- mice were found to carry four insertions of the PAC-Tg(SNCAA53T) transgene; two for the line 1 insert (on chomsome 3) and two for the line 2 insert (on chromosome 14). This double transgenic strain was maintained on a mixed FVB/N;129S6/SvEvTac background using multiple breeding units without repeated brother-sister matings: thus the only portions of the FVB/N or 129S6/SvEvTac genomes fixed in these mice are the FVB/N regions flanking the PAC-Tg(SNCAA53T) transgene insertion sites and the 129S6/SvEvTac regions around the Snca knockout allele. The dbl-PAC-Tg(SNCAA53T);Snca-/- mice were sent to The Jackson Laboratory Repository. Upon arrival, mice were bred together to establish the colony.
Control Information
| Control | ||
|---|---|---|
| None Available | ||
| Considerations for Choosing Controls | ||
Related Strains
Parkinson's Disease Models
View Parkinson's Disease Models (99 strains)
010710 FVB;129S6-Sncatm1Nbm Tg(SNCA)1Nbm/J 010788 FVB;129S6-Sncatm1Nbm Tg(SNCA*A30P)1Nbm Tg(SNCA*A30P)2Nbm/J
Additional Web Information
Visit the Parkinson's Disease Resource site for helpful information on Parkinson's and research resources.
Phenotype
Phenotype Information
Parkinson Disease 1, Autosomal Dominant; PARK1 - Models with phenotypic similarity to human disease where etiologies involve orthologs.1
1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s). assigned by genotype
Sncatm1Nbm/Sncatm1Nbm Tg(SNCA*A53T)1Nbm/Tg(SNCA*A53T)1Nbm Tg(SNCA*A53T)2Nbm/Tg(SNCA*A53T)2Nbm
involves: 129S6/SvEvTac * FVB/N
- growth/size phenotype
- *normal* growth/size phenotype
- body weigh does not differ from controls measured out to 18 months of age (MGI Ref ID J:156741)
- behavior/neurological phenotype
- hypoactivity
- total distance traveled in the open field apparatus is reduced compared to controls at 6 months and remains abnormal at 18 months (MGI Ref ID J:156741)
- distance traveled decreases with age, showing reduced ambulatory distance traveled compared to controls at 12 and 18 months; reduction is generalized, not specific to a particular type of movement or region (MGI Ref ID J:156741)
- impaired coordination
- males and females exhibit consistently reduced latency to fall beginning at 6 months; this persisted at 1 year of age and more pronounced at 18 months; endurance and coordination in the rotating rod test are abnormal (MGI Ref ID J:156741)
- nervous system phenotype
- *normal* nervous system phenotype
- dorsal motor nucleus of the vagus shows no abnormal alpha-synuclein aggregation and any widespread aggregates are not detected in brain homogenates of 5 and 18 month-old animals (MGI Ref ID J:156741)
- striatal tissue dopamine and dopamine metabolite content are not different from controls at 11 and 18 months (MGI Ref ID J:156741)
- no progressive loss of dopaminergic neurons in the substantia nigra, pars compacta (SNpc) is observed (MGI Ref ID J:156741)
- olfaction and cardiac innervation by the autonomic nervous system are not affected by the transgenes (MGI Ref ID J:156741)
- abnormal hippocampus morphology
- some dystrophic synapses are observed in rare instances at 12 or 22 months (MGI Ref ID J:156741)
- alpha-synuclein inclusion body
- protein is present in tyrosine hydroxylase (TH)-immunoreactive neuronal cell bodies within myenteric and submucosal plexuses; varicose TH-positive terminals of noradrenergic sympathetic neurons (MGI Ref ID J:156741)
- most alpha-synuclein positive neurons, especially in the myenteric plexus are not coincident with TH immunostaining (MGI Ref ID J:156741)
- proteinase K-resistant alpha-synuclein aggregates are observed in the nuclear and perinuclear cytoplasm of enteric nervous system neurons in mice showing gastrointestinal motility dysfunction (MGI Ref ID J:156741)
- digestive/alimentary phenotype
- abnormal digestive system physiology
- proteinase K-resistant alpha-synuclein aggregates are observed in the nuclear and perinuclear cytoplasm of enteric nervous system neurons in mice showing gastrointestinal motility dysfunction (MGI Ref ID J:156741)
- abnormal intestinal transit time
- whole-gut transit time (WGTT) is prolonged compared to controls starting at 3 months and is markedly prolonged at 6 months persisting through 18 months of age; this phenotype does not differ between males and females in contrast to bead expulsion time (distal colonic motility) (MGI Ref ID J:156741)
- abnormal large intestinal transit time
- motility of distal colon is reduced compared to controls with males showing around a 4-5 fold prolongation in expulsion compared to controls; reduction is exaggerated compared to females (MGI Ref ID J:156741)
- this phenotype is present at 3 months and persists through 18 months of age (MGI Ref ID J:156741)
- amount of stool passed/unit time and stool water content are unchanged at 3 months of age but by 6 months these parameters are reduced to comparable degrees (MGI Ref ID J:156741)
- cardiovascular system phenotype
- *normal* cardiovascular system phenotype
- no defects in autonomic cardiac innervation are detected (MGI Ref ID J:156741)
- taste/olfaction phenotype
- *normal* taste/olfaction phenotype
This mouse can be used to support research in many areas including:
Internal/Organ Research
Gastrointestinal Defects
Neurobiology Research
Ataxia (Movement) Defects
Neuromuscular Defects
Parkinson's Disease
synuclein mutants
Research Tools
Neurobiology Research
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Sncatm1Nbm | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Robert L Nussbaum | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | Scna-; Snca-; | ||
| Strain of Origin | 129S6/SvEvTac | ||
| Gene Symbol and Name | Snca, synuclein, alpha | ||
| Chromosome | 6 | ||
| Gene Common Name(s) | NACP; PARK1; PARK4; PD1; alpha-synuclein; alphaSYN; | ||
| Molecular Note | Exons 4 and 5 were replaced with a neomycin selection cassette inserted by homologous recombination. While the separation of Western blot results by 2D-PAGE showed various isoforms in total brain extract obtained from wild-type mice, protein was undetected in samples obtained from homozygous mutant mice. [MGI Ref ID J:79784] | ||
| Allele Symbol | Tg(SNCA*A53T)1Nbm | ||
| Allele Name | transgene insertion 1, Robert L Nussbaum | ||
| Allele Type | Transgenic (random, expressed) | ||
| Common Name(s) | PAC-Tg(SCNAA53T; | ||
| Strain of Origin | FVB/N | ||
| Expressed Gene | SNCA, synuclein, alpha (non A4 component of amyloid precursor), human | ||
| Promoter | SNCA, synuclein, alpha (non A4 component of amyloid precursor), human | ||
| Molecular Note | To generate the PAC-Tg(SNCAA53T) transgene, the 146 kb RPCI-1 human male P1 artificial chromosome (PAC) clone 27M07, containing the entire human SNCA (synuclein, alpha (non A4 component of amyloid precursor)) gene and 34 kb of its upstream region, was modified to have the A53T human mutation associated with autosomal dominant Parkinson's disease. This transgene was microinjected into the pronuclei of fertilized FVB/N ova. One transgenic insertion is present in the genome. [MGI Ref ID J:154972] [MGI Ref ID J:156741] | ||
| Allele Symbol | Tg(SNCA*A53T)2Nbm | ||
| Allele Name | transgene insertion 2, Robert L Nussbaum | ||
| Allele Type | Transgenic (random, expressed) | ||
| Common Name(s) | PAC-Tg(SCNAA53T; | ||
| Strain of Origin | FVB/N | ||
| Expressed Gene | SNCA, synuclein, alpha (non A4 component of amyloid precursor), human | ||
| Promoter | SNCA, synuclein, alpha (non A4 component of amyloid precursor), human | ||
| Molecular Note | To generate the PAC-Tg(SNCAA53T) transgene, the 146 kb RPCI-1 human male P1 artificial chromosome (PAC) clone 27M07, containing the entire human SNCA (synuclein, alpha (non A4 component of amyloid precursor)) gene and 34 kb of its upstream region, was modified to have the A53T human mutation associated with autosomal dominant Parkinson's disease. This transgene was microinjected into the pronuclei of fertilized FVB/N ova. One transgenic insertion is present in the genome. [MGI Ref ID J:154972] [MGI Ref ID J:156741] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Tg(Prnp-SNCA*A53T)83Vle, QPCR
Tg(SNCA), Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Cabin DE; Shimazu K; Murphy D; Cole NB; Gottschalk W; McIlwain KL; Orrison B; Chen A; Ellis CE; Paylor R; Lu B; Nussbaum RL. 2002. Synaptic vesicle depletion correlates with attenuated synaptic responses to prolonged repetitive stimulation in mice lacking alpha-synuclein. J Neurosci 22(20):8797-807. [PubMed: 12388586] [MGI Ref ID J:79784]
Kuo YM; Li Z; Jiao Y; Gaborit N; Pani AK; Orrison BM; Bruneau BG; Giasson BI; Smeyne RJ; Gershon MD; Nussbaum RL. 2010. Extensive enteric nervous system abnormalities in mice transgenic for artificial chromosomes containing Parkinson disease-associated {alpha}-synuclein gene mutations precede central nervous system changes. Hum Mol Genet :. [PubMed: 20106867] [MGI Ref ID J:156741]
Additional References
Sncatm1Nbm relatedTg(SNCA*A53T)1Nbm relatedAustin SA; Floden AM; Murphy EJ; Combs CK. 2006. Alpha-synuclein expression modulates microglial activation phenotype. J Neurosci 26(41):10558-63. [PubMed: 17035541] [MGI Ref ID J:113229]
Barcelo-Coblijn G; Golovko MY; Weinhofer I; Berger J; Murphy EJ. 2007. Brain neutral lipids mass is increased in alpha-synuclein gene-ablated mice. J Neurochem 101(1):132-41. [PubMed: 17250686] [MGI Ref ID J:122525]
Cabin DE; Gispert-Sanchez S; Murphy D; Auburger G; Myers RR; Nussbaum RL. 2005. Exacerbated synucleinopathy in mice expressing A53T SNCA on a Snca null background. Neurobiol Aging 26(1):25-35. [PubMed: 15585343] [MGI Ref ID J:124976]
Ekstrand MI; Terzioglu M; Galter D; Zhu S; Hofstetter C; Lindqvist E; Thams S; Bergstrand A; Hansson FS; Trifunovic A; Hoffer B; Cullheim S; Mohammed AH; Olson L; Larsson NG. 2007. Progressive parkinsonism in mice with respiratory-chain-deficient dopamine neurons. Proc Natl Acad Sci U S A 104(4):1325-30. [PubMed: 17227870] [MGI Ref ID J:119515]
Ellis CE; Murphy EJ; Mitchell DC; Golovko MY; Scaglia F; Barcelo-Coblijn GC; Nussbaum RL. 2005. Mitochondrial lipid abnormality and electron transport chain impairment in mice lacking alpha-synuclein. Mol Cell Biol 25(22):10190-201. [PubMed: 16260631] [MGI Ref ID J:102361]
Gispert S; Del Turco D; Garrett L; Chen A; Bernard DJ; Hamm-Clement J; Korf HW; Deller T; Braak H; Auburger G; Nussbaum RL. 2003. Transgenic mice expressing mutant A53T human alpha-synuclein show neuronal dysfunction in the absence of aggregate formation. Mol Cell Neurosci 24(2):419-29. [PubMed: 14572463] [MGI Ref ID J:86222]
Golovko MY; Faergeman NJ; Cole NB; Castagnet PI; Nussbaum RL; Murphy EJ. 2005. Alpha-synuclein gene deletion decreases brain palmitate uptake and alters the palmitate metabolism in the absence of alpha-synuclein palmitate binding. Biochemistry 44(23):8251-9. [PubMed: 15938614] [MGI Ref ID J:99690]
Golovko MY; Rosenberger TA; Faergeman NJ; Feddersen S; Cole NB; Pribill I; Berger J; Nussbaum RL; Murphy EJ. 2006. Acyl-CoA synthetase activity links wild-type but not mutant alpha-synuclein to brain arachidonate metabolism. Biochemistry 45(22):6956-66. [PubMed: 16734431] [MGI Ref ID J:109641]
Kurz A; Double KL; Lastres-Becker I; Tozzi A; Tantucci M; Bockhart V; Bonin M; Garcia-Arencibia M; Nuber S; Schlaudraff F; Liss B; Fernandez-Ruiz J; Gerlach M; Wullner U; Luddens H; Calabresi P; Auburger G; Gispert S. 2010. A53T-alpha-synuclein overexpression impairs dopamine signaling and striatal synaptic plasticity in old mice. PLoS One 5(7):e11464. [PubMed: 20628651] [MGI Ref ID J:163115]
Kurz A; Wohr M; Walter M; Bonin M; Auburger G; Gispert S; Schwarting RK. 2010. Alpha-synuclein deficiency affects brain Foxp1 expression and ultrasonic vocalization. Neuroscience 166(3):785-95. [PubMed: 20056137] [MGI Ref ID J:159729]
Steidinger TU; Standaert DG; Yacoubian TA. 2011. A neuroprotective role for angiogenin in models of Parkinson's disease. J Neurochem 116(3):334-41. [PubMed: 21091473] [MGI Ref ID J:170263]
Watson JB; Hatami A; David H; Masliah E; Roberts K; Evans CE; Levine MS. 2009. Alterations in corticostriatal synaptic plasticity in mice overexpressing human alpha-synuclein. Neuroscience 159(2):501-13. [PubMed: 19361478] [MGI Ref ID J:148932]
Westerlund M; Ran C; Borgkvist A; Sterky FH; Lindqvist E; Lundstromer K; Pernold K; Brene S; Kallunki P; Fisone G; Olson L; Galter D. 2008. Lrrk2 and alpha-synuclein are co-regulated in rodent striatum. Mol Cell Neurosci 39(4):586-91. [PubMed: 18790059] [MGI Ref ID J:142519]
Tg(SNCA*A53T)2Nbm relatedNussbaum RL. 2009. Generation of SNCA transgenes carrying A53T mutations MGI Direct Data Submission :. [MGI Ref ID J:154972]
Nussbaum RL. 2009. Generation of SNCA transgenes carrying A53T mutations MGI Direct Data Submission :. [MGI Ref ID J:154972]
Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Room Number AX11
Colony Maintenance
Breeding & Husbandry When maintaining a live colony, mice homozygous for the Snca targeted mutation and homozygous for both Tg(SNCAA53T) transgenes are bred together. The experimental control strain is Stock No. 010710. Mating System See Colony Maintenance under the Health & husbandry tab (Female x Male) 30-MAR-10 Diet Information LabDiet® 5K52/5K67
Purchasing information
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
|
 |
Live Mice
Price (US dollars $) Gender Genotypes Provided Individual Mouse $172.00 Female or Male Homozygous for Sncatm1Nbm, Homozygous for Tg(SNCA*A53T)1Nbm, Homozygous for Tg(SNCA*A53T)2Nbm/J
Pairs /Price (US dollars $) Pair Genotype $344.00 Homozygous for Sncatm1Nbm, Homozygous for Tg(SNCA*A53T)1Nbm, Homozygous for Tg(SNCA*A53T)2Nbm/J x Homozygous for Sncatm1Nbm, Homozygous for Tg(SNCA*A53T)1Nbm, Homozygous for Tg(SNCA*A53T)2Nbm/J Standard Supply
Repository-Live. The Repository Strains represent an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. We treat orders for these strains as custom orders. Within 2 business days, we respond to each availability inquiry or order 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.
| Pricing for International shipping destinations |
|
|
Live Mice
Price (US dollars $) Gender Genotypes Provided Individual Mouse $223.60 Female or Male Homozygous for Sncatm1Nbm, Homozygous for Tg(SNCA*A53T)1Nbm, Homozygous for Tg(SNCA*A53T)2Nbm/J
Pairs /Price (US dollars $) Pair Genotype $447.20 Homozygous for Sncatm1Nbm, Homozygous for Tg(SNCA*A53T)1Nbm, Homozygous for Tg(SNCA*A53T)2Nbm/J x Homozygous for Sncatm1Nbm, Homozygous for Tg(SNCA*A53T)1Nbm, Homozygous for Tg(SNCA*A53T)2Nbm/J Standard Supply
Repository-Live. The Repository Strains represent an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. We treat orders for these strains as custom orders. Within 2 business days, we respond to each availability inquiry or order 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.
|
|
|
Standard Supply
Repository-Live. The Repository Strains represent an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. We treat orders for these strains as custom orders. Within 2 business days, we respond to each availability inquiry or order 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.
General Supply Notes
- This strain is included in the Induced Mutant Resource Colony collection.
Control Information
| Control | ||
|---|---|---|
| None Available | ||
| 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
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form
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 inquiriesContracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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.