|Mice that are homozygous for this Tbce, tubulin-specific chaperone e, spontaneous mutation, pmn, are viable but die prematurely on the STOCK, NMRI/Pan outbred, background. This mutant mouse strain may be useful in studies of Spinal Muscular Atrophy, muscular atrophy, motor neuronopathy and neurodegeneration.|
Former Names FVB/N.Cg-Tbcepmn/J (Changed: 26-SEP-12 ) Type Congenic; Mutant Strain; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Generation N5pN1
Donating Investigator Michael Sendtner, University of Wuerzburg
Mice that are homozygous for this spontaneous mutation are viable but die prematurely. Onset of locomotor impairment with corresponding motor neuron and muscular degeneration occurs at 2 to 3 weeks of age. Atrophy and paralysis starts in the hind limbs and pelvic girdle and is progressive. Homozygotes die by 6 to 7 weeks of age due to respiratory failure. Neurodegeneration starts in the motor endplates, progresses to loss of axons and results in apoptosis of the cell bodies. Electrophysiological deficiencies are detected by 13 days of age, before the neurodegeneration is clinically visible. Electron microscopic analysis of sciatic and phrenic nerves reveals a reduced number of microtubules. TBCE protein is destabilized, producing a reduction in tubulin and microtubules in motor neuron axons. Progressive microtubule loss occurs in axons distal to proximal and corresponds to axon degeneration. The mutation arose in the NMRI/Pan outbred line and has been identified as a Trp524Gly substitution (T1570G transversion) of the Tbce, tubulin-specific chaperone e, gene. Heterozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of Spinal Muscular Atrohpy, muscular atrophy, motor neuronopathy and neurodegeneration.
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. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
The mutation was first recorded at the Panum Institute (Kopenhagen, Denmark) in 1988. The mutation arose in the NMRI/Pan outbred line and has been identified as a Trp524Gly substitution of the Tbce, tubulin-specific chaperone e, gene. The mice have been crossed to the NMRI outbred background for 32 generations. Upon arrival at The Jackson Laboratory the mice were backcrossed to FVB/NJ mice using a speed congenic protocol.
|Wild-type from the colony|
|Considerations for Choosing Controls|
Spinal Muscular Atrophy (SMA) Models
008849 B6.129(C)-Smn1tm1.1Jme/J 006146 B6.129-Smn1tm1Jme/J 008453 B6.129-Smn1tm4(SMN2)Mrph/J 008714 B6.129-Smn1tm5(Smn1/SMN2)Mrph/J 009378 B6.129-Smn1tm6(SMN2)Mrph/J 010921 B6.129P2(Cg)-Smn1tm1Msd/J 018439 B6.129S6-Tg(CAG-Bgeo,-SMN2)E9Dscd/J 009680 B6.B-Vps54wr/J 007963 B6.Cg-Smn1tm2Mrph/J 007966 B6.Cg-Smn1tm3(SMN2/Smn1)Mrph/J 006149 B6.Cg-Tg(ACTA1-cre)79Jme/J 006663 B6.Cg-Tg(Eno2-cre)39Jme/J 008629 B6.Cg-Tg(SMN2)11Tro Smn1tm1Msd/J 008631 B6.Cg-Tg(SMN2)11Tro Tg(SMN2)46Tro Smn1tm1Msd/J 008630 B6.Cg-Tg(SMN2)46Tro Smn1tm1Msd/J 007222 B6.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN1*A2G)2023Ahmb/J 006964 B6.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN2*delta7)4299Ahmb/J 006773 B6.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd/J 007246 B6;129-Smn1tm2Mrph/J 008383 B6;129-Smn1tm4(SMN2)Mrph/J 008384 B6;129-Smn1tm5(Smn1/SMN2)Mrph/J 008704 B6;129-Smn1tm6(SMN2)Mrph/J 006138 FVB.129(B6)-Smn1tm1Jme/J 008713 FVB.129(B6)-Smn1tm4(SMN2)Mrph/J 008604 FVB.129(B6)-Smn1tm5(Smn1/SMN2)Mrph/J 006214 FVB.129P2-Smn1tm1Msd/J 005058 FVB.Cg-Smn1tm1Hung Tg(SMN2)2Hung/J 008206 FVB.Cg-Smn1tm1Msd Tg(SMN2)566Ahmb/J 007955 FVB.Cg-Smn1tm2Mrph/J 007964 FVB.Cg-Smn1tm3(SMN2/Smn1)Mrph/J 009381 FVB.Cg-Smn1tm6(SMN2)Mrph/J 006139 FVB.Cg-Tg(ACTA1-cre)79Jme/J 006297 FVB.Cg-Tg(Eno2-cre)39Jme/J 008209 FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd Tg(ACTA1-SMN)69Ahmb/J 016573 FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd Tg(S100B-EGFP)1Wjt Tg(SMN2*delta7)4299Ahmb/J 007968 FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN1*A2G)2023Ahmb/2J 008782 FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN2*A111G)588Ahmb/J 009134 FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN2*A111G)591Ahmb/J 007952 FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN2*delta7)4299Ahmb/2J 005025 FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN2*delta7)4299Ahmb/J 005026 FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN1*A2G)2023Ahmb/J 007949 FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd/2J 005024 FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd/J 009682 NMRI-Tbcepmn/J 017596 STOCK Gt(ROSA)26Sortm1.1(rtTA,EGFP)Nagy Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN2*delta7)4299Ahmb Tg(tetO-SMN2,-luc)#aAhmb/J 017597 STOCK Gt(ROSA)26Sortm1.1(rtTA,EGFP)Nagy Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN2*delta7)4299Ahmb Tg(tetO-SMN2,-luc)#bAhmb/J 007022 STOCK Mnx1tm4(cre)Tmj Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN2*delta7)4299Ahmb/J 008783 STOCK Tg(CAG-cre/Esr1*)5Amc Smn1tm3(SMN2/Smn1)Mrph Tg(SMN2*delta7)4299Ahmb Tg(SMN2)89Ahmb/J 005938 STOCK Tg(Eno2-cre)39Jme/J 008203 STOCK Tg(SMN2)89Ahmb Smn1tm1Msd Tg(ACTA1-SMN)63Ahmb/J 006553 STOCK Tg(SMN2)89Ahmb Smn1tm1Msd Tg(H2-K1-tsA58)6Kio Tg(SMN2*delta7)4299Ahmb/J 006570 STOCK Tg(SMN2)89Ahmb Smn1tm1Msd Tg(Hlxb9-GFP)1Tmj/J 008212 STOCK Tg(SMN2)89Ahmb Smn1tm1Msd Tg(Prnp-SMN)92Ahmb/J 018916 STOCK Tg(SMN2)89Ahmb Smn1tm1Msd Tg(SMN1-SMN2*)16Cll/CllJ 007951 STOCK Tg(SMN2)89Ahmb Smn1tm3(SMN2/Smn1)Mrph Tg(SMN2*delta7)4299Ahmb/J 008359 STOCK Tg(SMN2)89Ahmb Smn1tm3(SMN2/Smn1)Mrph/J 017599 STOCK Tg(tetO-SMN2,-luc)#aAhmb/J 017600 STOCK Tg(tetO-SMN2,-luc)#bAhmb/JView Spinal Muscular Atrophy (SMA) Models (58 strains)Strains carrying Tbcepmn allele
009682 NMRI-Tbcepmn/JView Strains carrying Tbcepmn (1 strain)
View Related Disease (OMIM) TermsRelated Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.View Mammalian Phenotype TermsMammalian Phenotype Terms provided by MGIassigned by genotype
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.
- premature death
- muscle phenotype
- muscular atrophy
- progressive muscle weakness
- nervous system phenotype
- abnormal facial nerve morphology
- loss of motor axons here is reduced by ciliary neutrophic factor (CNTF) delivered via an engineered CNTF construct in tranfected mouse D3 cells (MGI Ref ID J:1717)
- abnormal phrenic nerve morphology
- axon degeneration
- the motor, but not the sensory, axons of the peripheral nerves degenerate, starting at the motor endplates and dying back proximally (MGI Ref ID J:30914)
- motor neuron degeneration
- progressive caudo-cranial degeneration (MGI Ref ID J:1717)
- respiratory system phenotype
- respiratory failure (MGI Ref ID J:1717)
- mice die of respiratory failure by 6-7 weeks of age (MGI Ref ID J:30914)
- behavior/neurological phenotype
- detectable by 2-3 weeks of age (MGI Ref ID J:30914)View Research ApplicationsResearch ApplicationsThis mouse can be used to support research in many areas including:
Spinal Muscular Atrophy (SMA)
|Allele Name||progressive motor neuronopathy|
|Common Name(s)||TbceG; pmn; progressive motor neuropathy;|
|Mutation Made By||Michael Sendtner, University of Wuerzburg|
|Strain of Origin||NMRI/Pan|
|Gene Symbol and Name||Tbce, tubulin-specific chaperone E|
|Gene Common Name(s)||2610206D02Rik; C530005D02Rik; HRD; KCS; KCS1; RIKEN cDNA 2610206D02 gene; RIKEN cDNA C530005D02 gene; pac2; pmn; progressive motor neuropathy;|
|General Note||This mutation was identified in 1988 at the Panum Institute in Copenhagen.|
|Molecular Note||The mutation has been identified as T to G transversion, resulting in a Trp524Gly amino acid substitution in the encoded protein. Northern analysis detected no difference in transcript levels between mutant and wild-type mice. That the mutation was duea defect in Tbce was demonstrated through complementation with a line expressing a Tbce transgene. [MGI Ref ID J:79895] [MGI Ref ID J:80606]|
Schmalbruch H; Jensen HJ; Bjaerg M; Kamieniecka Z; Kurland L. 1991. A new mouse mutant with progressive motor neuronopathy. J Neuropathol Exp Neurol 50(3):192-204. [PubMed: 2022963] [MGI Ref ID J:30914]
Bommel H; Xie G; Rossoll W; Wiese S; Jablonka S; Boehm T; Sendtner M. 2002. Missense mutation in the tubulin-specific chaperone E (Tbce) gene in the mouse mutant progressive motor neuronopathy, a model of human motoneuron disease. J Cell Biol 159(4):563-9. [PubMed: 12446740] [MGI Ref ID J:80606]
Bordet T; Schmalbruch H; Pettmann B; Hagege A; Castelnau-Ptakhine L; Kahn A; Haase G. 1999. Adenoviral cardiotrophin-1 gene transfer protects pmn mice from progressive motor neuronopathy. J Clin Invest 104(8):1077-85. [PubMed: 10525046] [MGI Ref ID J:58103]
Duong F; Fournier J; Keane PE; Guenet JL; Soubrie P; Warter JM; Borg J; Poindron P. 1998. The effect of the nonpeptide neurotrophic compound SR 57746A on the progression of the disease state of the pmn mouse. Br J Pharmacol 124(4):811-7. [PubMed: 9690875] [MGI Ref ID J:50995]
Ferrer-Alcon M; Winkler-Hirt C; Madani R; Perrin FE; Kato AC. 2008. Low intensity exercise attenuates disease progression and stimulates cell proliferation in the spinal cord of a mouse model with progressive motor neuronopathy. Neuroscience 152(2):291-5. [PubMed: 18295408] [MGI Ref ID J:135700]
Ferrer-Alcon M; Winkler-Hirt C; Perrin FE; Kato AC. 2007. Grafted neural stem cells increase the life span and protect motoneurons in pmn mice. Neuroreport 18(14):1463-8. [PubMed: 17712275] [MGI Ref ID J:125209]
Ferri A; Sanes JR; Coleman MP; Cunningham JM; Kato AC. 2003. Inhibiting axon degeneration and synapse loss attenuates apoptosis and disease progression in a mouse model of motoneuron disease. Curr Biol 13(8):669-73. [PubMed: 12699624] [MGI Ref ID J:82989]
Frey D; Schneider C; Xu L; Borg J; Spooren W; Caroni P. 2000. Early and selective loss of neuromuscular synapse subtypes with low sprouting competence in motoneuron diseases. J Neurosci 20(7):2534-42. [PubMed: 10729333] [MGI Ref ID J:109472]
Haase G; Kennel P; Pettmann B; Vigne E; Akli S; Revah F; Schmalbruch H ; Kahn A. 1997. Gene therapy of murine motor neuron disease using adenoviral vectors for neurotrophic factors [see comments] Nat Med 3(4):429-36. [PubMed: 9095177] [MGI Ref ID J:39440]
Haase G; Pettmann B; Vigne E; Castelnau-Ptakhine L; Schmalbruch H; Kahn A. 1998. Adenovirus-mediated transfer of the neurotrophin-3 gene into skeletal muscle of pmn mice: therapeutic effects and mechanisms of action. J Neurol Sci 160 Suppl 1:S97-105. [PubMed: 9851658] [MGI Ref ID J:51340]
Holtmann B; Zielasek J; Toyka KV; Sendtner M. 1999. Comparative analysis of motoneuron loss and functional deficits in PMN mice: implications for human motoneuron disease. J Neurol Sci 169(1-2):140-7. [PubMed: 10540023] [MGI Ref ID J:58379]
Jablonka S; Holtmann B; Sendtner M; Metzger F. 2011. Therapeutic effects of PEGylated insulin-like growth factor I in the pmn mouse model of motoneuron disease. Exp Neurol 232(2):261-9. [PubMed: 21963648] [MGI Ref ID J:178470]
Kennel P; Revah F; Bohme GA; Bejuit R; Gallix P; Stutzmann J; Imperato A; Pratt J. 2000. Riluzole prolongs survival and delays muscle strength deterioration in mice with progressive motor neuronopathy (pmn) J Neurol Sci 180(1-2):55-61. [PubMed: 11090865] [MGI Ref ID J:66163]
Kennel PF; Fonteneau P; Martin E; Schmidt JM; Azzouz M; Borg J; Guenet JL; Schmalbruch H; Warter JM; Poindron P. 1996. Electromyographical and motor performance studies in the pmn mouse model of neurodegenerative disease. Neurobiol Dis 3(2):137-47. [PubMed: 9173921] [MGI Ref ID J:43329]
Martin N; Jaubert J; Glaser P; Szatanik M; Guenet JL. 2001. Genetic and physical delineation of the region overlapping the progressive motor neuropathy (pmn) locus on mouse chromosome 13. Genomics 75(1-3):9-16. [PubMed: 11472062] [MGI Ref ID J:70256]
Martin N; Jaubert J; Gounon P; Salido E; Haase G; Szatanik M; Guenet JL. 2002. A missense mutation in Tbce causes progressive motor neuronopathy in mice. Nat Genet 32(3):443-7. [PubMed: 12389029] [MGI Ref ID J:79895]
Perrin FE; Boisset G; Lathuiliere A; Kato AC. 2006. Cell death pathways differ in several mouse models with motoneurone disease: analysis of pure motoneurone populations at a presymptomatic age. J Neurochem 98(6):1959-72. [PubMed: 16831193] [MGI Ref ID J:112591]
Rak K; Frenz S; Radeloff A; Groh J; Jablonka S; Martini R; Hagen R; Mlynski R. 2013. Mutation of the TBCE gene causes disturbance of microtubules in the auditory nerve and cochlear outer hair cell degeneration accompanied by progressive hearing loss in the pmn/pmn mouse. Exp Neurol 250:333-40. [PubMed: 24120439] [MGI Ref ID J:206608]
Sagot Y; Dubois-Dauphin M; Tan SA; de Bilbao F; Aebischer P; Martinou JC; Kato AC. 1995. Bcl-2 overexpression prevents motoneuron cell body loss but not axonal degeneration in a mouse model of a neurodegenerative disease. J Neurosci 15(11):7727-33. [PubMed: 7472523] [MGI Ref ID J:29787]
Sagot Y; Rosse T; Vejsada R; Perrelet D; Kato AC. 1998. Differential effects of neurotrophic factors on motoneuron retrograde labeling in a murine model of motoneuron disease. J Neurosci 18(3):1132-41. [PubMed: 9437033] [MGI Ref ID J:45539]
Sagot Y; Tan SA; Baetge E; Schmalbruch H; Kato AC; Aebischer P. 1995. Polymer encapsulated cell lines genetically engineered to release ciliary neurotrophic factor can slow down progressive motor neuronopathy in the mouse. Eur J Neurosci 7(6):1313-22. [PubMed: 7582105] [MGI Ref ID J:30394]
Sagot Y; Tan SA; Hammang JP; Aebischer P; Kato AC. 1996. GDNF slows loss of motoneurons but not axonal degeneration or premature death of pmn/pmn mice. J Neurosci 16(7):2335-41. [PubMed: 8601813] [MGI Ref ID J:32067]
Schaefer MK; Schmalbruch H; Buhler E; Lopez C; Martin N; Guenet JL; Haase G. 2007. Progressive motor neuronopathy: a critical role of the tubulin chaperone TBCE in axonal tubulin routing from the Golgi apparatus. J Neurosci 27(33):8779-89. [PubMed: 17699660] [MGI Ref ID J:124178]
Schmalbruch H; Jensen HJS. 1990. 'Progressive motor neuropathy' (pmn), a new neurological mutant in the mouse. Mouse Genome 87:113. [MGI Ref ID J:14295]
Sedehizade F; Klocke R; Jockusch H. 1997. Expression of nerve-regulated genes in muscles of mouse mutants affected by spinal muscular atrophies and muscular dystrophies. Muscle Nerve 20(2):186-94. [PubMed: 9040657] [MGI Ref ID J:53205]
Selvaraj BT; Frank N; Bender FL; Asan E; Sendtner M. 2012. Local axonal function of STAT3 rescues axon degeneration in the pmn model of motoneuron disease. J Cell Biol 199(3):437-51. [PubMed: 23109669] [MGI Ref ID J:195255]
Sendtner M; Gotz R; Holtmann B; Thoenen H. 1997. Endogenous ciliary neurotrophic factor is a lesion factor for axotomized motoneurons in adult mice. J Neurosci 17(18):6999-7006. [PubMed: 9278535] [MGI Ref ID J:42884]
Sendtner M; Schmalbruch H; Stockli KA; Carroll P; Kreutzberg GW; Thoenen H. 1992. Ciliary neurotrophic factor prevents degeneration of motor neurons in mouse mutant progressive motor neuronopathy [see comments] Nature 358(6386):502-4. [PubMed: 1641039] [MGI Ref ID J:1717]
Simonin Y; Charron Y; Sonderegger P; Vassalli JD; Kato AC. 2006. An inhibitor of serine proteases, neuroserpin, acts as a neuroprotective agent in a mouse model of neurodegenerative disease. J Neurosci 26(41):10614-9. [PubMed: 17035547] [MGI Ref ID J:113248]
Simonin Y; Ferrer-Alcon M; Ferri A; Kato AC. 2007. The neuroprotective effects of the WldS gene are correlated with proteasome expression rather than apoptosis. Eur J Neurosci 25(8):2269-74. [PubMed: 17445225] [MGI Ref ID J:125019]
Simonin Y; Perrin FE; Kato AC. 2007. Axonal involvement in the Wlds neuroprotective effect: analysis of pure motoneurons in a mouse model protected from motor neuron disease at a pre-symptomatic age. J Neurochem 101(2):530-42. [PubMed: 17402973] [MGI Ref ID J:122486]
Animal Health ReportsProduction of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.
Breeding & Husbandry When maintaining a live colony, these mice can be bred as heterozygotes. Homozygotes are viable but die by 6 to 7 weeks of age on the STOCK background.
|Pricing for USA, Canada and Mexico shipping destinations|
Cryopreserved Mice - Ready for Recovery
Price (US dollars $) Cryorecovery* $3300.00
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.
Cryorecovery - Standard.
Progeny testing is not required.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.
Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
|Pricing for International shipping destinations|
Cryopreserved Mice - Ready for Recovery
Price (US dollars $) Cryorecovery* $4290.00
Cryorecovery - Standard.
Progeny testing is not required.
|Wild-type from the colony|
|Considerations for Choosing Controls|
|Control Pricing Information for Genetically Engineered Mutant Strains.|
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.
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.