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- Description
- Disease & phenotype
- Genes & alleles
- Genotyping
- Health & care
- References
- Pricing & purchasing
- Terms of use
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
Former Names 129-Madh3tm1Par/J (Changed: 15-DEC-04 ) 129S2/SvPasIco-Madh3tm1Par/J (Changed: 15-DEC-04 ) Type Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Donating Investigator Dr. Luis F. Parada, UT Southwestern Medical Center Description
Mice homozygous for the targeted mutation are viable. Although fertile, they produce litters at reduced efficacy compared to wild type or heterozygous mice. Null mutants are approximately 20%-30% smaller than heterozygous or wildtype litter mates, with males exhibiting a more pronounced size reduction. Reporter lacZ expression is observed in many developing embryonic tissues with highest levels in mesenchymal derivatives. Expression in adult mutant mice is observed in the colon, with highest levels in the muscularis propria and submucosa with lower levels in the epithelium. At approximately 4-6 months of age, they develop gastric tumors. The donating investigator originally described spontaneous, deeply invasive colorectal adenocarcinomas that penetrate through all layers of the intestinal wall and metastasize to lymph nodes. Colorectal adenocarcinomas are not a component of the phenotype observed in this strain at The Jackson Laboratory. However, the gastric epithelium was found to contain neoplasms that were of a mixed nature. This deviation from the original phenotype may possibly be attributed to differing environmental conditions existing at The Jackson Laboratory facilities and those at the originating institution.Development
This targeted mutation was made in the laboratory of Dr. Luis F. Parada at The University of Texas Southwestern Medical Center. The targeting vector includes a neo cassette and was designed to disrupt the second exon of the locus. In addition, a lacZ gene and an internal ribosomal entry site (IRES) were introduced to permit translation of the beta galactosidase reporter from the interrupted transcript. The IRES-lacZ-neo inserted in the second exon truncates the gene and creates loss-of-function gene product proteins. Alternative splicing around exon 2 shifts the open reading frame. The 129X1/SvJ x 129S1/Sv-dervied R1 ES cell line was used. Chimeric mice carrying the targeted mutation were backcrossed to the 129S2/SvPasIco strain.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| Considerations for Choosing Controls | ||
Related Strains
lacZ Expression Strains
View lacZ Expression Strains (255 strains)
Additional Web Information
Fluorescent Proteins/lacZ Systems
New 129 Nomenclature Bulletin
Phenotype
Phenotype Information
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Loeys-Dietz Syndrome, Type 3; LDS3 (SMAD3)
assigned by genotype
Smad3tm1Par/Smad3tm1Par
either: (involves: 129S1/Sv * 129X1/SvJ) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6)
- mortality/aging
- premature death
- decreased life span; more pronounced in the 129/Sv background than in the mixed 129/Sv and C57BL/6 background, but evident in both (MGI Ref ID J:49839)
- tumorigenesis
- increased metastatic potential
- evidence of metastasis to lymph nodes is seen on the 129/Sv background (MGI Ref ID J:49839)
- intestinal adenocarcinoma
- penetrance of adenocarcinoma is about 30% on the mixed 129/Sv and C57BL/6 background and 100% on the 129/Sv background (MGI Ref ID J:49839)
- mutants on the mixed background show greater variability in the time course of tumors and tumors are less aggressive and smaller than in the 129/Sv background (MGI Ref ID J:49839)
- a wide range of tumors are found within a single mouse, including lesions that appear to be polyps (MGI Ref ID J:49839)
- growth/size phenotype
- decreased body size
- distended abdomen
- due to tumors (MGI Ref ID J:49839)
- reproductive system phenotype
- abnormal fertility/fecundity
- mice are fertile, but have reduced efficacy in producing litters (MGI Ref ID J:49839)
- behavior/neurological phenotype
- abnormal posture
- abnormal, rounded posture, but no associated skeletal defects (MGI Ref ID J:49839)
- lethargy
- as mutants age beyond 18 weeks, they exhibit signs of distress that include lethargy (MGI Ref ID J:49839)
- digestive/alimentary phenotype
- intestinal obstruction
- due to tumors (MGI Ref ID J:49839)
- rectal prolapse
- due to tumors; more pronounced on the 129/Sv background than on the mixed 129/Sv and C57BL/6 background, with 75% of mutants showing prolapse by 24 weeks of age (MGI Ref ID J:49839)
- integument phenotype
- ruffled hair
- as mutants age beyond 18 weeks, they exhibit signs of distress that include fur-ruffling (MGI Ref ID J:49839)
Smad3tm1Par/Smad3tm1Par
129-Smad3tm1Par/J
- tumorigenesis
- intestinal adenocarcinoma
- mutants maintained free of the gram-negative enterohepatic bacteria Helicobacter for up to 9 months do not develop colon cancer as do mutants housed under normal conditions (MGI Ref ID J:106572)
- infection of mutants with Helicobacter triggers colon cancer in 50-66% of mutants; mucinous adenocarcinomas develop 5 to 30 weeks after infection (MGI Ref ID J:106572)
- immune system phenotype
- abnormal circulating interleukin-6 level
- at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (25 min in duration), homozygotes fail to exhibit a significant increase in plasma IL-6 levels, unlike similarly-treated wild-type controls (MGI Ref ID J:175290)
- abnormal cytokine secretion
- at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury, homozygotes exhibit a significant reduction in the renal expression of IL-6 and endothelin-1 mRNA, unlike similarly-treated wild-type controls (MGI Ref ID J:175290)
- however, expression of other cytokines known to contribute to ischemic acute kidney injury is not significantly altered (MGI Ref ID J:175290)
- decreased interleukin-6 secretion
- at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury, homozygotes exhibit a drastic reduction in renal expression of IL-6, unlike similarly-treated wild-type controls (MGI Ref ID J:175290)
- increased inflammatory response
- colonic tissue of uninfected mutants is in a proinflammatory state as indicated by increased mRNA levels of IL-6, TNF-alpha, IFN-gamma, and IL-4, which is exacerbated by Helicobacter infection (MGI Ref ID J:106572)
- renal/urinary system phenotype
- decreased susceptibility to kidney reperfusion injury
- at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (either 22.5 or 25 min in duration), homozygotes exhibit better preservation of renal function as measured by serum BUN and creatinine levels (MGI Ref ID J:175290)
- renal histological injury is significantly reduced as shown by decreased acute tubular necrosis, intratubular sloughing and cast formation (MGI Ref ID J:175290)
- homeostasis/metabolism phenotype
- abnormal circulating interleukin-6 level
- at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (25 min in duration), homozygotes fail to exhibit a significant increase in plasma IL-6 levels, unlike similarly-treated wild-type controls (MGI Ref ID J:175290)
- decreased blood urea nitrogen level
- at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (either 22.5 or 25 min in duration), homozygotes exhibit significantly reduced serum BUN levels relative to wild-type controls (MGI Ref ID J:175290)
- decreased circulating creatinine level
- at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (either 22.5 or 25 min in duration), homozygotes exhibit significantly reduced serum creatinine levels relative to wild-type controls (MGI Ref ID J:175290)
- decreased susceptibility to kidney reperfusion injury
- at 24 hrs after bilateral renal ischemia reperfusion (I/R) injury (either 22.5 or 25 min in duration), homozygotes exhibit better preservation of renal function as measured by serum BUN and creatinine levels (MGI Ref ID J:175290)
- renal histological injury is significantly reduced as shown by decreased acute tubular necrosis, intratubular sloughing and cast formation (MGI Ref ID J:175290)
This mouse can be used to support research in many areas including:
Smad3tm1Par relatedCancer Research
Increased Tumor Incidence
Adenomas
Adenomas: intestinal adenomas
Other Tissues/Organs
Other Tissues/Organs: GI tract (stomach, intestine, colon)
Other
tumor metastasis
Internal/Organ Research
Gastrointestinal Defects
Reproductive Biology Research
Fertility Defects
Research Tools
lacZ Expression
Cancer Research
tumor immunology
Cancer Research
Increased Tumor Incidence
Other Tissues/Organs
Other Tissues/Organs: GI tract (stomach, intestine, colon)
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Smad3tm1Par | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Luis F Parada | ||
| Allele Type | Targeted (Reporter) | ||
| Common Name(s) | Madh3-; Smad3-; Smad3tm1par-; | ||
| Mutation Made By | Dr. Luis Parada, UT Southwestern Medical Center | ||
| Strain of Origin | (129X1/SvJ x 129S1/Sv)F1-Kitl<+> | ||
| ES Cell Line Name | R1 | ||
| ES Cell Line Strain | (129X1/SvJ x 129S1/Sv)F1-Kitl<+> | ||
| Site of Expression | lacZ expression is detected in many developing embryonic tissues with high levels detected in mesenchymal derivatives. In adult mice expression is detected in the colon, with highest levels in the muscularis propria and submucosa, lower levels are expressed in the epithelium. | ||
| Expressed Gene | lacZ, beta-galactosidase, E. coli | ||
| Molecular Note | An IRES-LacZ-neo cassette was inserted into exon 2 of the gene, truncating the carboxyl-terminal active domain of the protein. In addition, this cassette was inserted in a region where point mutations create loss-of-function proteins. Finally, alternative splicing around the disrupted exon would shift the open reading frame. [MGI Ref ID J:49839] | ||
| Gene Symbol and Name | Smad3, SMAD family member 3 | ||
| Chromosome | 9 | ||
| Gene Common Name(s) | AU022421; HSPC193; HsT17436; JV15-2; LDS1C; LDS3; MADH3; Madh3; Smad 3; expressed sequence AU022421; mad3; | ||
Genotyping
Genotyping Information
Genotyping Protocols
Smad3tm1Par, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Zhu Y; Richardson JA; Parada LF; Graff JM. 1998. Smad3 mutant mice develop metastatic colorectal cancer. Cell 94(6):703-14. [PubMed: 9753318] [MGI Ref ID J:49839]
Additional References
Smad3tm1Par relatedCheon SS; Wei Q; Gurung A; Youn A; Bright T; Poon R; Whetstone H; Guha A; Alman BA. 2006. Beta-catenin regulates wound size and mediates the effect of TGF-beta in cutaneous healing. FASEB J 20(6):692-701. [PubMed: 16581977] [MGI Ref ID J:129713]
Deane NG; Manning HC; Foutch AC; Washington MK; Aronow BA; Bornhop DJ; Coffey RJ. 2007. Targeted imaging of colonic tumors in smad3-/- mice discriminates cancer and inflammation. Mol Cancer Res 5(4):341-9. [PubMed: 17426249] [MGI Ref ID J:120907]
Domino SE; Karnak DM; Hurd EA. 2007. Cell surface fucosylation does not affect development of colon tumors in mice with germline Smad3 mutation. Tumour Biol 28(2):77-83. [PubMed: 17264540] [MGI Ref ID J:121796]
Giroux M; Delisle JS; Gauthier SD; Heinonen KM; Hinsinger J; Houde B; Gaboury L; Brochu S; Wu J; Hebert MJ; Perreault C. 2011. SMAD3 prevents graft-versus-host disease by restraining Th1 differentiation and granulocyte-mediated tissue damage. Blood 117(5):1734-44. [PubMed: 21119112] [MGI Ref ID J:169575]
Gu AD; Wang Y; Lin L; Zhang SS; Wan YY. 2012. Requirements of transcription factor Smad-dependent and -independent TGF-beta signaling to control discrete T-cell functions. Proc Natl Acad Sci U S A :. [PubMed: 22219364] [MGI Ref ID J:179925]
Itman C; Wong C; Hunyadi B; Ernst M; Jans DA; Loveland KL. 2011. Smad3 dosage determines androgen responsiveness and sets the pace of postnatal testis development. Endocrinology 152(5):2076-89. [PubMed: 21385936] [MGI Ref ID J:173836]
Jana S; Jailwala P; Haribhai D; Waukau J; Glisic S; Grossman W; Mishra M; Wen R; Wang D; Williams CB; Ghosh S. 2009. The role of NF-kappaB and Smad3 in TGF-beta-mediated Foxp3 expression. Eur J Immunol 39(9):2571-83. [PubMed: 19701891] [MGI Ref ID J:152150]
Jenkins BJ; Grail D; Nheu T; Najdovska M; Wang B; Waring P; Inglese M; McLoughlin RM; Jones SA; Topley N; Baumann H; Judd LM; Giraud AS; Boussioutas A; Zhu HJ; Ernst M. 2005. Hyperactivation of Stat3 in gp130 mutant mice promotes gastric hyperproliferation and desensitizes TGF-beta signaling. Nat Med 11(8):845-52. [PubMed: 16041381] [MGI Ref ID J:100160]
Le AV; Cho JY; Miller M; McElwain S; Golgotiu K; Broide DH. 2007. Inhibition of allergen-induced airway remodeling in Smad 3-deficient mice. J Immunol 178(11):7310-6. [PubMed: 17513781] [MGI Ref ID J:147829]
Li Q; Graff JM; O'connor AE; Loveland KL; Matzuk MM. 2007. SMAD3 Regulates Gonadal Tumorigenesis. Mol Endocrinol 21(10):2472-86. [PubMed: 17595316] [MGI Ref ID J:125355]
Li Q; Pangas SA; Jorgez CJ; Graff JM; Weinstein M; Matzuk MM. 2008. Redundant roles of SMAD2 and SMAD3 in ovarian granulosa cells in vivo. Mol Cell Biol 28(23):7001-11. [PubMed: 18809571] [MGI Ref ID J:142827]
Looyenga BD; Hammer GD. 2007. Genetic removal of smad3 from inhibin-null mice attenuates tumor progression by uncoupling extracellular mitogenic signals from the cell cycle machinery. Mol Endocrinol 21(10):2440-57. [PubMed: 17652186] [MGI Ref ID J:125349]
Maggio-Price L; Treuting P; Bielefeldt-Ohmann H; Seamons A; Drivdahl R; Zeng W; Lai L; Huycke M; Phelps S; Brabb T; Iritani BM. 2009. Bacterial infection of Smad3/Rag2 double-null mice with transforming growth factor-beta dysregulation as a model for studying inflammation-associated colon cancer. Am J Pathol 174(1):317-29. [PubMed: 19119184] [MGI Ref ID J:144197]
Maggio-Price L; Treuting P; Zeng W; Tsang M; Bielefeldt-Ohmann H; Iritani BM. 2006. Helicobacter infection is required for inflammation and colon cancer in SMAD3-deficient mice. Cancer Res 66(2):828-38. [PubMed: 16424015] [MGI Ref ID J:106572]
Nam KT; Lee HJ; Smith JJ; Lapierre LA; Kamath VP; Chen X; Aronow BJ; Yeatman TJ; Bhartur SG; Calhoun BC; Condie B; Manley NR; Beauchamp RD; Coffey RJ; Goldenring JR. 2010. Loss of Rab25 promotes the development of intestinal neoplasia in mice and is associated with human colorectal adenocarcinomas. J Clin Invest 120(3):840-9. [PubMed: 20197623] [MGI Ref ID J:158733]
Nam KT; O'Neal R; Lee YS; Lee YC; Coffey RJ; Goldenring JR. 2012. Gastric tumor development in Smad3-deficient mice initiates from forestomach/glandular transition zone along the lesser curvature. Lab Invest 92(6):883-95. [PubMed: 22411066] [MGI Ref ID J:184722]
Nath KA; Croatt AJ; Warner GM; Grande JP. 2011. Genetic deficiency of Smad3 protects against murine ischemic acute kidney injury. Am J Physiol Renal Physiol 301(2):F436-42. [PubMed: 21525133] [MGI Ref ID J:175290]
Philipp-Staheli J; Kim KH; Payne SR; Gurley KE; Liggitt D; Longton G; Kemp CJ. 2002. Pathway-specific tumor suppression. Reduction of p27 accelerates gastrointestinal tumorigenesis in Apc mutant mice, but not in Smad3 mutant mice. Cancer Cell 1(4):355-68. [PubMed: 12086850] [MGI Ref ID J:77135]
Romero MI; Lin L; Lush ME; Lei L; Parada LF; Zhu Y. 2007. Deletion of Nf1 in neurons induces increased axon collateral branching after dorsal root injury. J Neurosci 27(8):2124-34. [PubMed: 17314307] [MGI Ref ID J:118374]
Sodir NM; Chen X; Park R; Nickel AE; Conti PS; Moats R; Bading JR; Shibata D; Laird PW. 2006. Smad3 Deficiency Promotes Tumorigenesis in the Distal Colon of ApcMin/+ Mice. Cancer Res 66(17):8430-8. [PubMed: 16951153] [MGI Ref ID J:112366]
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]
Warner GM; Cheng J; Knudsen BE; Gray CE; Deibel A; Juskewitch JE; Lerman LO; Textor SC; Nath KA; Grande JP. 2012. Genetic deficiency of Smad3 protects the kidneys from atrophy and interstitial fibrosis in 2K1C hypertension. Am J Physiol Renal Physiol 302(11):F1455-64. [PubMed: 22378822] [MGI Ref ID J:185471]
Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
|
Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $1980.00 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.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Supply Notes
- 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 11 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
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2574.00 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.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Supply Notes
- 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 11 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).
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|
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Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
General Supply Notes
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 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.
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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
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JAX® Mice, Products & Services Conditions of Use
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