Strain Name:

NOD.129P2(B6)-Ctsltm1Cptr/RclJ

Stock Number:

008352

Order this mouse

Availability:

Cryopreserved - Ready for recovery

Use Restrictions Apply, see Terms of Use
Common Names: NOD.Catl;    
This congenic NOD strain contains a neomycin cassette disruption in exon 3 of cathepsin L (Ctsltm1Cptr). NOD Ctsl deficient mice exhibit defective CD4+T cell development and express Foxp3 on CD4+ T cells at a 2 fold higher frequency than controls. Homozygous mice are insulitis and diabetes resistant. This model provides a tool for detailed studies to identify the molecular pathways of major lysosomal cysteine proteases, specifically cathepsin L, in immune modulation.

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 NOD.129P2-Cstltm1Cptr/RclJ    (Changed: 07-OCT-08 )
Type Congenic; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain NOD
Donor Strain 129P2/OlaHsd (E14.1 ES cells)
GenerationN11F2+N?pN1
Generation Definitions
 
Donating InvestigatorDr. Renee C LeBoeuf,   Universtiy of Washington

Description
Mice homozygous for this Ctsl targeted mutation are viable, normal in size, and do not display any behavioral abnormalities. Western blot analysis failed to detect any signal in kidneys of homozygous mutant mice. No Ctsl enzymatic activity was detected in the kidney using a synthetic substrate. Donating investigator reports that homozygous females are infertile; while homozygous males breed well. As reported in the B6-Ctsltm1Cptr by Roth et al. 2000, the vibrissae of NOD congenic mutant mice have not penetrated the epidermis at birth and the first emergence of fur is delayed by approximately two days. Beginning around three weeks of age NOD mutant mice begin to lose their fur beginning at the head and progressing toward the tail region. Mature mutant mice are always partially devoid of fur. Unlike the observations of Roth et al. there appears to be no distortion of the the expected rates of homozygous NOD congenic mice weaned. Similar to Maehr et al. 2005, no throiditis, sialadenitis, diabetes or insulitis was detected in NOD.Ctsl deficient females aged to 10 months (Hsing et al, 2009). Ctsl deficient mice exhibit defective CD4+T cell development leading to a reduced CD4:CD8 ratio. CD4+T cells if naive NOD.Ctsl deficient mice exhibit Foxp3 expression at 2 fold higher frequency than wildtype controls (Hsing et al, 2009).

This model provides a tool for detailed studies to identify the molecular pathways of major lysosomal cysteine proteases, specifically cathepsin L in immune modulation.

Development
The Cathepsin L (Ctsl) gene was disrupted via homologous recombination in 129P2/OlaHsd-derived, E14.1 ES cells. A neomycin cassette was inserted into a NcoI site in exon 3 using a SalI linker containing stop codons in all reading frames of the Ctsl gene. The ES cell clone was injected into C57BL/6 blastocysts. The resulting chimeric founder's offspring were bred to C57BL/6J prior to 10 generations of crossing to NOD and intercrossing. Marker assisted analysis indicates 19 known Idd loci are of NOD origin. In 2008, the T1DR received this strain at generation N11F2.

Control Information

  Control
   001976 NOD/ShiLtJ
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Ctsl
000618   B6 x FSB/GnEi a/a Ctslfs/J
View Strains carrying other alleles of Ctsl     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Ctsltm1Cptr/Ctsl+

        NOD.129P2-Ctsltm1Cptr
  • immune system phenotype
  • decreased susceptibility to autoimmune diabetes
    • 55% of female mice exhibit blood glucose levels of greater than 250 mg/dl between 4-6 months of age as compared to 69% of NOD controls   (MGI Ref ID J:153355)
    • adoptive transfer of GITRhi-depleted Treg cells into NOD-Prkdcscid host results in a diabetes incidence of 41.7%   (MGI Ref ID J:153355)
  • insulitis
    • insulitis scores for diabetic animals are similar to diabetic NOD controls   (MGI Ref ID J:153355)
  • homeostasis/metabolism phenotype
  • hyperglycemia
    • 55% of female mice exhibit blood glucose levels of greater than 250 mg/dl between 4-6 months of age as compared to 69% of NOD controls   (MGI Ref ID J:153355)
  • endocrine/exocrine gland phenotype
  • insulitis
    • insulitis scores for diabetic animals are similar to diabetic NOD controls   (MGI Ref ID J:153355)

Ctsltm1Cptr/Ctsltm1Cptr

        NOD.129P2-Ctsltm1Cptr
  • immune system phenotype
  • decreased CD4-positive, alpha beta T cell number
    • number of CD4+ T cells is 3-fold reduced in thymus and lymph nodes as compared to NOD control   (MGI Ref ID J:153355)
  • decreased susceptibility to autoimmune diabetes
    • mice exhibit a complete resistance to diabetes   (MGI Ref ID J:153355)
    • adoptive transfer of GITRhi-depleted Treg cells into NOD-Prkdcscid host results in a diabetes incidence of 45.5%   (MGI Ref ID J:153355)
  • increased regulatory T cell number
    • homozygotes exhibit a 2-fold increase in Foxp3-expressing T cells in comparison to heterozygotes   (MGI Ref ID J:153355)
  • salivary gland inflammation
    • sialadenitis is observed in both diabetic and nondiabetic mice at 6 months of age, however, number of lesions observed is less than number found in NOD mice (6.5 vs. 12-20)   (MGI Ref ID J:153355)
  • endocrine/exocrine gland phenotype
  • salivary gland inflammation
    • sialadenitis is observed in both diabetic and nondiabetic mice at 6 months of age, however, number of lesions observed is less than number found in NOD mice (6.5 vs. 12-20)   (MGI Ref ID J:153355)
  • digestive/alimentary phenotype
  • salivary gland inflammation
    • sialadenitis is observed in both diabetic and nondiabetic mice at 6 months of age, however, number of lesions observed is less than number found in NOD mice (6.5 vs. 12-20)   (MGI Ref ID J:153355)
  • hematopoietic system phenotype
  • decreased CD4-positive, alpha beta T cell number
    • number of CD4+ T cells is 3-fold reduced in thymus and lymph nodes as compared to NOD control   (MGI Ref ID J:153355)
  • increased regulatory T cell number
    • homozygotes exhibit a 2-fold increase in Foxp3-expressing T cells in comparison to heterozygotes   (MGI Ref ID J:153355)
View Research Applications

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

Diabetes and Obesity Research
Type 1 Diabetes (IDDM)
      resistant

Immunology, Inflammation and Autoimmunity Research
Autoimmunity
      Type 1 Diabetes

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ctsltm1Cptr
Allele Name targeted mutation 1, Christoph Peters
Allele Type Targeted (Null/Knockout)
Common Name(s) CL-; Cat L-; L-; catL-; ctsl-;
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14.1
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Ctsl, cathepsin L
Chromosome 13
Gene Common Name(s) 1190035F06Rik; CATHL; CATL2; CTSL2; CTSU; Cat L; CatL; Ctsl1; MEP; RIKEN cDNA 1190035F06 gene; fs; furless; major excreted protein; nackt; nkt;
General Note In combination with Ctsbtm1Jde, double homozygous mutant have some similarities but distinct phenotypic characteristics compared to the human syndrome: Neuronal Ceroid Lipofuscinoses (NLCs)
Molecular Note Insertion of a neomycin resistance cassette into exon 3. Northern and Western analysis failed to detect any signal in homozygous mutant mice. No Ctsl enzymatic activity was detected using a synthetic substrate. [MGI Ref ID J:108004] [MGI Ref ID J:70118]

Genotyping

Genotyping Information

Genotyping Protocols

Cstltm1Cptr, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Ctsltm1Cptr related

Abboud-Jarrous G; Atzmon R; Peretz T; Palermo C; Gadea BB; Joyce JA; Vlodavsky I. 2008. Cathepsin L is responsible for processing and activation of proheparanase through multiple cleavages of a linker segment. J Biol Chem 283(26):18167-76. [PubMed: 18450756]  [MGI Ref ID J:138130]

Benavides F; Perez C; Blando J; Guenet JL; Conti CJ. 2006. The radiation-induced nackt (nkt) allele is a loss-of-function mutation of the mouse cathepsin L gene. J Immunol 176(2):702-3. [PubMed: 16393949]  [MGI Ref ID J:108004]

Dennemarker J; Lohmuller T; Mayerle J; Tacke M; Lerch MM; Coussens LM; Peters C; Reinheckel T. 2010. Deficiency for the cysteine protease cathepsin L promotes tumor progression in mouse epidermis. Oncogene 29(11):1611-21. [PubMed: 20023699]  [MGI Ref ID J:160397]

Dennemarker J; Lohmuller T; Muller S; Aguilar SV; Tobin DJ; Peters C; Reinheckel T. 2010. Impaired turnover of autophagolysosomes in cathepsin L deficiency. Biol Chem 391(8):913-22. [PubMed: 20536383]  [MGI Ref ID J:186898]

Duewell P; Kono H; Rayner KJ; Sirois CM; Vladimer G; Bauernfeind FG; Abela GS; Franchi L; Nunez G; Schnurr M; Espevik T; Lien E; Fitzgerald KA; Rock KL; Moore KJ; Wright SD; Hornung V; Latz E. 2010. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature 464(7293):1357-61. [PubMed: 20428172]  [MGI Ref ID J:159453]

Everts V; Korper W; Hoeben KA; Jansen ID; Bromme D; Cleutjens KB; Heeneman S; Peters C; Reinheckel T; Saftig P; Beertsen W. 2006. Osteoclastic bone degradation and the role of different cysteine proteinases and matrix metalloproteinases: differences between calvaria and long bone. J Bone Miner Res 21(9):1399-408. [PubMed: 16939398]  [MGI Ref ID J:128089]

Felbor U; Kessler B; Mothes W; Goebel HH; Ploegh HL; Bronson RT; Olsen BR. 2002. Neuronal loss and brain atrophy in mice lacking cathepsins B and L. Proc Natl Acad Sci U S A 99(12):7883-8. [PubMed: 12048238]  [MGI Ref ID J:77103]

Friedrichs B; Tepel C; Reinheckel T; Deussing J; von Figura K; Herzog V; Peters C; Saftig P; Brix K. 2003. Thyroid functions of mouse cathepsins B, K, and L. J Clin Invest 111(11):1733-45. [PubMed: 12782676]  [MGI Ref ID J:83877]

Funkelstein L; Toneff T; Hwang SR; Reinheckel T; Peters C; Hook V. 2008. Cathepsin L participates in the production of neuropeptide Y in secretory vesicles, demonstrated by protease gene knockout and expression. J Neurochem 106(1):384-91. [PubMed: 18410501]  [MGI Ref ID J:137265]

Funkelstein L; Toneff T; Mosier C; Hwang SR; Beuschlein F; Lichtenauer UD; Reinheckel T; Peters C; Hook V. 2008. Major role of cathepsin L for producing the peptide hormones ACTH, beta-endorphin, and alpha-MSH, illustrated by protease gene knockout and expression. J Biol Chem 283(51):35652-9. [PubMed: 18849346]  [MGI Ref ID J:144593]

Gocheva V; Wang HW; Gadea BB; Shree T; Hunter KE; Garfall AL; Berman T; Joyce JA. 2010. IL-4 induces cathepsin protease activity in tumor-associated macrophages to promote cancer growth and invasion. Genes Dev 24(3):241-55. [PubMed: 20080943]  [MGI Ref ID J:156936]

Gocheva V; Zeng W; Ke D; Klimstra D; Reinheckel T; Peters C; Hanahan D; Joyce JA. 2006. Distinct roles for cysteine cathepsin genes in multistage tumorigenesis. Genes Dev 20(5):543-56. [PubMed: 16481467]  [MGI Ref ID J:105935]

Hagemann S; Gunther T; Dennemarker J; Lohmuller T; Bromme D; Schule R; Peters C; Reinheckel T. 2004. The human cysteine protease cathepsin V can compensate for murine cathepsin L in mouse epidermis and hair follicles. Eur J Cell Biol 83(11-12):775-80. [PubMed: 15679121]  [MGI Ref ID J:102123]

Henningsson F; Yamamoto K; Saftig P; Reinheckel T; Peters C; Knight SD; Pejler G. 2005. A role for cathepsin E in the processing of mast-cell carboxypeptidase A. J Cell Sci 118(Pt 9):2035-42. [PubMed: 15860733]  [MGI Ref ID J:98827]

Honey K; Benlagha K; Beers C; Forbush K; Teyton L; Kleijmeer MJ; Rudensky AY; Bendelac A. 2002. Thymocyte expression of cathepsin L is essential for NKT cell development. Nat Immunol 3(11):1069-74. [PubMed: 12368909]  [MGI Ref ID J:109255]

Honey K; Nakagawa T; Peters C; Rudensky A. 2002. Cathepsin L regulates CD4+ T cell selection independently of its effect on invariant chain: a role in the generation of positively selecting peptide ligands. J Exp Med 195(10):1349-58. [PubMed: 12021314]  [MGI Ref ID J:112070]

Hsing LC; Kirk EA; McMillen TS; Hsiao SH; Caldwell M; Houston B; Rudensky AY; Leboeuf RC. 2009. Roles for cathepsins S, L, and B in insulitis and diabetes in the NOD mouse. J Autoimmun :. [PubMed: 19664906]  [MGI Ref ID J:153355]

Kalantari P; DeOliveira RB; Chan J; Corbett Y; Rathinam V; Stutz A; Latz E; Gazzinelli RT; Golenbock DT; Fitzgerald KA. 2014. Dual engagement of the NLRP3 and AIM2 inflammasomes by plasmodium-derived hemozoin and DNA during malaria. Cell Rep 6(1):196-210. [PubMed: 24388751]  [MGI Ref ID J:206874]

Kitamoto S; Sukhova GK; Sun J; Yang M; Libby P; Love V; Duramad P; Sun C; Zhang Y; Yang X; Peters C; Shi GP. 2007. Cathepsin L deficiency reduces diet-induced atherosclerosis in low-density lipoprotein receptor-knockout mice. Circulation 115(15):2065-75. [PubMed: 17404153]  [MGI Ref ID J:135371]

Koike M; Shibata M; Ohsawa Y; Nakanishi H; Koga T; Kametaka S; Waguri S; Momoi T; Kominami E; Peters C; Figura K; Saftig P; Uchiyama Y. 2003. Involvement of two different cell death pathways in retinal atrophy of cathepsin D-deficient mice. Mol Cell Neurosci 22(2):146-61. [PubMed: 12676526]  [MGI Ref ID J:82765]

Koike M; Shibata M; Waguri S; Yoshimura K; Tanida I; Kominami E; Gotow T; Peters C; von Figura K; Mizushima N; Saftig P; Uchiyama Y. 2005. Participation of autophagy in storage of lysosomes in neurons from mouse models of neuronal ceroid-lipofuscinoses (batten disease). Am J Pathol 167(6):1713-28. [PubMed: 16314482]  [MGI Ref ID J:103645]

Konjar S; Sutton VR; Hoves S; Repnik U; Yagita H; Reinheckel T; Peters C; Turk V; Turk B; Trapani JA; Kopitar-Jerala N. 2010. Human and mouse perforin are processed in part through cleavage by the lysosomal cysteine proteinase cathepsin L. Immunology 131(2):257-67. [PubMed: 20497254]  [MGI Ref ID J:166401]

Lennon-Dumenil AM; Roberts RA; Valentijn K; Driessen C; Overkleeft HS; Erickson A; Peters PJ; Bikoff E; Ploegh HL; Wolf Bryant P. 2001. The p41 isoform of invariant chain is a chaperone for cathepsin L. EMBO J 20(15):4055-64. [PubMed: 11483509]  [MGI Ref ID J:115604]

Maehr R; Hang HC; Mintern JD; Kim YM; Cuvillier A; Nishimura M; Yamada K; Shirahama-Noda K; Hara-Nishimura I; Ploegh HL. 2005. Asparagine endopeptidase is not essential for class II MHC antigen presentation but is required for processing of cathepsin L in mice. J Immunol 174(11):7066-74. [PubMed: 15905550]  [MGI Ref ID J:99005]

Maehr R; Mintern JD; Herman AE; Lennon-Dumenil AM; Mathis D; Benoist C; Ploegh HL. 2005. Cathepsin L is essential for onset of autoimmune diabetes in NOD mice. J Clin Invest 115(10):2934-43. [PubMed: 16184198]  [MGI Ref ID J:101527]

Miller G; Matthews SP; Reinheckel T; Fleming S; Watts C. 2011. Asparagine endopeptidase is required for normal kidney physiology and homeostasis. FASEB J 25(5):1606-17. [PubMed: 21292981]  [MGI Ref ID J:172774]

Minokadeh A; Funkelstein L; Toneff T; Hwang SR; Beinfeld M; Reinheckel T; Peters C; Zadina J; Hook V. 2010. Cathepsin L participates in dynorphin production in brain cortex, illustrated by protease gene knockout and expression. Mol Cell Neurosci 43(1):98-107. [PubMed: 19837164]  [MGI Ref ID J:158324]

Nakagawa T; Roth W; Wong P; Nelson A; Farr A; Deussing J; Villadangos JA; Ploegh H; Peters C; Rudensky AY. 1998. Cathepsin L: critical role in Ii degradation and CD4 T cell selection in the thymus. Science 280(5362):450-3. [PubMed: 9545226]  [MGI Ref ID J:82888]

Nepal RM; Vesosky B; Turner J; Bryant P. 2008. DM, but not cathepsin L, is required to control an aerosol infection with Mycobacterium tuberculosis. J Leukoc Biol 84(4):1011-8. [PubMed: 18591414]  [MGI Ref ID J:140231]

Nishimura F; Naruishi H; Naruishi K; Yamada T; Sasaki J; Peters C; Uchiyama Y; Murayama Y. 2002. Cathepsin-L, a key molecule in the pathogenesis of drug-induced and I-cell disease-mediated gingival overgrowth: a study with cathepsin-L-deficient mice. Am J Pathol 161(6):2047-52. [PubMed: 12466121]  [MGI Ref ID J:80536]

Ohkouchi S; Shibata M; Sasaki M; Koike M; Safig P; Peters C; Nagata S; Uchiyama Y. 2013. Biogenesis and proteolytic processing of lysosomal DNase II. PLoS One 8(3):e59148. [PubMed: 23516607]  [MGI Ref ID J:199384]

Petermann I; Mayer C; Stypmann J; Biniossek ML; Tobin DJ; Engelen MA; Dandekar T; Grune T; Schild L; Peters C; Reinheckel T. 2006. Lysosomal, cytoskeletal, and metabolic alterations in cardiomyopathy of cathepsin L knockout mice. FASEB J 20(8):1266-8. [PubMed: 16636100]  [MGI Ref ID J:111345]

Reinheckel T; Hagemann S; Dollwet-Mack S; Martinez E; Lohmuller T; Zlatkovic G; Tobin DJ; Maas-Szabowski N; Peters C. 2005. The lysosomal cysteine protease cathepsin L regulates keratinocyte proliferation by control of growth factor recycling. J Cell Sci 118(Pt 15):3387-95. [PubMed: 16079282]  [MGI Ref ID J:100201]

Rocken C; Fandrich M; Stix B; Tannert A; Hortschansky P; Reinheckel T; Saftig P; Kahne T; Menard R; Ancsin JB; Buhling F. 2006. Cathepsin protease activity modulates amyloid load in extracerebral amyloidosis. J Pathol 210(4):478-87. [PubMed: 17068745]  [MGI Ref ID J:116135]

Roth W; Deussing J; Botchkarev VA; Pauly-Evers M; Saftig P; Hafner A; Schmidt P; Schmahl W; Scherer J; Anton-Lamprecht I; Von Figura K; Paus R; Peters C. 2000. Cathepsin L deficiency as molecular defect of furless: hyperproliferation of keratinocytes and pertubation of hair follicle cycling. FASEB J 14(13):2075-86. [PubMed: 11023992]  [MGI Ref ID J:70118]

Roy KC; Maricic I; Khurana A; Smith TR; Halder RC; Kumar V. 2008. Involvement of Secretory and Endosomal Compartments in Presentation of an Exogenous Self-Glycolipid to Type II NKT Cells. J Immunol 180(5):2942-50. [PubMed: 18292516]  [MGI Ref ID J:131541]

Sever S; Altintas MM; Nankoe SR; Moller CC; Ko D; Wei C; Henderson J; del Re EC; Hsing L; Erickson A; Cohen CD; Kretzler M; Kerjaschki D; Rudensky A; Nikolic B; Reiser J. 2007. Proteolytic processing of dynamin by cytoplasmic cathepsin L is a mechanism for proteinuric kidney disease. J Clin Invest 117(8):2095-104. [PubMed: 17671649]  [MGI Ref ID J:123953]

Shen L; Sigal LJ; Boes M; Rock KL. 2004. Important role of cathepsin S in generating peptides for TAP-independent MHC class I crosspresentation in vivo. Immunity 21(2):155-65. [PubMed: 15308097]  [MGI Ref ID J:93590]

Shimada N; Ohno-Matsui K; Iseki S; Koike M; Uchiyama Y; Wang J; Yoshida T; Sato T; Peters C; Mochizuki M; Morita I. 2010. Cathepsin L in bone marrow-derived cells is required for retinal and choroidal neovascularization. Am J Pathol 176(5):2571-80. [PubMed: 20304958]  [MGI Ref ID J:160772]

Spira D; Stypmann J; Tobin DJ; Petermann I; Mayer C; Hagemann S; Vasiljeva O; Gunther T; Schule R; Peters C; Reinheckel T. 2007. Cell Type-specific Functions of the Lysosomal Protease Cathepsin L in the Heart. J Biol Chem 282(51):37045-37052. [PubMed: 17942402]  [MGI Ref ID J:129020]

Steenhuis P; Froemming J; Reinheckel T; Storch S. 2012. Proteolytic cleavage of the disease-related lysosomal membrane glycoprotein CLN7. Biochim Biophys Acta 1822(10):1617-28. [PubMed: 22668694]  [MGI Ref ID J:188065]

Stypmann J; Glaser K; Roth W; Tobin DJ; Petermann I; Matthias R; Monnig G; Haverkamp W; Breithardt G; Schmahl W; Peters C; Reinheckel T. 2002. Dilated cardiomyopathy in mice deficient for the lysosomal cysteine peptidase cathepsin L. Proc Natl Acad Sci U S A 99(9):6234-9. [PubMed: 11972068]  [MGI Ref ID J:76333]

Sugita S; Horie S; Nakamura O; Maruyama K; Takase H; Usui Y; Takeuchi M; Ishidoh K; Koike M; Uchiyama Y; Peters C; Yamamoto Y; Mochizuki M. 2009. Acquisition of T regulatory function in cathepsin L-inhibited T cells by eye-derived CTLA-2alpha during inflammatory conditions. J Immunol 183(8):5013-22. [PubMed: 19801522]  [MGI Ref ID J:153812]

Sun J; Sukhova GK; Zhang J; Chen H; Sjoberg S; Libby P; Xiang M; Wang J; Peters C; Reinheckel T; Shi GP. 2011. Cathepsin L activity is essential to elastase perfusion-induced abdominal aortic aneurysms in mice. Arterioscler Thromb Vasc Biol 31(11):2500-8. [PubMed: 21868704]  [MGI Ref ID J:191463]

Tobin DJ; Foitzik K; Reinheckel T; Mecklenburg L; Botchkarev VA; Peters C; Paus R. 2002. The lysosomal protease cathepsin L is an important regulator of keratinocyte and melanocyte differentiation during hair follicle morphogenesis and cycling. Am J Pathol 160(5):1807-21. [PubMed: 12000732]  [MGI Ref ID J:109246]

Urbich C; Heeschen C; Aicher A; Sasaki K; Bruhl T; Farhadi MR; Vajkoczy P; Hofmann WK; Peters C; Pennacchio LA; Abolmaali ND; Chavakis E; Reinheckel T; Zeiher AM; Dimmeler S. 2005. Cathepsin L is required for endothelial progenitor cell-induced neovascularization. Nat Med 11(2):206-13. [PubMed: 15665831]  [MGI Ref ID J:99594]

Wilson SR; Peters C; Saftig P; Bromme D. 2009. Cathepsin K activity-dependent regulation of osteoclast actin ring formation and bone resorption. J Biol Chem 284(4):2584-92. [PubMed: 19028686]  [MGI Ref ID J:146945]

Yang M; Zhang Y; Pan J; Sun J; Liu J; Libby P; Sukhova GK; Doria A; Katunuma N; Peroni OD; Guerre-Millo M; Kahn BB; Clement K; Shi GP. 2007. Cathepsin L activity controls adipogenesis and glucose tolerance. Nat Cell Biol 9(8):970-7. [PubMed: 17643114]  [MGI Ref ID J:129484]

Zeeuwen PL; van Vlijmen-Willems IM; Cheng T; Rodijk-Olthuis D; Hitomi K; Hara-Nishimura I; John S; Smyth N; Reinheckel T; Hendriks WJ; Schalkwijk J. 2010. The cystatin M/E-cathepsin L balance is essential for tissue homeostasis in epidermis, hair follicles, and cornea. FASEB J 24(10):3744-55. [PubMed: 20495178]  [MGI Ref ID J:165312]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryRecommended breeding scheme is to mate heterozygous females with homozygous males.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2140.00
Animals Provided

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 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 View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2782.00
Animals Provided

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 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).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

General Supply Notes

Control Information

  Control
   001976 NOD/ShiLtJ
 
  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 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.


(6.8)