Description

Strain Information

Former Names NOD/LtJ    (Changed: 23-FEB-07 ) Type Inbred Strain; Additional information on Inbred Strains. Visit our online Nomenclature tutorial. Mating System Sibling x Sibling         (Female x Male) Species laboratory mouse H2 Haplotype g7 Generation F120 (03-JAN-08)

Appearance
albino
Related Genotype: A/A Tyr^c/Tyr^c

Important Note
This strain is homozygous for Cdh23^ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss that is already severe by three months of age.

Description
Diabetes in NOD/ShiLtJ mice is characterized by insulitis, a leukocytic infiltrate of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. Onset of diabetes is marked by moderate glycosuria and by a non-fasting plasma glucose higher than 250 mg/dl. Diabetic mice are hypoinsulinemic and hyperglucagonemic, indicating a selective destruction of pancreatic islet beta cells. Susceptibility to IDDM in NOD/ShiLtJ mice is polygenic, and environment, including housing conditions, health status, and diet, exerts a strong effect on penetrance. NOD/ShiLtJ females are more widely used than males because the onset of IDDM symptoms occurs earlier and with a higher incidence (90-100% by 30 weeks of age). NOD/ShiLtJ males develop IDDM at a frequency of between 40-60% by 30-40 weeks of age. Male mice are useful for certain applications, including pharmaceutical studies, "accelerated transfer" of IDDM, and some in vitro studies. The major component of diabetes susceptibility in NOD mice is the unique MHC haplotype (H2^g7 = K^d, Aa^d, Ab^g7, E^null, D^b). NOD mice also exhibit multiple aberrant immunophenotypes including defective antigen presenting cell immunoregulatory functions, defects in the regulation of theT lymphocyte repertoire, defective NK cell function, defective cytokine production from macrophages (Fan et al., 2004) and impaired wound healing. They also lack hemolytic complement, C5. NOD/ShiLtJ mice also are severely hearing-impaired. A variety of mutations causing immunodeficiencies, targeted mutations in cytokine genes, as well as transgenes affecting immune functions, have been backcrossed into the NOD/ShiLt inbred strain background.

Development
NOD inbred mice originated early on in the inbreeding of the Cataract Shionogi (CTS) strain. These mice were originally outbred Jcl:ICR mice. At F6, the progenitors of the future NOD/Shi mice were inbred on the basis of an elevated fasting blood glucose level in cataract-free mice. At F13, the NOD progenitors were separated from what is now the NON/Shi strain. High fasting blood glucose levels continued to be the basis for selection of the latter strain, while the NOD progenitors at F13 and later were selected on the basis of a normal fasting blood glucose level. In 1974, at F20, a female in the "normoglycemic" line spontaneously developed overt insulin-dependent diabetes mellitus with insulitis (IDDM). Selective breeding of the progeny of this diabetic female produced the nonobese diabetic (NOD) strain. Originally restricted to distribution in Japan, NOD substrains were distributed during the early 1980s to Australia and the United States. NOD and NON strains were imported from a colony in Kyoto, Japan by Dr. M. Hattori to the Joslin Diabetes Ceneter in Boston in 1984. Breeder pairs from this importation were sent from The Joslin Diabetes Center to Dr. E Leiter at The Jackson Laboratory, and are the source of the production strains NOD/ShiLtJ and NON/ShiLtJ. The current generation of inbreeding is F83.

Related Strains

NOD Strains

001289	NOD/ShiLt
006778	NOD/ShiLt-Tg(GFAP-Cd80)9Mdos/MdosJ
004939	NOD/ShiLtJ-Leprdb-5J/LtJ

View NOD Strains     (3 strains)

Strains carrying   Cdh23^ahl allele

001137	129P1/ReJ
000690	129P3/J
000691	129X1/SvJ
000646	A/J
000647	A/WySnJ
003070	ALR/LtJ
003072	ALS/LtJ
004502	B6;AKR-Lxl2/J
001026	BALB/cByJ
000653	BUB/BnJ
005494	C3.129S1(B6)-Grm1rcw/J
000664	C57BL/6J
004764	C57BL/6J-Cdh23v-8J/J
003129	C57BL/6J-Epha4rb-2J/J
004820	C57BL/6J-Kcne12J/J
004703	C57BL/6J-Kcnq2Nmf134/J
004811	C57BL/6J-nmf110/J
004812	C57BL/6J-nmf111/J
004747	C57BL/6J-nmf118/J
004656	C57BL/6J-nmf88/J
004391	C57BL/6J-Chr 13A/J/NaJ
004385	C57BL/6J-Chr 7A/J/NaJ
000662	C57BLKS/J
000667	C57BR/cdJ
000668	C57L/J
000669	C58/J
000657	CE/J
000670	DBA/1J
001140	DBA/1LacJ
000671	DBA/2J
007048	DBA/2J-Gpnmb+/SjJ
002106	KK/HlJ
000675	LG/J
000676	LP/J
000677	MA/MyJ
002050	NOR/LtJ
000679	P/J
002747	SENCARB/PtJ
002335	SKH2/J
003392	STOCK Crb1rd8/J

View Strains carrying   Cdh23^ahl     (40 strains)

Strains carrying   Hc⁰ allele

000645	A/HeJ
000646	A/J
000647	A/WySnJ
000648	AKR/J
000460	B10.D2-Hc0 H2d H2-T18c/o2SnJ
000461	B10.D2-Hc0 H2d H2-T18c/oSnJ
000657	CE/J
000671	DBA/2J
007048	DBA/2J-Gpnmb+/SjJ
001800	FVB/NJ
001491	FVB/NMob
000674	I/LnJ
001303	NOD.CB17-Prkdcscid/J
000684	NZB/BlNJ
000682	RF/J
000688	ST/bJ
000689	SWR/J

View Strains carrying   Hc⁰     (17 strains)

Strains carrying other alleles of Cdh23

008288	B6(Cg)-Cdh23v-11J/J
002756	B6.CAST-Cdh23Ahl+/Kjn
002432	B6J x B6.C-H2bm1/ByJ-Cdh23v-J/J
002552	C57BL/6J-Cdh23v-2J/J
004764	C57BL/6J-Cdh23v-8J/J
004819	C57BL/6J-Cdh23v-9J/J
005016	CByJ;B6-Cdh23v-10J/J
000275	V/LeJ

View Strains carrying other alleles of Cdh23     (8 strains)

Strains carrying other alleles of Hc

000470	AK.M-H2m H2-T18a/nSnJ
005308	B10.Cg-H2d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ
000463	B10.D2-Hc1 H2d H2-T18c/nSnJ
003147	B10.D2-Hc1 H2d H2-T18c/nSnJ-Tg(DO11.10)10Dlo/J
004306	NOD.CBALs-Hc1/LtJ

View Strains carrying other alleles of Hc     (5 strains)

Additional Web Information

Genetic Quality Control Annual Report
JAX^® NOTES, Spring 1999; 477. Control Strains for NOD/LtJ Mice in Diabetes Research.
JAX^® NOTES, Spring 2003; 489. Malocclusion in the Laboratory Mouse.
JAX^® NOTES, Spring 2003; 489. Role of NK and NKT Cells in Immunity and Disease.
JAX^® NOTES, Spring 2007; 505. Research Using NOD/ShiLtJ Mouse Suggests Novel Therapies for Type 1 Diabetes.
JAX^® NOTES, Summer 1992; 450. Myoepitheliomas in Inbred Laboratory Mice.
JAX^® NOTES, Summer 2003; 490. Hydrocephalus in Laboratory Mice.
JAX^® NOTES, Winter 1993; 452. NOD/LtJ Mice Available.
JAX^® NOTES, Winter 1999; 476. Using NOD/LtJ Males in Diabetes Research.
JAX^® NOTES, Winter 2006; 504. JAX^® Mice: the Gold Standard Just Got Better.

Phenotype

Phenotype Information

View Phenotypic Data

Phenotypic Data

Body Weight Information - JAX^® Mice Strain NOD/ShiLtJ (001976)
(This chart reflects the typical correlation between body weight and age for mice maintained in production colonies at The Jackson Laboratory.)

Mouse Phenome Database
Festing Inbred Strain Characteristics: NOD
JAX^® Physiological Data Summary [pdf]
JAX^® Physiological Data Protocol [pdf]

View Research Applications

Research Applications

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

Developmental Biology Research
Lymphoid Tissue Defects (hematopoietic defects)

Diabetes and Obesity Research
Hyperglycemia
Hypoinsulinemia
Impaired Wound Healing
Islet Transplantation Studies
Type 1 Diabetes (IDDM)

Immunology and Inflammation Research
Autoimmunity (Type 1 Diabetes)

Internal/Organ Research
Wound Healing (delayed/impaired)

Neurobiology Research
Vestibular and Hearing Defects (Age related hearing loss)

Research Tools
Immunology and Inflammation Research (NK Cell Deficiency)

Sensorineural Research
Vestibular and Hearing Defects (Age related hearing loss)

Cdh23^ahl related

Neurobiology Research
Vestibular and Hearing Defects (Age related hearing loss)

Sensorineural Research
Vestibular and Hearing Defects (Age related hearing loss)

Hc⁰ related

Immunology and Inflammation Research
Immunodeficiency (specific complement deficiency)

Research Tools
Immunology and Inflammation Research (specific complement deficiency) (C5 complement)

Genes & Alleles

Gene & Allele Information

Allele Symbol		Cdh23ahl
Allele Name		age related hearing loss 1
Allele Type		QTL
Common Name(s)		Cdh23753A; mdfw;
Strain of Origin		multiple strains
Gene Symbol and Name		Cdh23, cadherin 23 (otocadherin)
Chromosome		10
Gene Common Name(s)		4930542A03Rik; DFNB12; DKFZp434P2350; FLJ00233; FLJ36499; KIAA1774; KIAA1812; MGC102761; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; bob; bobby; bus; bustling; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf181; nmf252; v; waltzer;
Molecular Note		Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has identified an association between ahl and a G to A transition at nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7 and reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD1, RBF/DnJ, PL/J, AKR/J, RF/J, BALB/cBy, A/WySnJ, P/J, SENCARA/PtJ, DBA/1J, ALS/LtJ, C58/J, C57BLKS/J, 129P1/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129X1/SvJ, NOR/LtJ, A/J, C57BL/6, NOD/LyJ, DBA/2J, ALR/LtJ, C57L/J. Strains classified with ahl that DO NOT carry this mutation include: C3H/HeSnJ, I/LnJ,YBR/Ei, MRL/MpJ. [MGI Ref ID J:86905]
Allele Symbol		Hc0
Allele Name		deficient
Allele Type		Spontaneous
Common Name(s)		C5-; C5-d; C5-def; C5-deficient; hco;
Gene Symbol and Name		Hc, hemolytic complement
Chromosome		2
Gene Common Name(s)		C5; C5a; CPAMD4; FLJ17816; FLJ17822; He; MGC142298; RGD1561905;
General Note		This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ Hc was identified as a candidate gene for Abhr2 in a microarray analysis of lung mRNA from A/J, C3H/HeJ, and (A/J x C3H/HeJ)F1 x A/J backcross animals. Hc genotype shows statistically significant correlation to allergen-induced bronchial hyperresponsive phenotype. The A/J allele contains a 2 bp deletion resulting in deficient Hc mRNA and protein production and is associated with susceptibility to allergen-induced bronchial hyperresponsiveness. (J:108211)
Molecular Note		A 2 base "TA" deletion at positions 62 and 63 of an 83 base pair exon near the 5' end of the gene is found in the following mouse strains: A/HeJ, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ. The consequence of this deletion is the creation of a stop codon starting four bases after the deletion. A truncated product of 216 amino acids is predicted as a result although contradictory reports exist that a larger pro-C5 protein may be synthesized. Nevertheless, macrophages from mouse strains carrying this allele do not secrete complement 5. [MGI Ref ID J:23983]

Genotyping

Genotyping Information

This strain will not have a genotyping protocol or one is not currently available.

Helpful Links

Optimizing PCR Protocols

References

References

Selected Reference(s)

Makino S; Kunimoto K; Muraoka Y; Mizushima Y; Katagiri K; Tochino Y. 1980. Breeding of a non-obese, diabetic strain of mice. Jikken Dobutsu 29(1):1-13. [PubMed: 6995140]  [MGI Ref ID J:25411]

Serreze DV; Chapman HD; Varnum DS; Gerling I; Leiter EH; Shultz LD. 1997. Initiation of autoimmune diabetes in NOD/Lt mice is MHC class I-dependent. J Immunol 158(8):3978-86. [PubMed: 9103469]  [MGI Ref ID J:39473]

Additional References

Bowman MA; Leiter EH; Atkinson MA. 1994. Prevention of diabetes in the NOD mouse: implications for therapeutic intervention in human disease. Immunol Today 15(3):115-20. [PubMed: 8172643]  [MGI Ref ID J:17091]

Chun T; Hermel E; Gaskins HR; Aldrich CJ. 2001. Cytotoxic T lymphocyte and cDNA sequence analyses of the MHC class Ib molecule Qa1 in nonobese diabetic mice. Immunogenetics 53(6):506-10. [PubMed: 11685462]  [MGI Ref ID J:72438]

Darby IA; Bisucci T; Hewitson TD; MacLellan DG. 1997. Apoptosis is increased in a model of diabetes-impaired wound healing in genetically diabetic mice. Int J Biochem Cell Biol 29(1):191-200. [PubMed: 9076954]  [MGI Ref ID J:40898]

DiLorenzo TP; Lieberman SM; Takaki T; Honda S; Chapman HD; Santamaria P; Serreze DV; Nathenson SG. 2002. During the early prediabetic period in NOD mice, the pathogenic CD8(+) T-cell population comprises multiple antigenic specificities. Clin Immunol 105(3):332-41. [PubMed: 12498815]  [MGI Ref ID J:94192]

Leiter EH. 1998. NOD Mice and Related Strains: Origins, Husbandry and Biology Introduction. In: NOD Mice and Related Strains: Research Applications in Diabetes, AIDS, Cancer, and Other Diseases. RG Landes, Austin.  [MGI Ref ID J:110093]

Lynch DM; Kay PH. 1995. Studies on the polymorphism of the fifth component of complement in laboratory mice. Exp Clin Immunogenet 12(4):253-60. [PubMed: 8919358]  [MGI Ref ID J:31912]

Moy SS; Nadler JJ; Young NB; Nonneman RJ; Segall SK; Andrade GM; Crawley JN; Magnuson TR. 2008. Social approach and repetitive behavior in eleven inbred mouse strains. Behav Brain Res 191(1):118-29. [PubMed: 18440079]  [MGI Ref ID J:138681]

Nagy A; Nagashima H; Cha S; Oxford GE; Zelles T; Peck AB; Humphreys-Beher MG. 2001. Reduced oral wound healing in the NOD mouse model for type 1 autoimmune diabetes and its reversal by epidermal growth factor supplementation. Diabetes 50(9):2100-4. [PubMed: 11522677]  [MGI Ref ID J:71049]

Pierce MA; Chapman HD; Post CM; Svetlanov A; Efrat S; Horwitz M; Serreze DV. 2003. Adenovirus early region 3 antiapoptotic 10.4K, 14.5K, and 14.7K genes decrease the incidence of autoimmune diabetes in NOD mice. Diabetes 52(5):1119-27. [PubMed: 12716741]  [MGI Ref ID J:83195]

Quintana FJ; Cohen IR. 2001. Autoantibody Patterns in Diabetes-prone NOD Mice and in Standard C57BL/6 Mice. J Autoimmun 17(3):191-7. [PubMed: 11712856]  [MGI Ref ID J:72893]

Serreze DV; Leiter EH. 1994. Genetic and pathogenic basis of autoimmune diabetes in NOD mice. Curr Opin Immunol 6(6):900-6. [PubMed: 7710714]  [MGI Ref ID J:22216]

Serreze DV; Post CM; Chapman HD; Johnson EA; Lu B; Rothman PB. 2000. Interferon-gamma receptor signaling is dispensable in the development of autoimmune type 1 diabetes in NOD mice. Diabetes 49(12):2007-11. [PubMed: 11118001]  [MGI Ref ID J:65986]

Trembleau S; Gregori S; Penna G; Gorny I; Adorini L. 2001. Il-12 administration reveals diabetogenic t cells in genetically resistant i-ealpha-transgenic nonobese diabetic mice: resistance to autoimmune diabetes is associated with binding of ealpha-derived peptides to the i-a(g7) molecule. J Immunol 167(7):4104-14. [PubMed: 11564833]  [MGI Ref ID J:71651]

Xie C; Sharma R; Wang H; Zhou XJ; Mohan C. 2004. Strain distribution pattern of susceptibility to immune-mediated nephritis. J Immunol 172(8):5047-55. [PubMed: 15067087]  [MGI Ref ID J:122988]

Cdh23^ahl related

Davis RR; Newlander JK; Ling X; Cortopassi GA; Krieg EF; Erway LC. 2001. Genetic basis for susceptibility to noise-induced hearing loss in mice. Hear Res 155(1-2):82-90. [PubMed: 11335078]  [MGI Ref ID J:69679]

Di Palma F; Pellegrino R; Noben-Trauth K. 2001. Genomic structure, alternative splice forms and normal and mutant alleles of cadherin 23 (Cdh23). Gene 281(1-2):31-41. [PubMed: 11750125]  [MGI Ref ID J:73941]

Johnson KR; Erway LC; Cook SA; Willott JF; Zheng QY. 1997. A major gene affecting age-related hearing loss in C57BL/6J mice Hear Res 114(1-2):83-92. [PubMed: 9447922]  [MGI Ref ID J:44966]

Johnson KR; Longo-Guess C; Gagnon LH; Yu H; Zheng QY. 2008. A locus on distal chromosome 11 (ahl8) and its interaction with Cdh23 ahl underlie the early onset, age-related hearing loss of DBA/2J mice. Genomics 92(4):219-25. [PubMed: 18662770]  [MGI Ref ID J:139223]

Johnson KR; Zheng QY; Noben-Trauth K. 2006. Strain background effects and genetic modifiers of hearing in mice. Brain Res 1091(1):79-88. [PubMed: 16579977]  [MGI Ref ID J:110459]

Johnson KR; Zheng QY; Weston MD; Ptacek LJ; Noben-Trauth K. 2005. The Mass1(frings) mutation underlies early onset hearing impairment in BUB/BnJ mice, a model for the auditory pathology of Usher syndrome IIC. Genomics 85(5):582-90. [PubMed: 15820310]  [MGI Ref ID J:97534]

Keithley EM; Canto C; Zheng QY; Fischel-Ghodsian N; Johnson KR. 2004. Age-related hearing loss and the ahl locus in mice. Hear Res 188(1-2):21-8. [PubMed: 14759567]  [MGI Ref ID J:87783]

Liu X; Bulgakov OV; Darrow KN; Pawlyk B; Adamian M; Liberman MC; Li T. 2007. Usherin is required for maintenance of retinal photoreceptors and normal development of cochlear hair cells. Proc Natl Acad Sci U S A 104(11):4413-8. [PubMed: 17360538]  [MGI Ref ID J:118927]

Mathews CE; Leiter EH. 1999. Resistance of ALR/Lt islets to free radical-mediated diabetogenic stress is inherited as a dominant trait. Diabetes 48(11):2189-96. [PubMed: 10535453]  [MGI Ref ID J:109893]

Noben-Trauth K; Zheng QY; Johnson KR. 2003. Association of cadherin 23 with polygenic inheritance and genetic modification of sensorineural hearing loss. Nat Genet 35(1):21-3. [PubMed: 12910270]  [MGI Ref ID J:86905]

Noben-Trauth K; Zheng QY; Johnson KR; Nishina PM. 1997. mdfw: a deafness susceptibility locus that interacts with deaf waddler (dfw). Genomics 44(3):266-72. [PubMed: 9325047]  [MGI Ref ID J:38429]

Vazquez AE; Jimenez AM; Martin GK; Luebke AE; Lonsbury-Martin BL. 2004. Evaluating cochlear function and the effects of noise exposure in the B6.CAST+Ahl mouse with distortion product otoacoustic emissions. Hear Res 194(1-2):87-96. [PubMed: 15276680]  [MGI Ref ID J:117746]

Zheng QY; Johnson KR. 2001. Hearing loss associated with the modifier of deaf waddler (mdfw) locus corresponds with age-related hearing loss in 12 inbred strains of mice. Hear Res 154(1-2):45-53. [PubMed: 11423214]  [MGI Ref ID J:70964]

Hc⁰ related

Actor JK; Breij E; Wetsel RA; Hoffmann H; Hunter RL Jr; Jagannath C. 2001. A role for complement C5 in organism containment and granulomatous response during murine tuberculosis. Scand J Immunol 53(5):464-74. [PubMed: 11309154]  [MGI Ref ID J:103981]

Addis-Lieser E; Kohl J; Chiaramonte MG. 2005. Opposing regulatory roles of complement factor 5 in the development of bleomycin-induced pulmonary fibrosis. J Immunol 175(3):1894-902. [PubMed: 16034133]  [MGI Ref ID J:107269]

Anderson AL; Sporici R; Lambris J; Larosa D; Levinson AI. 2006. Pathogenesis of B-cell superantigen-induced immune complex-mediated inflammation. Infect Immun 74(2):1196-203. [PubMed: 16428769]  [MGI Ref ID J:104987]

Bauer K; Yu X; Wernhoff P; Koczan D; Thiesen HJ; Ibrahim SM. 2004. Identification of new quantitative trait loci in mice with collagen-induced arthritis. Arthritis Rheum 50(11):3721-8. [PubMed: 15529344]  [MGI Ref ID J:94347]

Bora NS; Kaliappan S; Jha P; Xu Q; Sohn JH; Dhaulakhandi DB; Kaplan HJ; Bora PS. 2006. Complement activation via alternative pathway is critical in the development of laser-induced choroidal neovascularization: role of factor B and factor H. J Immunol 177(3):1872-8. [PubMed: 16849499]  [MGI Ref ID J:138026]

Borders CW; Courtney A; Ronen K; Pilar Laborde-Lahoz M; Guidry TV; Hwang SA; Olsen M; Hunter RL Jr; Hollmann TJ; Wetsel RA; Actor JK. 2005. Requisite role for complement C5 and the C5a receptor in granulomatous response to mycobacterial glycolipid trehalose 6,6'-dimycolate. Scand J Immunol 62(2):123-30. [PubMed: 16101818]  [MGI Ref ID J:114316]

Carter WO; Bull C; Bortolon E; Yang L; Jesmok GJ; Gundel RH. 1998. A murine skeletal muscle ischemia-reperfusion injury model: differential pathology in BALB/c and DBA/2N mice. J Appl Physiol 85(5):1676-83. [PubMed: 9804569]  [MGI Ref ID J:51187]

Chen J; Reifsnyder PC; Scheuplein F; Schott WH; Mileikovsky M; Soodeen-Karamath S; Nagy A; Dosch MH; Ellis J; Koch-Nolte F; Leiter EH. 2005. 'Agouti NOD': identification of a CBA-derived Idd locus on Chromosome 7 and its use for chimera production with NOD embryonic stem cells. Mamm Genome 16(10):775-83. [PubMed: 16261419]  [MGI Ref ID J:102639]

Cunnion KM; Benjamin DK Jr; Hester CG; Frank MM. 2004. Role of complement receptors 1 and 2 (CD35 and CD21), C3, C4, and C5 in survival by mice of Staphylococcus aureus bacteremia. J Lab Clin Med 143(6):358-65. [PubMed: 15192652]  [MGI Ref ID J:101948]

Daniel DS; Dai G; Singh CR; Lindsey DR; Smith AK; Dhandayuthapani S; Hunter RL Jr; Jagannath C. 2006. The reduced bactericidal function of complement C5-deficient murine macrophages is associated with defects in the synthesis and delivery of reactive oxygen radicals to mycobacterial phagosomes. J Immunol 177(7):4688-98. [PubMed: 16982908]  [MGI Ref ID J:139313]

Deguchi Y; Andoh A; Inatomi O; Araki Y; Hata K; Tsujikawa T; Kitoh K; Fujiyama Y. 2005. Development of dextran sulfate sodium-induced colitis is aggravated in mice genetically deficient for complement C5. Int J Mol Med 16(4):605-8. [PubMed: 16142393]  [MGI Ref ID J:107581]

Fairweather D; Frisancho-Kiss S; Njoku DB; Nyland JF; Kaya Z; Yusung SA; Davis SE; Frisancho JA; Barrett MA; Rose NR. 2006. Complement receptor 1 and 2 deficiency increases coxsackievirus B3-induced myocarditis, dilated cardiomyopathy, and heart failure by increasing macrophages, IL-1beta, and immune complex deposition in the heart. J Immunol 176(6):3516-24. [PubMed: 16517720]  [MGI Ref ID J:129509]

Flierl MA; Rittirsch D; Nadeau BA; Day DE; Zetoune FS; Sarma JV; Huber-Lang MS; Ward PA. 2008. Functions of the complement components C3 and C5 during sepsis. FASEB J 22(10):3483-90. [PubMed: 18587006]  [MGI Ref ID J:140250]

Girardi G; Berman J; Redecha P; Spruce L; Thurman JM; Kraus D; Hollmann TJ; Casali P; Caroll MC; Wetsel RA; Lambris JD; Holers VM; Salmon JE. 2003. Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome. J Clin Invest 112(11):1644-54. [PubMed: 14660741]  [MGI Ref ID J:86845]

Hillebrandt S; Wasmuth HE; Weiskirchen R; Hellerbrand C; Keppeler H; Werth A; Schirin-Sokhan R; Wilkens G; Geier A; Lorenzen J; Kohl J; Gressner AM; Matern S; Lammert F. 2005. Complement factor 5 is a quantitative trait gene that modifies liver fibrogenesis in mice and humans. Nat Genet 37(8):835-43. [PubMed: 15995705]  [MGI Ref ID J:100159]

Karp CL; Grupe A; Schadt E; Ewart SL; Keane-Moore M; Cuomo PJ; Kohl J; Wahl L; Kuperman D; Germer S; Aud D; Peltz G; Wills-Karp M. 2000. Identification of complement factor 5 as a susceptibility locus for experimental allergic asthma. Nat Immunol 1(3):221-6. [PubMed: 10973279]  [MGI Ref ID J:108211]

Kawikova I; Paliwal V; Szczepanik M; Itakura A; Fukui M; Campos RA; Geba GP; Homer RJ; Iliopoulou BP; Pober JS; Tsuji RF; Askenase PW. 2004. Airway hyper-reactivity mediated by B-1 cell immunoglobulin M antibody generating complement C5a at 1 day post-immunization in a murine hapten model of non-atopic asthma. Immunology 113(2):234-45. [PubMed: 15379984]  [MGI Ref ID J:92933]

Kerepesi LA; Hess JA; Nolan TJ; Schad GA; Abraham D. 2006. Complement component C3 is required for protective innate and adaptive immunity to larval strongyloides stercoralis in mice. J Immunol 176(7):4315-22. [PubMed: 16547268]  [MGI Ref ID J:129872]

Kim DD; Miwa T; Kimura Y; Schwendener RA; van Lookeren Campagne M; Song WC. 2008. Deficiency of decay-accelerating factor and complement receptor 1-related gene/protein y on murine platelets leads to complement-dependent clearance by the macrophage phagocytic receptor CRIg. Blood 112(4):1109-19. [PubMed: 18524992]  [MGI Ref ID J:138410]

Kirimanjeswara GS; Mann PB; Pilione M; Kennett MJ; Harvill ET. 2005. The complex mechanism of antibody-mediated clearance of Bordetella from the lungs requires TLR4. J Immunol 175(11):7504-11. [PubMed: 16301658]  [MGI Ref ID J:122156]

Kyriakides C; Austen W Jr; Wang Y; Favuzza J; Kobzik L; Moore FD Jr; Hechtman HB. 1999. Membrane attack complex of complement and neutrophils mediate the injury of acid aspiration. J Appl Physiol 87(6):2357-61. [PubMed: 10601189]  [MGI Ref ID J:103341]

Mahesh J; Daly J; Cheadle WG; Kotwal GJ. 1999. Elucidation of the early events contributing to zymosan-induced multiple organ dysfunction syndrome using MIP-1alpha, C3 knockout, and C5-deficient mice. Shock 12(5):340-9. [PubMed: 10565608]  [MGI Ref ID J:59655]

Mastellos D; Papadimitriou JC; Franchini S; Tsonis PA; Lambris JD. 2001. A novel role of complement: mice deficient in the fifth component of complement (C5) exhibit impaired liver regeneration. J Immunol 166(4):2479-86. [PubMed: 11160308]  [MGI Ref ID J:111000]

Miller CG; Cook DN; Kotwal GJ. 1996. Two chemotactic factors, C5a and MIP-1alpha, dramatically alter the mortality from zymosan-induced multiple organ dysfunction syndrome (MODS): C5a contributes to MODS while MIP-1alpha has a protective role. Mol Immunol 33(14):1135-7. [PubMed: 9047380]  [MGI Ref ID J:38592]

Miller CG; Justus DE; Jayaraman S; Kotwal GJ. 1995. Severe and prolonged inflammatory response to localized cowpox virus infection in footpads of C5-deficient mice: investigation of the role of host complement in poxvirus pathogenesis. Cell Immunol 162(2):326-32. [PubMed: 7743560]  [MGI Ref ID J:25289]

Mocco J; Mack WJ; Ducruet AF; Sosunov SA; Sughrue ME; Hassid BG; Nair MN; Laufer I; Komotar RJ; Claire M; Holland H; Pinsky DJ; Connolly ES Jr. 2006. Complement component C3 mediates inflammatory injury following focal cerebral ischemia. Circ Res 99(2):209-17. [PubMed: 16778128]  [MGI Ref ID J:123658]

Mori L; de Libero G. 1998. Genetic control of susceptibility to collagen-induced arthritis in T cell receptor beta-chain transgenic mice. Arthritis Rheum 41(2):256-62. [PubMed: 9485083]  [MGI Ref ID J:134111]

Moulton RA; Mashruwala MA; Smith AK; Lindsey DR; Wetsel RA; Haviland DL; Hunter RL; Jagannath C. 2007. Complement C5a anaphylatoxin is an innate determinant of dendritic cell-induced Th1 immunity to Mycobacterium bovis BCG infection in mice. J Leukoc Biol 82(4):956-67. [PubMed: 17675563]  [MGI Ref ID J:125190]

Mullick A; Elias M; Picard S; Bourget L; Jovcevski O; Gauthier S; Tuite A; Harakidas P; Bihun C; Massie B; Gros P. 2004. Dysregulated inflammatory response to Candida albicans in a C5-deficient mouse strain. Infect Immun 72(10):5868-76. [PubMed: 15385488]  [MGI Ref ID J:93132]

Mullick A; Leon Z; Min-Oo G; Berghout J; Lo R; Daniels E; Gros P. 2006. Cardiac failure in C5-deficient A/J mice after Candida albicans infection. Infect Immun 74(8):4439-51. [PubMed: 16861630]  [MGI Ref ID J:112405]

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Patel SN; Berghout J; Lovegrove FE; Ayi K; Conroy A; Serghides L; Min-oo G; Gowda DC; Sarma JV; Rittirsch D; Ward PA; Liles WC; Gros P; Kain KC. 2008. C5 deficiency and C5a or C5aR blockade protects against cerebral malaria. J Exp Med 205(5):1133-43. [PubMed: 18426986]  [MGI Ref ID J:136298]

Pickering MC; Warren J; Rose KL; Carlucci F; Wang Y; Walport MJ; Cook HT; Botto M. 2006. Prevention of C5 activation ameliorates spontaneous and experimental glomerulonephritis in factor H-deficient mice. Proc Natl Acad Sci U S A 103(25):9649-54. [PubMed: 16769899]  [MGI Ref ID J:111031]

Pilione MR; Agosto LM; Kennett MJ; Harvill ET. 2006. CD11b is required for the resolution of inflammation induced by Bordetella bronchiseptica respiratory infection. Cell Microbiol 8(5):758-68. [PubMed: 16611225]  [MGI Ref ID J:135740]

Pritchard MT; McMullen MR; Stavitsky AB; Cohen JI; Lin F; Medof ME; Nagy LE. 2007. Differential contributions of C3, C5, and decay-accelerating factor to ethanol-induced fatty liver in mice. Gastroenterology 132(3):1117-26. [PubMed: 17383432]  [MGI Ref ID J:128218]

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Refici ML; Metzger DW; Arulanandam BP; Lennartz MR; Loegering DJ. 2001. Fcgamma-receptor signaling augments the LPS-stimulated increase in serum tumor necrosis factor-alpha levels. Am J Physiol Regul Integr Comp Physiol 280(4):R1037-44. [PubMed: 11247825]  [MGI Ref ID J:114295]

Rittirsch D; Flierl MA; Day DE; Nadeau BA; McGuire SR; Hoesel LM; Ipaktchi K; Zetoune FS; Sarma JV; Leng L; Huber-Lang MS; Neff TA; Bucala R; Ward PA. 2008. Acute lung injury induced by lipopolysaccharide is independent of complement activation. J Immunol 180(11):7664-72. [PubMed: 18490769]  [MGI Ref ID J:136379]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX8

Colony Maintenance

Mating System	Sibling x Sibling         (Female x Male)
Diet Information	LabDiet® 5K52/5K67

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Supply Details

Standard Supply	JAX Ready Strain® (Level 1). Most popular strains. Readily available in any quantity you need.
Supply Notes	Females are not available after eight weeks of age. Shipped at a specific age in weeks. Mice at a precise age in days and littermates are also available. Strains that must be genotyped are not available until five to seven weeks of age. Genomic DNA is available for this strain from the Mouse DNA Resource.
Important Note	This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss that is already severe by three months of age.

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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.

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phone:	207-288-6470
fax:	207-288-6655

JAX^® Mice & Services Conditions of Use

“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (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 with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”

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, The Jackson Laboratory will, at its option, provide credit or replacement for the MICE or product received or the services provided.

No Liability

In no event shall The Jackson Laboratory, 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 The Jackson Laboratory, its agents or employees. In purchasing or receiving MICE, products or services from The Jackson Laboratory, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges The Jackson Laboratory from all such causes of action or damages, and further agrees to defend and indemnify The Jackson Laboratory from any costs or damages arising out of any third party claims.

MICE and biological materials 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 The Jackson Laboratory’s MICE, products and services. In addition, special terms and conditions of sale of certain MICE, products and services may be set forth separately in The Jackson Laboratory 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 The Jackson Laboratory, 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 The Jackson Laboratory, 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 services by The Jackson Laboratory.