Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered Mutant Mice. Mating System Homozygote x Homozygote         (Female x Male) Species laboratory mouse Background Strain C57BL/6J Donor Strain 129S7 via AB1 ES cell line (+Hprt-bm2) Generation N10F37 (12-NOV-08)   Donating Investigator Arthur Beaudet,   Baylor College of Medicine

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for the Itgb2^tm1Bay mutation are viable and fertile. Homozygous mutant mice show an increased neutrophil count, and a decreased inflammatory response to peritonitis. Responses to delayed-type hypersensitivity and rejection of transplanted tissue are impaired. PLEASE NOTE: The Itgb2^tm1Bay allele is not a null mutation; it is a hypomorphic mutation which results in the expression of very low levels of Itgb2 protein. This strain serves as a model for the moderate form of human CD18 deficiency.

Development
The Itgb2^tm1Bay mutant strain was developed in the laboratory of Dr. Arthur Beaudet at Baylor College of Medicine. The 129-derived AB1 ES cell line was used. The C57BL/6J strain was produced by backcrossing the Itgb2^tm1Bay mutation 10 times to C57BL/6J inbred mice.

Control Information

	Control
	000664 C57BL/6J
Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Itgb2

003329

B6.129S7-Itgb2tm2Bay/J

View Strains carrying other alleles of Itgb2     (1 strain)

Additional Web Information

Congenic Nomenclature

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms

	Leukocyte Adhesion Deficiency, Type I; LAD - Models with phenotypic similarity to human disease where etiologies involve orthologs.1
NOT	Psoriasis Susceptibility 1; PSORS1 - Models with phenotypic similarity to human disease where etiologies involve orthologs.1
	Psoriasis Susceptibility 1; PSORS1 - Models with phenotypic similarity to human disease where etiologies are distinct.2

1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s). 2 Human genes are associated with this disease. Orthologs of those genes do not appear in the mouse genotype(s).

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

Itgb2^tm1Bay/Itgb2^tm1Bay

        B6.129S7-Itgb2^tm1Bay/J

• life span-post-weaning/aging
• premature death (MGI Ref ID J:118466)
  • mutants and wild-type mice treated with streptozotocin to induce diabetes display significantly increased mortality after 12 months of disease compared to untreated controls
• vision/eye phenotype
• abnormal eye physiology (MGI Ref ID J:118466)
  • in the diabetes models, 11-month diabetic mutants have decreased numbers of injured endothelial cells (<5%) compared to diabetic wild-type controls
• abnormal retina morphology (MGI Ref ID J:118466)
  • in the galactose- and streptozotocin-induced diabetes models, after 11 months, mutants have fewer adherent leukocytes in the retina compared to diabetic controls; number of adherent leukocytes in the retina in 11-month diabetic mutants does not differ from number in non-diabetic controls
  • diabetic wild-type mice at 11 months of disease have a 3.1-fold increase in adherent leukocyte number compared with non-diabetic controls
  • compared to diabetic wild-type controls, number of endothelial cells in diabetic mutants are higher and comparable to non-diabetic wild-type controls
  • 11-month diabetic wild-type mice have 3.8-fold more acellular capillaries compared to non-diabetic controls; in diabetic mutants, this pathology is suppressed by 60% with number of acellular capillaries similar to that in non-diabetic wild-type controls
  • at 11 months, numbers of normal appearing pericytes in retinas of diabetic mutants are significantly greater than number in diabetic wild-type controls
  • at 22 months, galactosemic mutants show almost no endothelial cell loss, no pericyte loss, and less acellular capillary formation (by 60%) than galactosemic wild-type controls compared to euglycemic wild-type mice
  • no basement membrane thickening is observed in diabetic and galactosemic mutants compared to that observed in diabetic and galactosemic wild-type controls
  • following laser photocoagulation (1,2, and 4 weeks after), significantly less pathologically significant leakage (fewer grade-2B lesions) develops in mutants compared to wild-type
  • less mice have 3 or more grade-2B lesions in each eye compared with wild-type
• abnormal retinal vasculature (MGI Ref ID J:118466)
  • in diabetes models, mutants exhibit decreased retinal-blood barrier breakdown compared to diabetic controls at 11 months
• increased resistance to induced choroidal neovascularization (MGI Ref ID J:119416)
  • at 2 weeks after laser injury, volume of choroidal neovascularization (CNV) is reducedby ~67.0% compared to wild-type mice
  • mutants have markedly smaller CNV membranes 2 weeks after injury compared to wild-type
• homeostasis/metabolism phenotype
• increased circulating glucose level (MGI Ref ID J:118466)
  • blood glucose levels are significantly increased in mutants and controls with streptozotocin treatment or high galactose diet
• cardiovascular system phenotype
• abnormal retinal vasculature (MGI Ref ID J:118466)
  • in diabetes models, mutants exhibit decreased retinal-blood barrier breakdown compared to diabetic controls at 11 months
• increased resistance to induced choroidal neovascularization (MGI Ref ID J:119416)
  • at 2 weeks after laser injury, volume of choroidal neovascularization (CNV) is reducedby ~67.0% compared to wild-type mice
  • mutants have markedly smaller CNV membranes 2 weeks after injury compared to wild-type

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Itgb2^tm1Bay/Itgb2^tm1Bay

        involves: 129S7/SvEvBrd

• immune system phenotype
• decreased inflammatory response (MGI Ref ID J:13599)
  • decreased inflammatory response to i.p. injection of thioglycollate showing decreased migration of neutrophils into the peritoneal cavity
  • delayed rejection of cardiac transplants
• increased leukocyte cell number (MGI Ref ID J:13599)
  • increased total leukocyte counts however less elevated than on the PL/J background
• increased granulocyte number (MGI Ref ID J:13599)
• increased lymphocyte cell number (MGI Ref ID J:13599)
• hematopoietic system phenotype
• increased leukocyte cell number (MGI Ref ID J:13599)
  • increased total leukocyte counts however less elevated than on the PL/J background
• increased granulocyte number (MGI Ref ID J:13599)
• increased lymphocyte cell number (MGI Ref ID J:13599)
• skin/coat/nails phenotype
• *normal* skin/coat/nails phenotype (MGI Ref ID J:32126)
  • did not develop progressive dermatitis in the 129S7/SvEvBrd background

Itgb2^tm1Bay/Itgb2^tm1Bay

        involves: 129S7/SvEvBrd * PL/J

• skin/coat/nails phenotype
• *normal* skin/coat/nails phenotype (MGI Ref ID J:32126)
  • associated phenotypes appear on the PL/J background but not on a C57BL/6 or 129S7/SvEvBrd background
• abnormal dermal layer morphology (MGI Ref ID J:32126)
  • dermal collagen appeared disorganized
• mixed cellular infiltration to dermis (MGI Ref ID J:32126)
  • progressive dermatitis with a dermal infiltrate consisting of granulocytes, lymphocytes, histiocytes and scattered mast cells
• abnormal dermal papilla (MGI Ref ID J:32126)
  • vessels within the dermal papillae were dilated
• abnormal epidermal layer morphology (MGI Ref ID J:32126)
  • occasionally developed focal spongiosis and erosion of the epidermis
• epidermal hyperplasia (MGI Ref ID J:32126)
  • irregular psoriasiform hyperplasia of the epidermis
• hyperkeratosis (MGI Ref ID J:32126)
  • skin exhibited orthohyperkeratosis
• parakeratosis (MGI Ref ID J:32126)
• abnormal skin condition (MGI Ref ID J:32126)
• psoriasis (MGI Ref ID J:32126)
  • had irregular psoriasiform hyperplasia of the epidermis and subcorneal microabscesses
• reddish skin (MGI Ref ID J:32126)
  • dermatitis was characterized by erythema
• scaly skin (MGI Ref ID J:32126)
  • severely affected mice developed scales and crusts in the dorsum of the trunk, the abdomen, and the neck
• alopecia (MGI Ref ID J:32126)
  • progressively developed in the facial region and/or base of the tail
• dermatitis (MGI Ref ID J:32126)
  • developed a progressive dermatitis, characterized by erythema, alopecia, and scale and crust formation
• immune system phenotype
• abnormal spleen morphology (MGI Ref ID J:32126)
  • exhibited myeloid hyperplasia in the spleen
• dermatitis (MGI Ref ID J:32126)
  • developed a progressive dermatitis, characterized by erythema, alopecia, and scale and crust formation
• enlarged lymph nodes (MGI Ref ID J:32126)
  • displayed reactive lymphadenopathy
• increased leukocyte cell number (MGI Ref ID J:32126)
  • numbers of white blood cells were increased to a higher extent than on a 129S7/SvEvBrd background
• increased basophil cell number (MGI Ref ID J:32126)
• increased eosinophil cell number (MGI Ref ID J:32126)
• increased lymphocyte cell number (MGI Ref ID J:32126)
• increased monocyte cell number (MGI Ref ID J:32126)
• increased neutrophil cell number (MGI Ref ID J:32126)
• hematopoietic system phenotype
• abnormal bone marrow cell morphology/development (MGI Ref ID J:32126)
  • exhibited myeloid hyperplasia in the bone marrow
• increased basophil cell number (MGI Ref ID J:32126)
• increased eosinophil cell number (MGI Ref ID J:32126)
• increased platelet cell number (MGI Ref ID J:32126)
• abnormal spleen morphology (MGI Ref ID J:32126)
  • exhibited myeloid hyperplasia in the spleen
• increased leukocyte cell number (MGI Ref ID J:32126)
  • numbers of white blood cells were increased to a higher extent than on a 129S7/SvEvBrd background
• increased basophil cell number (MGI Ref ID J:32126)
• increased eosinophil cell number (MGI Ref ID J:32126)
• increased lymphocyte cell number (MGI Ref ID J:32126)
• increased monocyte cell number (MGI Ref ID J:32126)
• increased neutrophil cell number (MGI Ref ID J:32126)
• pigmentation phenotype
• *normal* pigmentation phenotype (MGI Ref ID J:32126)
  • associated phenotype appears on the PL/J background but not on a C57BL/6 or 129S7/SvEvBrd background

Itgb2^tm1Bay/Itgb2^tm1Bay

        involves: 129S7/SvEvBrd * C57BL/6J

• immune system phenotype
• abnormal spleen red pulp morphology (MGI Ref ID J:13599)
  • myeloid hyperplasia of splenic red pulp
• hematopoietic system phenotype
• abnormal spleen red pulp morphology (MGI Ref ID J:13599)
  • myeloid hyperplasia of splenic red pulp
• increased bone marrow cell number (MGI Ref ID J:13599)
  • myeloid hyperplasia in bone marrow
• skin/coat/nails phenotype
• *normal* skin/coat/nails phenotype (MGI Ref ID J:32126)
  • did not develop progressive dermatitis in the C57BL/6J background

Itgb2^tm1Bay/Itgb2^tm1Bay

        involves: 129S7/SvEvBrd * C57BL/6J * PL/J

• skin/coat/nails phenotype
• *normal* skin/coat/nails phenotype (MGI Ref ID J:84126)
  • F1 mice from intercrosses of homozygotes on PL/J and C57BL/6J backgrounds did not develop progressive dermatitis, however when F1 mice were backcrossed to homozygotes on the PL/J background, 50% developed dermatitis
• alopecia (MGI Ref ID J:84126)
  • approximately half of affected F2 mice develop severe disease with various degrees of alopecia
• dermatitis (MGI Ref ID J:84126)
  • 23.5% of the F2 progeny from a PL/J x C57BL/6J intercross develop psoriasiform dermatitis, which is not observed on a 129S7/SvEvBrd or a mixed 129S7/SvEvBrd and C57BL/6J background
• psoriasis (MGI Ref ID J:84126)
  • 23.5% of the F2 progeny from a PL/J x C57BL/6J intercross develop chronic inflammatory skin disease with highly variable severity
• reddish skin (MGI Ref ID J:84126)
  • approximately half of affected F2 mice develop only mild disease with erythema and/or dry skin, which is not observed on a 129S7/SvEvBrd or a mixed 129S7/SvEvBrd and C57BL/6J background
• immune system phenotype
• dermatitis (MGI Ref ID J:84126)
  • 23.5% of the F2 progeny from a PL/J x C57BL/6J intercross develop psoriasiform dermatitis, which is not observed on a 129S7/SvEvBrd or a mixed 129S7/SvEvBrd and C57BL/6J background

View Research Applications

Research Applications

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

Itgb2^tm1Bay related

Cell Biology Research
Defects in Cell Adhesion Molecules

Dermatology Research
Skin and Hair Texture Defects

Developmental Biology Research
Defects in Cell Adhesion Molecules
Defects in Extracellular Matrix Molecules

Immunology and Inflammation Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Inflammation

Mouse/Human Gene Homologs
leukocyte adhesion deficiency, type I

Genes & Alleles

Gene & Allele Information

Allele Symbol		Itgb2tm1Bay
Allele Name		targeted mutation 1, Baylor College of Medicine
Allele Type		Targeted (knock-out)
Common Name(s)		CD18-; CD18hypo;
Mutation Made By		Arthur Beaudet,   Baylor College of Medicine
Strain of Origin		129S7/SvEvBrd-Hprt1<+>
ES Cell Line Name		AB1
ES Cell Line Strain		129S7/SvEvBrd-Hprt1<+>
Gene Symbol and Name		Itgb2, integrin beta 2
Chromosome		10
Gene Common Name(s)		2E6; AI528527; CD18; CD18 antigen; Cd18; LAD; LCAMB; LFA-1; MAC-1; MF17; MFI7; MGC116306; Mac-1 beta; expressed sequence AI528527;
Molecular Note		An insertion mutation that duplicates exons 2 and 3 with interruption of one copy of exon 3 with a neomycin cassette. This is not a null mutation but rather a hypomorph expressing very low levels of ITGB2 protein. [MGI Ref ID J:13599]

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)

Wilson RW; Ballantyne CM; Smith CW; Montgomery C; Bradley A; O'Brien WE; Beaudet AL. 1993. Gene targeting yields a CD18-mutant mouse for study of inflammation. J Immunol 151(3):1571-8. [PubMed: 8101543]  [MGI Ref ID J:13599]

Additional References

Bullard DC; Scharffetter-Kochanek K; McArthur MJ; Chosay JG; McBride ME; Montgomery CA; Beaudet AL. 1996. A polygenic mouse model of psoriasiform skin disease in CD18-deficient mice. Proc Natl Acad Sci U S A 93(5):2116-21. [PubMed: 8700894]  [MGI Ref ID J:32126]

Kadono T; Venturi GM; Steeber DA; Tedder TF. 2002. Leukocyte rolling velocities and migration are optimized by cooperative L-selectin and intercellular adhesion molecule-1 functions. J Immunol 169(8):4542-50. [PubMed: 12370391]  [MGI Ref ID J:79530]

Papayannopoulou T; Priestley GV; Nakamoto B; Zafiropoulos V; Scott LM; Harlan JM. 2001. Synergistic mobilization of hemopoietic progenitor cells using concurrent beta1 and beta2 integrin blockade or beta2-deficient mice. Blood 97(5):1282-8. [PubMed: 11222371]  [MGI Ref ID J:67767]

Wu HS; Kolonoski P; Chang YY; Bermudez LE. 2000. Invasion of the brain and chronic central nervous system infection after systemic Mycobacterium avium complex infection in mice. Infect Immun 68(5):2979-84. [PubMed: 10768998]  [MGI Ref ID J:61694]

Itgb2^tm1Bay related

Baker PJ; DuFour L; Dixon M; Roopenian DC. 2000. Adhesion molecule deficiencies increase Porphyromonas gingivalis-induced alveolar bone loss in mice. Infect Immun 68(6):3103-7. [PubMed: 10816450]  [MGI Ref ID J:62266]

Barlow SC; Collins RG; Ball NJ; Weaver CT; Schoeb TR; Bullard DC. 2003. Psoriasiform Dermatitis Susceptibility in Itgb2(tm1Bay) PL/J Mice Requires Low-Level CD18 Expression and at Least Two Additional Loci for Progression to Severe Disease. Am J Pathol 163(1):197-202. [PubMed: 12819024]  [MGI Ref ID J:84126]

Barlow SC; Xu H; Weaver CT; Lindsey JR; Schoeb TR; Bullard DC. 2004. Development of dermatitis in CD18-deficient PL/J mice is not dependent on bacterial flora, and requires both CD4+ and CD8+ T lymphocytes. Int Immunol 16(2):345-51. [PubMed: 14734620]  [MGI Ref ID J:88930]

Bullard DC; Scharffetter-Kochanek K; McArthur MJ; Chosay JG; McBride ME; Montgomery CA; Beaudet AL. 1996. A polygenic mouse model of psoriasiform skin disease in CD18-deficient mice. Proc Natl Acad Sci U S A 93(5):2116-21. [PubMed: 8700894]  [MGI Ref ID J:32126]

Daley JM; Ivanenko-Johnston T; Reichner JS; Albina JE. 2005. Transcriptional regulation of TNF-alpha production in neutropenia. Am J Physiol Regul Integr Comp Physiol 288(2):R409-12. [PubMed: 15458967]  [MGI Ref ID J:104758]

Eppihimer MJ; Russell J; Anderson DC; Wolitzky BA; Granger DN. 1997. Endothelial cell adhesion molecule expression in gene-targeted mice. Am J Physiol 273(4 Pt 2):H1903-8. [PubMed: 9362259]  [MGI Ref ID J:43907]

Guerau-de-Arellano M; Alroy J; Huber BT. 2005. Beta2 integrins control the severity of murine Lyme carditis. Infect Immun 73(6):3242-50. [PubMed: 15908348]  [MGI Ref ID J:99145]

Gujral JS; Farhood A; Bajt ML; Jaeschke H. 2003. Neutrophils aggravate acute liver injury during obstructive cholestasis in bile duct-ligated mice. Hepatology 38(2):355-63. [PubMed: 12883479]  [MGI Ref ID J:105960]

Hoefer IE; van Royen N; Rectenwald JE; Deindl E; Hua J; Jost M; Grundmann S; Voskuil M; Ozaki CK; Piek JJ; Buschmann IR. 2004. Arteriogenesis proceeds via ICAM-1/Mac-1- mediated mechanisms. Circ Res 94(9):1179-85. [PubMed: 15059933]  [MGI Ref ID J:98899]

Huleatt JW; Lefrancois L. 1996. Beta2 integrins and ICAM-1 are involved in establishment of the intestinal mucosal T cell compartment. Immunity 5(3):263-73. [PubMed: 8808681]  [MGI Ref ID J:35355]

Jones SP; Trocha SD; Strange MB; Granger DN; Kevil CG; Bullard DC; Lefer DJ. 2000. Leukocyte and endothelial cell adhesion molecules in a chronic murine model of myocardial reperfusion injury Am J Physiol Heart Circ Physiol 279(5):H2196-201. [PubMed: 11045953]  [MGI Ref ID J:65658]

Joussen AM; Poulaki V; Le ML; Koizumi K; Esser C; Janicki H; Schraermeyer U; Kociok N; Fauser S; Kirchhof B; Kern TS; Adamis AP. 2004. A central role for inflammation in the pathogenesis of diabetic retinopathy. FASEB J 18(12):1450-2. [PubMed: 15231732]  [MGI Ref ID J:118466]

Kadono T; Venturi GM; Steeber DA; Tedder TF. 2002. Leukocyte rolling velocities and migration are optimized by cooperative L-selectin and intercellular adhesion molecule-1 functions. J Immunol 169(8):4542-50. [PubMed: 12370391]  [MGI Ref ID J:79530]

Kess D; Lindqvist AK; Peters T; Wang H; Zamek J; Nischt R; Broman KW; Blakytny R; Krieg T; Holmdahl R; Scharffetter-Kochanek K. 2006. Identification of susceptibility loci for skin disease in a murine psoriasis model. J Immunol 177(7):4612-9. [PubMed: 16982899]  [MGI Ref ID J:117544]

Kess D; Peters T; Zamek J; Wickenhauser C; Tawadros S; Loser K; Varga G; Grabbe S; Nischt R; Sunderkotter C; Muller W; Krieg T; Scharffetter-Kochanek K. 2003. CD4+ T cell-associated pathophysiology critically depends on CD18 gene dose effects in a murine model of psoriasis. J Immunol 171(11):5697-706. [PubMed: 14634077]  [MGI Ref ID J:109598]

Kodali P; Wu P; Lahiji PA; Brown EJ; Maher JJ. 2006. ANIT toxicity toward mouse hepatocytes in vivo is mediated primarily by neutrophils via CD18. Am J Physiol Gastrointest Liver Physiol 291(2):G355-63. [PubMed: 16614373]  [MGI Ref ID J:112906]

Lejtenyi D; Osmond DG; Miller SC. 2003. Natural killer cells and B lymphocytes in L-selectin and Mac-1/LFA-1 knockout mice: marker-dependent, but not cell lineage-dependent changes in the spleen and bone marrow. Immunobiology 207(2):129-35. [PubMed: 12675270]  [MGI Ref ID J:102758]

Matynia A; Anagnostaras SG; Wiltgen BJ; Lacuesta M; Fanselow MS; Silva AJ. 2008. A high through-put reverse genetic screen identifies two genes involved in remote memory in mice. PLoS ONE 3(5):e2121. [PubMed: 18464936]  [MGI Ref ID J:136217]

Oldenborg PA; Gresham HD; Lindberg FP. 2001. CD47-signal regulatory protein alpha (SIRPalpha) regulates Fcgamma and complement receptor-mediated phagocytosis. J Exp Med 193(7):855-62. [PubMed: 11283158]  [MGI Ref ID J:120547]

Papayannopoulou T; Priestley GV; Nakamoto B; Zafiropoulos V; Scott LM; Harlan JM. 2001. Synergistic mobilization of hemopoietic progenitor cells using concurrent beta1 and beta2 integrin blockade or beta2-deficient mice. Blood 97(5):1282-8. [PubMed: 11222371]  [MGI Ref ID J:67767]

Sakurai E; Taguchi H; Anand A; Ambati BK; Gragoudas ES; Miller JW; Adamis AP; Ambati J. 2003. Targeted disruption of the CD18 or ICAM-1 gene inhibits choroidal neovascularization. Invest Ophthalmol Vis Sci 44(6):2743-9. [PubMed: 12766082]  [MGI Ref ID J:119416]

Sumagin R; Lomakina E; Sarelius IH. 2008. Leukocyte-endothelial cell interactions are linked to vascular permeability via ICAM-1-mediated signaling. Am J Physiol Heart Circ Physiol 295(3):H969-H977. [PubMed: 18641276]  [MGI Ref ID J:141283]

Tu L; Poe JC; Kadono T; Venturi GM; Bullard DC; Tedder TF; Steeber DA. 2002. A functional role for circulating mouse L-selectin in regulating leukocyte/endothelial cell interactions in vivo. J Immunol 169(4):2034-43. [PubMed: 12165530]  [MGI Ref ID J:120206]

Wang H; Kess D; Lindqvist AK; Peters T; Sindrilaru A; Wlaschek M; Blakytny R; Holmdahl R; Scharffetter-Kochanek K. 2008. A 9-centimorgan interval of chromosome 10 controls the T cell-dependent psoriasiform skin disease and arthritis in a murine psoriasis model. J Immunol 180(8):5520-9. [PubMed: 18390736]  [MGI Ref ID J:134251]

Wang H; Peters T; Kess D; Sindrilaru A; Oreshkova T; Van Rooijen N; Stratis A; Renkl AC; Sunderkotter C; Wlaschek M; Haase I; Scharffetter-Kochanek K. 2006. Activated macrophages are essential in a murine model for T cell-mediated chronic psoriasiform skin inflammation. J Clin Invest 116(8):2105-14. [PubMed: 16886059]  [MGI Ref ID J:113121]

Wang H; Peters T; Sindrilaru A; Kess D; Oreshkova T; Yu XZ; Seier AM; Schreiber H; Wlaschek M; Blakytny R; Rohrbein J; Schulz G; Weiss JM; Scharffetter-Kochanek K. 2008. TGF-beta-dependent suppressive function of Tregs requires wild-type levels of CD18 in a mouse model of psoriasis. J Clin Invest 118(7):2629-39. [PubMed: 18521187]  [MGI Ref ID J:137678]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX12

Colony Maintenance

Breeding & Husbandry	The Itgb2tm1Bay strain is maintained by homozygous sibling matings. Homozygous mice may be ordered. Expected coat color from breeding:Black
Mating System	Homozygote x Homozygote         (Female x Male)
Diet Information	LabDiet® 5K52/5K67

Purchasing information

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

Pricing

Supply Details

Standard Supply

Repository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement.

Supply Notes

Usually shipped between four and eight weeks of age. This strain is included in the Induced Mutant Resource Colony collection. Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	000664 C57BL/6J
Considerations for Choosing Controls
USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
International - Control Pricing Information for Genetically Engineered Mutant Strains.

General Terms and Conditions

See Terms of Use

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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Contact Information
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Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
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Terms of Use

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General Terms and Conditions

For Licensing and Use Restrictions view the link(s) below:
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Contact information

General inquiries

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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.”

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