Overview

BXSB mice develop a spontaneous autoimmune syndrome similar to lupus, which is accelerated in males (BXSB males have the mutant Yaa-containing Y chromosome). These mice may be useful in applications related to systemic lupus erythematosus.

Genetic overview

Genetic Background	Generation
	F165 (2019-03-18 00:00:00)

Yaa

Allele Type	Gene Symbol	Gene Name
Spontaneous	Yaa	accelerated autoimmunity and lymphoproliferation transposition

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Research Applications

Immunology, Inflammation and Autoimmunity Research

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Base Price

Starting at:

$218.00 Domestic price for male 5-week

296.51 Domestic price for breeder pair

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Details

Important Note

Males of this strain carry the BXSB-derived Yaa mutation on the Y chromosome.

Detailed Description

The Y-linked autoimmune accelerator locus (Yaa) on the Y chromosome of BXSB inbred male mice is the result of a duplication of an ~4 Mbp telomeric segment near the pseudoautosomal region of the X chromosome onto the Y chromosome. The duplicated segment contains 19 genes, including toll-like receptor 7 (Tlr7) and phosphoribosyl pyrophosphate synthetase 2 (Prps2). BXSB males have the mutant Yaa-containing Y chromosome, and are a model for a severe form of systemic lupus erythematosus (SLE). Their spontaneously arising autoimmune disease is characterized by the robust development of follicular T cells and germinal centers. Marginal zone B cells are depleted in BXSB-Yaa mice and a dramatic increase in number of peripheral monocytes is seen beginning at two months of age. Disease progression is characterized by lymph node and spleen enlargement, hemolytic anemia, hypergammaglobulinemia, anti-nuclear antibodies, and immune complex glomerulonephritis. This leads to morbidity on average of six months of age. BXSB females develop a greatly attenuated form of autoimmune disease; indicating that autoimmune disease acceleration is due to the presence of the Yaa mutation carried on the Y chromosome.

A duplicated copy of the Tlr7 gene is primarily responsible for the autoimmune phenotype attributed to the Yaa mutation. The BXSB-Yaa mouse therefore provides a model for investigating the effects copy number variation of Tlr7 on autoimmune disease. Therapeutic treatment of BXSB-Yaa mice with an anti-Type I interferon receptor antibody attenuates their autoimmune disease; indicating that Type I interferon signaling involved is in the pathogenesis of this disease.

The most suitable control animals are sex-matched, autoimmune disease-resistant BXSB.B6-Yaa⁺ consomic males carrying the C57BL/6-derived Y chromosome in place of the BXSB-derived mutant Yaa-containing Y chromosome. BXSB.B6-Yaa⁺ consomic mice (backcrossed to BXSB/MpJ inbred females for at least 40 generations) are described and available at The Jackson Laboratory as Stock No. 021330.

A note on outcrossing BXSB males with other inbred females: similar autoimmune disease acceleration occurs in males (but not in females) from an outcross of BXSB males to NZB females. Acceleration does not occur in offspring of the reciprocal cross. The same effect of Yaa is seen in offspring of outcrosses to strains SJL, C57BL/6, and AKR.

In addition, BXSB males lacking the interleukin 21 receptor (BXSB-Yaa/Il21r^-/- or BXSB-Yaa/Il21^-/-) are highly resistant to disease and are therefore a model for investigating the role of interleukin 21 in disease pathogenesis. Populations of regulatory CD8+ and potentially natural killer cells are also actively retarding disease in this model; making them useful to investigate the roles of such regulatory cells in autoimmune disease.

Control Suggestions

The most suitable control animals are sex-matched, autoimmune disease-resistant BXSB.B6-Yaa⁺ consomic males carrying the C57BL/6-derived Y chromosome in place of the BXSB-derived mutant Yaa-containing Y chromosome. BXSB.B6-Yaa⁺ consomic mice are available with different amounts of backcrossing to BXSB/MpJ inbred females:
--Stock No. 021330 are backcrossed at least 40 generations,
--Stock No. 001925 are backcrossed at least 22 generations, and
--Stock No. 000742 are backcrossed at least 10 generations.
Female from the colony
021330 BXSB.B6-Yaa⁺/MobJDcrJ

Additional Information

Considerations for Choosing Controls

Selected References

Bubier JA; Sproule TJ; Foreman O; Spolski R; Shaffer DJ; Morse HC 3rd; Leonard WJ; Roopenian DC. 2009. A critical role for IL-21 receptor signaling in the pathogenesis of systemic lupus erythematosus in BXSB-Yaa mice. Proc Natl Acad Sci U S A 106(5):1518-23PubMed: 19164519 MGI: J:144484
McPhee CG; Sproule TJ; Shin DM; Bubier JA; Schott WH; Steinbuck MP; Avenesyan L; Morse HC 3rd; Roopenian DC. 2011. MHC class I family proteins retard systemic lupus erythematosus autoimmunity and B cell lymphomagenesis. J Immunol 187(9):4695-704PubMed: 21964024 MGI: J:179430
Baccala R; Gonzalez-Quintial R; Schreiber RD; Lawson BR; Kono DH; Theofilopoulos AN. 2012. Anti-IFN-alpha/beta Receptor Antibody Treatment Ameliorates Disease in Lupus-Predisposed Mice. J Immunol 189(12):5976-84PubMed: 23175700 MGI: J:190844

View All References

Genetics

Yaa

Allele Symbol: Yaa

Allele Name	accelerated autoimmunity and lymphoproliferation
Allele Type	Spontaneous
Allele Synonym(s)	Yaa; accelerated autoimmunity and lymphoproliferation
Gene Symbol and Name	Yaa, accelerated autoimmunity and lymphoproliferation transposition
Gene Synonym(s)	Tp(X;Y)1Ekw
Strain of Origin	SB/Le
Chromosome	Y
Molecular Note	An approximately 4 MB region of the X chromosome that includes at least 13 known genes (spanning from Ofd1 to Mid1) was translocated to the Y chromosome adjacent to the pseudoautosomal region. Increased RNA expression of Msl3, Tlr7, Tmsb4x and Rab9 was detected in follicular B cells.

Disease/Phenotype

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

systemic lupus erythematosus

Research Areas By Genotype

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

Immunology, Inflammation and Autoimmunity Research
- Growth Factors/Receptors/Cytokines
- Autoimmunity
  - lupus erythematosus

Genotype: Yaa related

Immunology, Inflammation and Autoimmunity Research
- Autoimmunity
  - lupus erythematosus

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: X/Yaa
(SJL/J x BXSB)F1

immune system phenotype

enlarged lymph nodes
- at 18 to 25 weeks the combined weight of the axillary, mesenteric, and renal lymph nodes is increased 5-fold compared to C57BL/6J males
- moderately enlarged

increased susceptibility to autoimmune disorder
- accelerated autoimmune syndrome relative to reciprocal hybrid males

mortality/aging

premature death
- mean longevity for males is 308 +/- 26 days while only 8 of 16 reciprocal hybrid males died between 270 and 684 days

Genotype: X/Yaa
(C57BL/6J x BXSB)F1

immune system phenotype

enlarged lymph nodes
- at 18 to 25 weeks the combined weight of the axillary, mesenteric, and renal lymph nodes is increased 5-fold compared to C57BL/6J males
- moderately enlarged

increased susceptibility to autoimmune disorder
- accelerated autoimmune syndrome relative to reciprocal hybrid males

mortality/aging

premature death
- mean longevity for males is 332 +/- 14 days compared to 716 +/- 28 days for littermate females

Genotype: X/Yaa
(NZB x B6.SB/Le-Yaa)F1

hematopoietic system phenotype

increased monocyte cell number
- CD11b⁺ monocyte numbers increase as mice age with a 3-fold increase by 10 months of age

immune system phenotype

increased monocyte cell number
- CD11b⁺ monocyte numbers increase as mice age with a 3-fold increase by 10 months of age

Genotype: X/Yaa
B6.SB-Yaa/J

cellular phenotype

increased splenocyte proliferation
- hyperresponsive to imiquimod induced splenocyte proliferation

hematopoietic system phenotype

decreased marginal zone B cell number

increased splenocyte proliferation
- hyperresponsive to imiquimod induced splenocyte proliferation

immune system phenotype

decreased marginal zone B cell number

increased splenocyte proliferation
- hyperresponsive to imiquimod induced splenocyte proliferation

The following phenotype relates to a compound genotype created using this strain

Genotype: X/Yaa
BXSB/MpJ

hematopoietic system phenotype

abnormal B cell differentiation
- frequency of C3d receptor bearing cells is increased in young mice but declines with age

abnormal spleen B cell follicle morphology
- scattered follicular distribution in the spleen and large extrafollicular accumulations of CD138+ plasma cells and plasmablasts are found at 14 weeks of age

abnormal T cell subpopulation ratio
- at 14 weeks of age, more than normal splenic CD4+ Foxp3+ CD25+ T cells and very few splenic CD8+ Foxp3+ CD25+ T cells and higher than normal expression of CD122 on CD8+ splenic T cells

decreased erythrocyte cell number
- decreased at 16 weeks of age compared to C57BL/6J males

increased IgG1 level

increased IgG2a level
- relative to BXSB.B6-Yaa+ controls

increased IgG2b level
- relative to BXSB.B6-Yaa+ controls

increased IgG3 level

increased monocyte cell number
- at 8 months of age a 16-fold increase in monocytes is seen in males compared to females
- increase in peripheral blood mononuclear cells lacking T and B cells markers is seen by 2 months of age and bemose more severe with age

increased plasma cell number
- frequency of Ig-bearing cells is increased in the thymus
- increase in the frequency and absolute numbers of Ig-bearing cells associated with advanced autoimmune disease is seen in males but not females

increased spleen weight
- 4-fold increase in spleen weight

increased splenocyte number
- relative to BXSB.B6-Yaa+ at 14 weeks of age but not at 6 weeks of age

homeostasis/metabolism phenotype

increased circulating interleukin-21 level

increased urine protein level
- seen at 4 months of age

immune system phenotype

abnormal B cell differentiation
- frequency of C3d receptor bearing cells is increased in young mice but declines with age

abnormal lymph node morphology
- infiltrated with a mixed population of lymphocytes, plasma cells, and histiocytes often blurring the architecture of the node

abnormal spleen B cell follicle morphology
- scattered follicular distribution in the spleen and large extrafollicular accumulations of CD138+ plasma cells and plasmablasts are found at 14 weeks of age

abnormal T cell subpopulation ratio
- at 14 weeks of age, more than normal splenic CD4+ Foxp3+ CD25+ T cells and very few splenic CD8+ Foxp3+ CD25+ T cells and higher than normal expression of CD122 on CD8+ splenic T cells

enlarged lymph nodes
- at 18 to 25 weeks the combined weight of the axillary, mesenteric, and renal lymph nodes is increased 5-fold compared to C57BL/6J males
- moderately enlarged

glomerulonephritis
- acute to subacute exudative and proliferative glomerulonephritis

increased anti-erythrocyte antigen antibody level
- erythrocyte autoantibodies were found in 7 of 13 males between 16 and 25 weeks of age

increased anti-nuclear antigen antibody level
- serum anti-nuclear antibodies are found at 6 weeks of age and increased levels at 14 weeks of age

increased circulating interleukin-21 level

increased IgG1 level

increased IgG2a level
- relative to BXSB.B6-Yaa+ controls

increased IgG2b level
- relative to BXSB.B6-Yaa+ controls

increased IgG3 level

increased monocyte cell number
- at 8 months of age a 16-fold increase in monocytes is seen in males compared to females
- increase in peripheral blood mononuclear cells lacking T and B cells markers is seen by 2 months of age and bemose more severe with age

increased plasma cell number
- frequency of Ig-bearing cells is increased in the thymus
- increase in the frequency and absolute numbers of Ig-bearing cells associated with advanced autoimmune disease is seen in males but not females

increased spleen weight
- 4-fold increase in spleen weight

increased splenocyte number
- relative to BXSB.B6-Yaa+ at 14 weeks of age but not at 6 weeks of age

increased susceptibility to autoimmune disorder
- accelerated autoimmune syndrome relative to females of the same strain

mortality/aging

premature death
- castration does not significantly alter longevity
- mean longevity for males is 155 +/- 13 days compared to 442 +/- 29 days for littermate females
- median survival is 8 months

renal/urinary system phenotype

glomerulonephritis
- acute to subacute exudative and proliferative glomerulonephritis

increased urine protein level
- seen at 4 months of age

renal glomerular immunoglobulin deposits
- glomerular depositions of IgG are found at 14 weeks of age

Genotype: X/Yaa
BXSB/MpJScr

hematopoietic system phenotype

decreased CD4-positive, alpha beta T cell number
- pronounced decrease in CD4+ T cells with age

increased IgG level

increased monocyte cell number
- monocytosis

mortality/aging

premature death

renal/urinary system phenotype

glomerulonephritis
- develop severe proliferative glomerulonephritis by 3 to 5 months of age

immune system phenotype

decreased CD4-positive, alpha beta T cell number
- pronounced decrease in CD4+ T cells with age

glomerulonephritis
- develop severe proliferative glomerulonephritis by 3 to 5 months of age

increased anti-nuclear antigen antibody level
- anti-nuclear antibody levels are elevated at 3 to 5 months of age

increased IgG level

increased monocyte cell number
- monocytosis

increased susceptibility to autoimmune disorder
- accelerated autoimmune syndrome

Phenotype Information

Festing Inbred Strain Characteristics: BXSB

References

Bubier JA; Sproule TJ; Foreman O; Spolski R; Shaffer DJ; Morse HC 3rd; Leonard WJ; Roopenian DC. 2009. A critical role for IL-21 receptor signaling in the pathogenesis of systemic lupus erythematosus in BXSB-Yaa mice. Proc Natl Acad Sci U S A 106(5):1518-23PubMed: 19164519 MGI: J:144484
McPhee CG; Sproule TJ; Shin DM; Bubier JA; Schott WH; Steinbuck MP; Avenesyan L; Morse HC 3rd; Roopenian DC. 2011. MHC class I family proteins retard systemic lupus erythematosus autoimmunity and B cell lymphomagenesis. J Immunol 187(9):4695-704PubMed: 21964024 MGI: J:179430
Baccala R; Gonzalez-Quintial R; Schreiber RD; Lawson BR; Kono DH; Theofilopoulos AN. 2012. Anti-IFN-alpha/beta Receptor Antibody Treatment Ameliorates Disease in Lupus-Predisposed Mice. J Immunol 189(12):5976-84PubMed: 23175700 MGI: J:190844

Additional References

Zheng QY; Tong YC; Alagramam KN; Yu H. 2007. Tympanometry assessment of 61 inbred strains of mice. Hear Res 231(1-2):23-31PubMed: 17611057 MGI: J:123543
Rowland SL; Riggs JM; Gilfillan S; Bugatti M; Vermi W; Kolbeck R; Unanue ER; Sanjuan MA; Colonna M. 2014. Early, transient depletion of plasmacytoid dendritic cells ameliorates autoimmunity in a lupus model. J Exp Med 211(10):1977-91PubMed: 25180065 MGI: J:267843
Masum MA; Ichii O; Elewa YHA; Nakamura T; Otani Y; Hosotani M; Kon Y. 2018. Modified scanning electron microscopy reveals pathological crosstalk between endothelial cells and podocytes in a murine model of membranoproliferative glomerulonephritis. Sci Rep 8(1):10276PubMed: 29980767 MGI: J:268475
Kimura J; Ichii O; Miyazono K; Nakamura T; Horino T; Otsuka-Kanazawa S; Kon Y. 2014. Overexpression of Toll-like receptor 8 correlates with the progression of podocyte injury in murine autoimmune glomerulonephritis. Sci Rep 4:7290PubMed: 25468389 MGI: J:269052
Andrews BS; Eisenberg RA; Theofilopoulos AN; Izui S; Wilson CB; McConahey PJ; Murphy ED; Roths JB; Dixon FJ. 1978. Spontaneous murine lupus-like syndromes. Clinical and immunopathological manifestations in several strains. J Exp Med 148(5):1198-215PubMed: 309911 MGI: J:27634
Murphy ED; Roths JB. 1979. A Y chromosome associated factor in strain BXSB producing accelerated autoimmunity and lymphoproliferation. Arthritis Rheum 22(11):1188-94PubMed: 315777 MGI: J:6235
Eisenberg RA; Izui S; McConahey PJ; Hang L; Peters CJ; Theofilopoulos AN; Dixon FJ. 1980. Male determined accelerated autoimmune disease in BXSB mice: transfer by bone marrow and spleen cells. J Immunol 125(3):1032-6PubMed: 7410826 MGI: J:6372
Gilbert D; Lopez B; Parain J; Koutouzov S; Tron F. 2000. Overlap of the anti-cardiolipin and anti-nucleosome responses of the (NZW X BXSB)F1 mouse strain: a new pattern of cross-reactivity for lupus-related autoantibodies Eur J Immunol 30(11):3271-80PubMed: 11093143 MGI: J:65821
Luzina IG; Atamas SP; Storrer CE; daSilva LC; Kelsoe G; Papadimitriou JC; Handwerger BS. 2001. Spontaneous formation of germinal centers in autoimmune mice. J Leukoc Biol 70(4):578-84PubMed: 11590194 MGI: J:72513

Additional - Yaa related

Technical Support

Contact Technical Support

Genotyping Protocols
- QPCR: Yaa Alternate1
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This is an inbred strain. Males carry the BXSB-derived Yaa mutation on the Y chromosome. To maintain the live inbred colony, unaffected females (+/+) may be bred with affected males (Yaa/Y).
- Additional Breeding and Husbandry Support
Mating System
- +/+ sibling x Hemizygote
Appearance
- white-bellied agouti, affected
  Related Genotype: A^w/A^w X/Yaa (male)
  
  white-bellied agouti, unaffected
  Related Genotype: A^w/A^w X/X (female)
Citation
When using the BXSB/MpJ mouse strain in a publication, please cite the originating article(s) and include JAX stock #000740 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX10 (Standard)

Pricing & Availability

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Genotype

Price

weeks

Breeder Pair

Sex

Genotype

Price

Female
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Cryorecovery - Pricing

Service	Genotype	Price
	Inbred, 1 pair minimum will be supplied

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We 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.

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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.

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Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Control Suggestions

Additional Information

Selected References

Yaa

Allele Symbol: Yaa

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Research Areas By Genotype

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

Genotype: Yaa related

Mammalian Phenotype Terms by Genotype

Genotype: X/Yaa(SJL/J x BXSB)F1

immune system phenotype

mortality/aging

Genotype: X/Yaa(C57BL/6J x BXSB)F1

immune system phenotype

mortality/aging

Genotype: X/Yaa(NZB x B6.SB/Le-Yaa)F1

hematopoietic system phenotype

immune system phenotype

Genotype: X/YaaB6.SB-Yaa/J

cellular phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: X/YaaBXSB/MpJ

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

mortality/aging

renal/urinary system phenotype

Genotype: X/YaaBXSB/MpJScr

hematopoietic system phenotype

mortality/aging

renal/urinary system phenotype

immune system phenotype

Phenotype Information

References

Additional References

Additional - Yaa related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Appearance

Citation

Animal Health Reports

Live Mouse

Breeder Pair

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Genotype: X/Yaa
(SJL/J x BXSB)F1

Genotype: X/Yaa
(C57BL/6J x BXSB)F1

Genotype: X/Yaa
(NZB x B6.SB/Le-Yaa)F1

Genotype: X/Yaa
B6.SB-Yaa/J

Genotype: X/Yaa
BXSB/MpJ

Genotype: X/Yaa
BXSB/MpJScr