JAX Mice Database - *F1 Hybrid

Search Criteria: Strain Type is "*F1 Hybrid"

JAX^® Mice Strains

Stock Number	Strain Name Phenotype	Standard Supply
100006	B6D2F1/J	Level 1

101043	B6129SF1/J	Level 2

100010	B6C3F1/J	Level 2

100011	B6CBAF1/J	Level 2

100012	B6SJLF1/J	Level 2

100007	CB6F1/J	Level 2

100008	NZBWF1/J	Level 2
	Systemic lupus erythematosus (SLE), is a chronic, inflammatory, autoimmune disease of unknown origin. There is strong evidence supporting the role of genetics in determining susceptibility and resistance to the disease. NZBWF1/J develop an autoimmune disease resembling human systemic lupus erythematosus. Autoimmunity is characterized by high levels of antinuclear antibodies, hemolytic anemia, proteinuria, and progressive immune complex glomerulonephritis. The incidence and severity of with symptoms more pronounced in females. The average lifespan for NZBWF1 is 245 days for females and 406 days for males. NZBWF1/J mice have been used as a model for autoimmune disease since the early 1960s elucidating not only the complex immunobiological responses and mechanisms but also the genetic basis for the complex multifactorial disease.
100410	WBB6F1/J-Kit^W/Kit^W-v/J	Level 2
	Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Kit^W/Kit^W-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. Kit^W/Kit^W-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment.
100492	B6129PF1/J	Level 3

100299	PLSJLF1/J	Level 3

100409	B6129PF1/J-A^w-J/A^w	Level 4

100002	B6AF1/J	Level 4

100016	C3FeB6F1/J	Level 4

100003	CAF1/J	Level 4

100009	CByB6F1/J	Level 4

100015	CByD2F1/J	Level 4

100019	CSJLF1/J	Level 4

008215	(C57BL/6-Tg(TRAMP)8247Ng/J X FVB/NJ)F1/J	Repository- Live
	Mice carrying the TRAMP (Transgenic Adenocarcinoma of Mouse Prostate) transgene develop progressive forms of prostate cancer with distant site metastasis, primarily to the lymph nodes and lungs. These transgenic mice express the simian virus 40 (SV40) large tumor T antigen (Tag) under the control of the rat probasin promoter. Expression of the transgene is specific to the prostate epithelium. Transgenic mice exhibit various forms of disease from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. The median survival time for these F1 transgenic mice is 19 weeks, very few mice survive past 33 weeks of age, which is significantly shorter than the lifespan of transgenic mice on the C57BL/6 background. Comparative histological analysis of tumors from these F1 transgenic mice and from transgenic mice on the C57BL/6 background reveals that the tumors found in these F1 mutants arise from the dorsolateral and ventral lobes of the prostate and are more spherical, hig ..... For more information please see the full phenotype on the strain data sheet
001022	B6C3FeF1/J a/a	Repository- Live

001201	B6CBACaF1/J-A^w-J/A	Repository- Live

001875	B6EiC3SnF1/J	Repository- Live

003550	B6EiD2F1/J	Repository- Live

100004	C3D2F1/J	Repository- Live

001203	C3FeB6F1/J A/A^w-J	Repository- Live

100401	WCB6F1/J Kitl^Sl Kitl^Sl-d	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., Kitl^Sl/Kitl^Sl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full phenotype on the strain data sheet
003301	(C57BL/6J x C3H-Eya1^bor)F1/J	Repository-Cryopreserved
	The human Branchio-Oto-Renal Syndrome is generally a dominant disorder with incomplete penetrance and variable expressivity resulting from null mutations in the EYA1 gene. The mouse Eya1^bor allele is primarily a recessive hypomorphic mutation. Nevertheless, homozygous mice with this hypomorphic allele offer a good model for Branchio-Oto-Renal Syndrome. The phenotype of Eya1^bor/Eya1^bor mice parallels that of the human Branchio-Oto-Renal Syndrome and both are thought to result from reduced gene dosage. The Eya1^bor/Eya1^bor mice are deaf and their behavior is marked by circling and head-bobbing. They lack all but the most basal one-quarter of the cochlea, and the organ of Corti is completely absent. They have foreshortened, narrower semicircular canals and in some the common crus is incomplete. Their kidneys are absent or dysmorphic with greater severity generally on the left side. Fewe ..... For more information please see the full phenotype on the strain data sheet

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JAX® Mice Strains

JAX^® Mice Strains