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B6 albino b6 cg tyrc 2j j

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B6-Albino (B6(Cg)-Tyrc-2J/J) is a laboratory mouse strain that carries the Tyrc-2J mutation, which results in albinism. This strain is on a C57BL/6J (B6) genetic background. The Tyrc-2J mutation causes a reduction in melanin production, leading to the characteristic white coat color and pink eyes of albino mice.

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C57bl 6, by Jackson ImmunoResearch (2 mentions) Nod cg prkdcscid il2rgtm1wjl szj nsg, by Jackson ImmunoResearch (1 mentions)

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B6(Cg)-Tyrc-2J/J (19 citations) B6(Cg)-Tyrc-2J/J albino mice (10 citations) B6(Cg)-TyrC-2J/J (B6 albino) mice (8 citations) B6 albino (3 citations) Albino C57BL/6 (B6(Cg)-Tyrc-2J/J), (3 citations) Albino B6(Cg)-Tyrc-2J/J (2 citations)

4 protocols using b6 albino b6 cg tyrc 2j j

1

Mouse Strain Characterization and Maintenance

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C57BL/6 and B6-Albino (B6(Cg)-Tyrc-2J/J) were purchased from Jackson Laboratory. Mir22−/− (miR-22-null) mice used here were generated as previously described27 (link) and backcrossed at least five generations onto the C57BL/6 background) and then maintained as a homozygous stock. Hdac4flox/flox mice were provided by E. Olson (University of Texas Southwestern Medical Center, Dallas, Texas, USA)48 (link). CD11c-Cre transgenic mice (8 generations backcrossed to the C57BL/6 background) were provided by J. Levitt at Baylor College of Medicine. For all mouse experiments, wild-type littermate syngeneic animals were used as controls. All mice were bred and maintained in the specific pathogen free Transgenic Mouse Facility at Baylor College of Medicine, fed water and standard rodent chow ad libitum and used in accordance with all federal and institutional guidelines for the humane treatment of animals.
Lu W., You R., Yuan X., Yang T., Samuel E.L., Marcano D.C., Sikkema W.K., Tour J.M., Rodriguez A., Kheradmand F, & Corry D.B. (2015). MicroRNA-22 Inhibits Histone Deacetylase 4 to Promote T Helper-17 Cell-Dependent Emphysema. Nature immunology, 16(11), 1185-1194.
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2

Mouse Strain Characterization and Maintenance

Cited 1 time
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C57BL/6 and B6-Albino (B6(Cg)-Tyrc-2J/J) were purchased from Jackson Laboratory. Mir22−/− (miR-22-null) mice used here were generated as previously described27 (link) and backcrossed at least five generations onto the C57BL/6 background) and then maintained as a homozygous stock. Hdac4flox/flox mice were provided by E. Olson (University of Texas Southwestern Medical Center, Dallas, Texas, USA)48 (link). CD11c-Cre transgenic mice (8 generations backcrossed to the C57BL/6 background) were provided by J. Levitt at Baylor College of Medicine. For all mouse experiments, wild-type littermate syngeneic animals were used as controls. All mice were bred and maintained in the specific pathogen free Transgenic Mouse Facility at Baylor College of Medicine, fed water and standard rodent chow ad libitum and used in accordance with all federal and institutional guidelines for the humane treatment of animals.
Lu W., You R., Yuan X., Yang T., Samuel E.L., Marcano D.C., Sikkema W.K., Tour J.M., Rodriguez A., Kheradmand F, & Corry D.B. (2015). MicroRNA-22 Inhibits Histone Deacetylase 4 to Promote T Helper-17 Cell-Dependent Emphysema. Nature immunology, 16(11), 1185-1194.
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3

G291T Mutation in Tyrosinase Mice

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B6 (CG)-Tyrc-2j/J (B6 albino) (Jackson Laboratory, Bar Harbor, Maine, USA), G291T mutation in Tyr gene mice generated using the CRISPR /Cas9 system23 (link), C57BL/6J (B6 black) mice and Balb/c mice (8–12 weeks old) were bred in a specific pathogen free area in the Animal Resource Center of the University of Tsukuba, maintained at 23.5 ± 2.5 °C and 52.5 ± 12.5% humidity with 14/10 h light/dark period. Food and water were supplied ad libitum. HCD (1.25% cholesterol; Oriental Yeast Co. Ltd., Japan) was used.
Kulathunga K., Wakimoto A., Hiraishi Y., Yadav M.K., Gentleman K., Warabi E., Sakasai T., Miwa Y., Mizuno S., Takahashi S, & Hamada M. (2021). Albino mice with the point mutation at the tyrosinase locus show high cholesterol diet-induced NASH susceptibility. Scientific Reports, 11, 21827.
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4

Glioma mouse model using immunocompetent mice

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Male NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG)16 (link) and B6(Cg)-Tyrc-2J/J (B6 Albino) mice aged 8–12 weeks old were purchased from Jackson Laboratories. The 3–8 weeks immunocompetent Ntv-a Ink4a-Arf-/- PTENfl/fl mice on FVB/N, C57BL/6, BALB/C and 129 backgrounds were used for the mouse glioma model.17 (link)
Brempelis K.J., Cowan C.M., Kreuser S.A., Labadie K.P., Prieskorn B.M., Lieberman N.A., Ene C.I., Moyes K.W., Chinn H., DeGolier K.R., Matsumoto L.R., Daniel S.K., Yokoyama J.K., Davis A.D., Hoglund V.J., Smythe K.S., Balcaitis S.D., Jensen M.C., Ellenbogen R.G., Campbell J.S., Pierce R.H., Holland E.C., Pillarisetty V.G, & Crane C.A. (2020). Genetically engineered macrophages persist in solid tumors and locally deliver therapeutic proteins to activate immune responses. Journal for Immunotherapy of Cancer, 8(2), e001356.
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