B6.129s6 cg spp1tm1blh j

Manufactured by Jackson ImmunoResearch

Sourced in United States, Montenegro

The B6.129S6(Cg)-Spp1tm1Blh/J is a genetically modified mouse strain. It is a model for the study of osteopontin (Spp1) gene function.

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Lab products found in correlation

C57bl 6j, by Jackson ImmunoResearch (3 mentions) C57bl 6j mice, by Jackson ImmunoResearch (2 mentions) C57bl 6jrj mice, by Janvier Labs (2 mentions) Balb c mice, by Inotiv (1 mentions) Mrl mpj faslpr j, by Jackson ImmunoResearch (1 mentions) Balb colahsd, by Inotiv (1 mentions) Mrl lpr, by Jackson ImmunoResearch (1 mentions) B6 cg tg sod1 g93a 1gur j, by Jackson ImmunoResearch (1 mentions) B6.129 cg cd44tm1hbg j, by Jackson ImmunoResearch (1 mentions) D12492, by Research Diets (1 mentions) C57bl 6 mice, by Jackson ImmunoResearch (1 mentions)

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B6.Cg-Spp1tm1Blh/J) (4 citations)

9 protocols using b6.129s6 cg spp1tm1blh j

Diverse Mouse Strains for Comprehensive Research

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For this study, adult female mice from the following four standard inbred strains were used: C57BL/6 J (The Jackson Laboratory, Bar Harbor, ME, USA); B6.129S6(Cg)-Spp1^tm1Blh/J, also known as OPN−/− (The Jackson Laboratory); B6.129P2-Icos/J also know as ICOS−/− (The Jackson Laboratory), BALB/cOlaHsd, or BALB/c mice (Envigo, Huntingdon, UK); and MRL/MpJ-Fas^lpr/J, commonly known as MRL-lpr (The Jackson Laboratory). Mice of the first four strains were used at 8–10 weeks of age, while those of the latter strain were 12 weeks old. All animals were maintained under pathogen-free conditions in the animal facility of Università del Piemonte Orientale; they were fed ad libitum on rodent chow and water was freely available in the home cages, the ambient temperature was maintained at 21 ± 1 °C. All experimental procedures were conducted during the light phase of a 12:12-h light:dark cycle. Experimental procedures were conducted, following European guidelines, in accordance with both the University Ethical Committee and the National Institutes of Health Ministry and Care Committee (protocol number DB064.42), both of which approved the protocol.

Raineri D., Dianzani C., Cappellano G., Maione F., Baldanzi G., Iacobucci I., Clemente N., Baldone G., Boggio E., Gigliotti C.L., Boldorini R., Rojo J.M., Monti M., Birolo L., Dianzani U, & Chiocchetti A. (2020). Osteopontin binds ICOSL promoting tumor metastasis. Communications Biology, 3, 615.

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Transgenic Mouse Models of ALS

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Transgenic mice carrying the human mutant SOD1^G93A gene (B6.Cg-Tg(SOD1*G93A)1Gur/J), mice with targeted disruption of the OPN gene (B6.129S6(Cg)-Spp1^tm1Blh/J), and mice with targeted disruption of the CD44 gene (B6.129(Cg)-Cd44^tm1Hbg/J) were purchased from Jackson Laboratory. Mice carrying the human SOD1^G85R gene (line 148) or the wild-type human SOD1 gene (B6.Cg-Tg(SOD1)76Dpr) were kind gifts from Dr. Don Cleveland (University of California, San Diego). LoxSOD1^G37R mice were described previously62 (link). Mice were genotyped for human SOD1 as described62 (link).

Morisaki Y., Niikura M., Watanabe M., Onishi K., Tanabe S., Moriwaki Y., Okuda T., Ohara S., Murayama S., Takao M., Uchida S., Yamanaka K, & Misawa H. (2016). Selective Expression of Osteopontin in ALS-resistant Motor Neurons is a Critical Determinant of Late Phase Neurodegeneration Mediated by Matrix Metalloproteinase-9. Scientific Reports, 6, 27354.

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High-fat Diet Effects on OPN-deficient Mice

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All of the procedures were performed according to the “Guide for the Care and Use of Laboratory Animals” published by the National Institutes of Health (publication 86–23 revised 1985) and under the ethical approval of the Committee of Animal Experimental Ethical Inspection of the First Affiliated Hospital, College of Medicine, Zhejiang University, China. The specific pathogen-free female mice and OPN-deficient mice (B6.129S6(Cg)-Spp1^tm1Blh/J) were both of the same background (C57BL/6J) and were both originally from Jackson Laboratory (Bar Harbor, ME, USA). 4-week-old female wild-type (WT) mice and OPN-deficient (KO) mice were sacrificed after a continuous, 24-week high-fat diet (HFD, 60% kcal of fat, cat. number: D12492; Research Diets, Inc.) or a normal diet (ND) containing approximately 4% kcal of fat.

Chen J., Zeng P., Gong L., Zhang X., Ling Z., Bi K., Shi F., Wang K., Zhang Q., Jiang J., Zhang Y., Uede T., El-Omar E.M, & Diao H. (2022). Osteopontin Exacerbates High-Fat Diet-Induced Metabolic Disorders in a Microbiome-Dependent Manner. mBio, 13(6), e02531-22.

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Aging and Osteopontin Knockout in Mice

Cited 1 time

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C57BL/6JRj mice (referred to as WT) were purchased from Janvier Labs. OPN-knockout mice (B6.129S6(Cg)-Spp1^tm1Blh/J), purchased from The Jackson Laboratory, had been backcrossed with C57/BL6J mice more than 10 generations and were bred by heterozygous mice to yield homozygous (referred to as OPN^–/–) and WT littermates. The p16-luciferase mice (strain code 01XBT--B6.Cg-Cdkn2a tm3.1Nesh Tyr c-2J/Nci) were obtained from the National Cancer Institute mouse repository (courtesy of Norman Sharpless, University of North Carolina, Chapel Hill, North Carolina, USA) (25 (link)). All mice were housed in a pathogen-free platform at a constant temperature (22°C), with a 12-hour light-dark cycle and unrestricted access to a chow diet (CD, A0310; Safe Diets) and water. Chow diet composition was 13.5% fat, 61.3% carbohydrate, and 25.2% protein. During follow-up, animals underwent monthly body weight evaluation. The experiments comparing the young (3-month-old) and aged (12-month-old) WT and transgenic animals were performed contemporaneously.

Sawaki D., Zhang Y., Mohamadi A., Pini M., Mezdari Z., Lipskaia L., Naushad S., Lamendour L., Altintas D.M., Breau M., Liang H., Halfaoui M., Delmont T., Surenaud M., Rousseau D., Yoshimitsu T., Louache F., Adnot S., Henegar C., Gual P., Czibik G, & Derumeaux G. (2023). Osteopontin promotes age-related adipose tissue remodeling through senescence-associated macrophage dysfunction. JCI Insight, 8(8), e145811.

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Osteopontin Knockout Bone Analysis

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All bone samples were taken from female mice from C57BL/6 background. OPN knock-out mice were 8 weeks old (B6.129S6(Cg)-Spp1tm1Blh/J, The Jackson Laboratory) and control Wild Type were between 8 and 10 weeks of age. The bones for all the experiments were taken from the same mice.

Depalle B., McGilvery C.M., Nobakhti S., Aldegaither N., Shefelbine S.J, & Porter A.E. (2021). Osteopontin regulates type I collagen fibril formation in bone tissue. Acta Biomaterialia, 120, 194-202.

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OPN Deficiency in Mouse Model

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OPN deficient mice (B6.129S6(Cg)-Spp^1tm1Blh/J) were obtained from Jackson Laboratories (Bar Harbor, ME; stock #004936) and bred at The Scripps Research Institute. The genotype was confirmed by PCR analysis. All animals were housed in a specific pathogen-free facility with unlimited access to water and laboratory chow. The experiments were approved by the TSRI Institutional Animal Use and Care Committee of our institute and were conducted in accordance with the guidelines of the institutional animal care policy.

Marcondes M.C., Ojakian R., Bortell N., Flynn C., Conti B, & Fox H.S. (2014). Osteopontin Expression in the Brain Triggers Localized Inflammation and Cell Death When Immune Cells Are Activated by Pertussis Toxin. Mediators of Inflammation, 2014, 358218.

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Muscle Injury and Exercise in Mice

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All animal experimental procedures were approved by the Animal Care and Use Committee of the First Affiliated Hospital, School of Medicine, Zhejiang University (reference number 2015‐186). The specific pathogen-free female mice and OPN-deficient mice (B6.129S6(Cg)-Spp1tm1Blh/J) were both of the same background (C57BL/6J) and both originally from Jackson Laboratory (Bar Harbor, ME, USA). 7-10 weeks old female wild-type (WT) mice and OPN-deficient (KO) mice were used to establish muscle injury model and exercise model.

Wang Y., Hong L., Jiang J., Zhang X., Chen J, & Diao H. (2023). Osteopontin May Improve Postinjury Muscle Repair Via Matrix Metalloproteinases And tgf-β Activation in Regular Exercise. International Journal of Medical Sciences, 20(9), 1202-1211.

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Osteopontin Knockout Mouse Model

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Specific pathogen-free adult (8–10 weeks) female C57BL/6 mice (WT) and B6.129S6(Cg)-Spp1^tm1Blh/J osteopontin knockout mice (OPN-KO) were supplied by Jackson Lab (Bar Harbor, ME) and weighed 20.0 ± 1.6 g at the beginning of treatment. OPN KO mice were created through targeted disruption of the OPN gene in 129S6/SvEvTac derived mouse TL-1 embryonic stem cells. Successfully targeted cells were injected into C57BL6 blastocysts and the resulting chimeras crossed to outbred Black Swiss mice. Once established in this breed, heterozygotes were backcrossed for 10 generations with C57BL/6 mice. Animals were housed one per cage receiving HEPA-filtered air in the National Institute for Occupational Safety and Health (NIOSH) animal facilities accredited by AAALAC International. Animals were supplied with water and irradiated NIH-31 modified 6% mouse food (Envigo RMS, Inc.) ad libitum and were acclimated in the animal facility under controlled temperature and humidity for one week prior to use. All experimental procedures were conducted in accordance with the Guide for the Care and Use of Laboratory Animals, 7^th ed. and approved by the National Institute for Occupational Safety and Health (NIOSH) Institutional Animal Care and Use Committee.

Khaliullin T.O., Kisin E.R., Murray A.R., Yanamala N., Shurin M.R., Gutkin D.W., Fatkhutdinova L.M., Kagan V.E, & Shvedova A.A. (2017). Mediation of the single-walled carbon nanotubes induced pulmonary fibrogenic response by osteopontin and TGF-β1. Experimental lung research, 43(8), 311-326.

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Osteopontin Knockout Mice Model

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C57/BL6JRj mice (referred to as wild-type [WT]) were purchased from Janvier Labs (France). Osteopontin knockout mice (B6.129S6[Cg]-Spp1tm1Blh/J) were purchased from The Jackson Laboratory (Bar Harbor, ME), which had been backcrossed with C57/BL6J mice more than 10 generations, and kept as homozygous (referred to as OPN -/-). All mice were housed in a specific pathogen-free platform at constant temperature (22°C), with a 12-hour light-dark cycle and unrestricted access to a chow diet (CD, A0310; Safe Diets, France) and water. During follow-up, animals underwent monthly body-weight, metabolic, and echocardiography evaluations. Before euthanization, animals also underwent hemodynamic evaluation. All animal experiments were approved by the Institutional Animal Care and Use Committee of the French National Institute of Health and Medical Research (INSERM)-Unit 955, Créteil, France (ComEth 15-001).

Sawaki D., Czibik G., Pini M., Ternacle J., Suffee N., Mercedes R., Marcelin G., Surenaud M., Marcos E., Gual P., Clément K., Hue S., Adnot S., Hatem S.N., Tsuchimochi I., Yoshimitsu T., Hénégar C, & Derumeaux G. (2018). Visceral Adipose Tissue Drives Cardiac Aging Through Modulation of Fibroblast Senescence by Osteopontin Production. Circulation, 138(8).

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