C57bl 10scsn dmdmdx j

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C57BL/10ScSn-Dmdmdx/J is a mouse strain that carries a spontaneous mutation in the dystrophin gene, resulting in a model for Duchenne muscular dystrophy. This strain is commonly used in research related to muscular dystrophy and related disorders.

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C57BL/10ScSn (18 citations) C57BL/10ScSn-Dmdmdx/J (mdx) mice (18 citations) C57BL/10ScSn-Dmdmdx/J (mdx) (17 citations) C57BL/10ScSn-Dmdmdx/J mice (14 citations) C57Bl/10ScSn-DMDmdx (10 citations) C57BL/10ScSn-Dmdmdx/J(mdx) (JAX (2 citations)

75 protocols using c57bl 10scsn dmdmdx j

Muscular Dystrophy in Mice

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Wild-type (C57BL/10ScSnJ, n = 25) and mdx (C57BL/10ScSn-Dmdmdx/J, n = 25) mice were obtained from Jackson Laboratories (Bar Harbor, ME) and were studied between the ages of 4–10 weeks. The mice were housed in an approved Association for Assessment and Accreditation of Laboratory Animal Care facility at the University of Florida (12-h light/dark, 22°C, 42% humidity) and provided food ad libitum. The study was approved by our Institutional Animal Care and Use Committee (IACUC) review board at the University of Florida (Gainesville, FL).

Lopez C., Batra A., Moslemi Z., Rennick A., Guice K., Zeng H., Walter G.A, & Forbes S.C. (2021). Effects of muscle damage on 31phosphorus magnetic resonance spectroscopy indices of energetic status and sarcolemma integrity in young mdx mice. NMR in biomedicine, 35(3), e4659.

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Genetically Engineered Mouse Models for Duchenne Muscular Dystrophy

Cited 1 time

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The mdx mice were obtained from Jackson laboratories (C57BL/10ScSn-Dmdmdx/J). The mdx:S2808A mice were generated by crossing mdx mice with RyR2-S2808A, in which S2808 on RyR2 is substituted by alanine to inhibit PKA phosphorylation of RyR2 in mdx mice [3 (link)]. The mdx:S2814A mice were generated by crossing mdx mice with RyR2-S2814 mice, in which S2814 on RyR2 is genetically inactivated to prevent CaMKII phosphorylation of RyR2 [4 (link)]. Only male mice were used for experiments, and all lines were backcrossed for at least 20 generations. All studies were performed according to protocols approved by the Institutional Animal Care and Use Committee of Baylor College of Medicine conforming to the Guide for the Care and Use of Laboratory Animals published by the U.S. National Institutes of Health (NIH Publication No. 85-23, revised 1996).

Wang Q., Wang W., Wang G., Rodney G, & Wehrens X.H. (2015). Crosstalk between RyR2 Oxidation and Phosphorylation Contributes to Cardiac dysfunction in Mice with Duchenne Muscular Dystrophy. Journal of molecular and cellular cardiology, 89(0 0), 177-184.

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Transgenic Mice for Muscle Stem Cell Studies

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The mice strains were obtained from Jackson Laboratories, including C57BL/6J mice (Stock no. 000664, adult mice at 8 weeks and aged mice at 18 months), mdx mice (C57BL/10ScSn-Dmdmdx/J, Stock No: 001801), Rosa26-tdTomato (Stock no. 7909), Pax7-cre/ERT2 (Stock no. 017763), and Rosa26-EYFP (Stock no. 006148). Pax7-cre/ERT2 and Rosa26-EYFP were crossed to produce Pax7-CreER:Rosa26-EYFP offspring. The genotypes of all transgenic mice were confirmed with genotyping analyses according to the manufacturer’s instructions. All mice were bred and maintained in specific pathogen-free conditions. All animal work was conducted under protocols approved by the UC Berkeley or UCLA Animal Research Committee.

Fang J., Sia J., Soto J., Wang P., Li L.K., Hsueh Y.Y., Sun R., Francis Faull K., Tidball J.G, & Li S. (2021). Skeletal-muscle regeneration via the chemical induction and expansion of myogenic stem cells in situ or in vitro. Nature biomedical engineering, 5(8), 864-879.

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Duchenne Muscular Dystrophy Combination Therapy

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Mdx (C57BL/10ScSn-Dmd^mdx/J) mice and wild type C57BL/10J mice were obtained from The Jackson Laboratory. The phosphorodiamidate morpholino modified antisense oligomer against the exon 23 of DMD gene (PPMO23) was synthesized and conjugated to the cell-penetrating peptide (RXRRBRRXRRBRXB) (Gene-Tools, LLC.). Male mdx mice were subjected to PPMO23 (15 mg/kg, i.v., biweekly), from 4 week of age, and combined with AGR-H19 (10 mg/kg s.q., every three days) or Nifenazone (10 mg/kg i.p. daily), and the experiment was terminated at 24 week of age. Male wild type C57BL/10J mice of same age were included as control group. The human antisense oligonucleotide (AON) against the exon 44 (h44AON1) of the human DMD gene was synthesized using phosphorothioated 2’O-Methyl RNA oligomers (Biosynthesis Inc.) and delivered to iPS-SkMCs/-CMs, scramble RNA was delivered as the negative control. H19 mimics and Nifenazone was used to treat the iPS-SkMCs/-CMs in combined with h44AON1, vehicle was used as the negative control. All cells were harvested 7 days post-treatment. Oligonucleotide sequences are included in the Supplementary Table 9.

Zhang Y., Li Y., Hu Q., Xi Y., Xing Z., Zhang Z., Huang L., Wu J., Liang K., Nguyen T.K., Egranov S.D., Sun C., Zhao Z., Hawke D.H., Li J., Sun D., Kim J.J., Zhang P., Cheng J., Farida A., Hung M.C., Han L., Darabi R., Lin C, & Yang L. (2020). LncRNA H19 Alleviates Muscular Dystrophy Through Stabilizing Dystrophin. Nature cell biology, 22(11), 1332-1345.

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mdx Mouse Model for DMD Research

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Three-month-old male mdx mice (C57BL/10ScSn-DMDmdx/J) were generated using founders purchased from Jackson Laboratory (Bar Harbor, ME, USA). All mice were housed in groups of 3–4 per cage on a 14/10-h light/dark cycle with food and water provided ad libitum.

Lindsay A., Baumann C.W., Rebbeck R.T., Yuen S.L., Southern W.M., Hodges J.S., Cornea R.L., Thomas D.D., Ervasti J.M, & Lowe D.A. (2020). Mechanical factors tune the sensitivity of mdx muscle to eccentric strength loss and its protection by antioxidant and calcium modulators. Skeletal Muscle, 10, 3.

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Longitudinal Evaluation of Muscle Growth and Myopathy in Mice

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All mice used in this study were maintained under protocols approved by Institutional Animal Care and Use Committee at the New York University School of Medicine. Male C57BL6 (n=22, C57BL/10ScSn, The Jackson Laboratory, ME) and mdx (n=8, male C57BL/10ScSn-Dmd^mdx/J, The Jackson Laboratory, ME) mice were used to observe myofiber size and sarcolemma permeability during normal muscle growth and myopathy, respectively. The WT mice were imaged at time points of 4 (n=4), 5 (n=4), 7 (n=7), 9 (n=4) and 13 (n=3) weeks old to measure skeletal muscle properties at these time points of normal muscular growth. All WTs were sacrificed immediately after the MRI study for a given time point for ex vivo imaging and immunohistochemistry (IHC) staining of Wheat Germ Agglutinin (WGA). The mdx mice (n=8) were longitudinally studied at the same time points (n=8, 6, 6, 6, and 4 for week 4, 5, 7, 9 and 13 time points, respectively), while subsets of the mdx mice were sacrificed at 4 (n=2), 5 (n=2) and 13 weeks (n=4) for MRI-pathology correlations. The changes in the muscle between week 4 and week 13 in the WT and mdx mice were used to assess the association of the RPBM with other MRI and histopathological measures of the muscle.

Winters K.V., Reynaud O., Novikov D.S., Fieremans E, & Kim S.G. (2018). Quantifying Myofiber Integrity using Diffusion MRI and Random Permeable Barrier Modeling in Skeletal Muscle Growth and Duchenne Muscular Dystrophy Model in Mice. Magnetic resonance in medicine, 80(5), 2094-2108.

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Utilizing Dystrophin-Deficient Mice for DMD

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The study is reported in accordance with ARRIVE guidelines (https://arriveguidelines.org). C57BL/10ScSnJ (B10, #000476) wildtype (WT) and C57BL/10ScSn-Dmdmdx/J (mdx, #001801) mice were purchased from Jackson Laboratories (Bar Harbor, ME, USA) and were used as WT control and DMD model for all experiments. As DMD occurs primarily in males, only male mice were used in the current study. These mice had free access to drinking water and regular chow, unless otherwise noted. All animal experiments were performed in accordance with the relevant guidelines and regulations approved by the Animal Care and Use Committee of Wright State University.

Brown A., Morris B., Kamau J.K., Alshudukhi A.A., Jama A, & Ren H. (2023). Automated Image Analysis Pipeline Development to Monitor Disease Progression in Muscular Dystrophy Using Cell Profiler. Archives of microbiology & immunology, 7(3), 178-187.

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Transgenic Dystrophin Mice for Muscular Dystrophy

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All mice used in this study were adult males (3–5 months of age). Animals were cared for in accordance with, and all experimental protocols were approved by, the University of Minnesota Institutional Animal Care and Use Committee standards. All National Institutes of Health laboratory animal ethical regulations were followed in these studies. C57BL/10 (wildtype) and mdx mice were obtained from The Jackson Laboratory. Transgenic dystrophin lines were previously generated: Dys^ΔH2-R15-mdx [25 (link)], Dys^{ΔH2-R19/ΔCT}-mdx [24 (link)], Dys^ΔR4-23/ΔCT-mdx [29 (link)], Dys^{ΔR2-15/ΔR18-23/ΔCT}-mdx [29 (link)], Dp116-mdx [30 (link)] and flμDys (Jeffrey Chamberlain Lab). All transgenic dystrophin lines are skeletal muscle specific via the human skeletal actin promoter (HSA) and were backcrossed onto the mdx (C57BL/10ScSn-Dmd^mdx/J) mouse strain from The Jackson Laboratory (Bar Harbor, ME). ActB-msCT, Actg1-msCT, ActB-msKO and Actg1-msKO have been previously generated via loxP flanking sites with the knockout mice expressing HSA-Cre [31 (link),32 (link)]. Mdx/PrxII-TG, mdx/mb^−/⁻ were previously generated [28 (link)] as were the mdx/Actg1-TG [33 (link)] and Adbn^−/⁻ [34 (link)]. The genotypes of mini- and micro-dystrophin transgenic mice were verified via amplification of the HSA promoter followed by protein confirmation based upon expected molecular weights and antibody reactivities (S1 Fig).

Nelson D.M., Fasbender E.K., Jakubiak M.C., Lindsay A., Lowe D.A, & Ervasti J.M. (2020). Rapid, redox-mediated mechanical susceptibility of the cortical microtubule lattice in skeletal muscle. Redox Biology, 37, 101730.

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Murine Models for Muscular Dystrophy Research

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C57BL/10 (no. 000476), mdx mice (C57BL/10ScSn-Dmdmdx/J) (no. 001801), and mdx mice in the DBA2/J background (D2-mdx) (no. 013141) were obtained from The Jackson Laboratory. CD45.1 congenic mice (no. 002014) were also obtained from The Jackson Laboratory and crossed with mdx mice at the UCI. B6A/J (no. 012767) and C57BL/6 mice (no. 000664) were bred in vivariums at Children’s National Hospital. VCP (77 (link)) and double homeobox 4 (DUX4) (78 (link)) mice were provided by collaborators at the UCI and Ohio State University, respectively. Animal experiments were approved by the Institutional Animal Care and Use Committee of UCI and performed under Institutional Animal Care and Use Committee guidelines.

Coulis G., Jaime D., Guerrero-Juarez C., Kastenschmidt J.M., Farahat P.K., Nguyen Q., Pervolarakis N., McLinden K., Thurlow L., Movahedi S., Hughes B.S., Duarte J., Sorn A., Montoya E., Mozaffar I., Dragan M., Othy S., Joshi T., Hans C.P., Kimonis V., MacLean A.L., Nie Q., Wallace L.M., Harper S.Q., Mozaffar T., Hogarth M.W., Bhattacharya S., Jaiswal J.K., Golann D.R., Su Q., Kessenbrock K., Stec M., Spencer M.J., Zamudio J.R, & Villalta S.A. (2023). Single-cell and spatial transcriptomics identify a macrophage population associated with skeletal muscle fibrosis. Science Advances, 9(27), eadd9984.

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Dystrophin-Deficient Mouse Model Study

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Seven-week old male C57BL/10J mice (stock number: 000665), hereafter referred to as wild type (WT, n = 12) and dystrophin-deficient (MDX, n = 12) mice (C57BL/10ScSn-Dmd^mdx/J; stock number 001801) were purchased from the Jackson Laboratory (Bar Harbor, ME). Mice were housed in groups (20–23 °C, 12-h photoperiod) and fed ad libitum. The study was approved by the Institutional Animal Care and Use Committee at Boston University.

Kwak D., Wei G., Thompson L.V, & Kim J.H. (2020). Short-Term ONX-0914 Administration: Performance and Muscle Phenotype in Mdx Mice. International Journal of Environmental Research and Public Health, 17(14), 5211.

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