Mss51 deletion increases endurance and ameliorates histopathology in the mdx mouse model of Duchenne muscular dystrophy.

Autor: Rovira Gonzalez YI; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD, USA.; Cellular and Molecular Medicine Graduate Program, Johns Hopkins School of Medicine, Baltimore, MD, USA., Moyer AL; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD, USA.; Cellular and Molecular Medicine Graduate Program, Johns Hopkins School of Medicine, Baltimore, MD, USA., LeTexier NJ; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD, USA., Bratti AD; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD, USA., Feng S; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD, USA., Peña V; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD, USA., Sun C; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD, USA.; Departments of Neurology and Neuroscience, Johns Hopkins School of Medicine, Baltimore, MD, USA., Pulcastro H; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD, USA., Liu T; Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA., Iyer SR; Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD, USA., Lovering RM; Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD, USA., O'Rourke B; Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA., Wagner KR; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD, USA.; Departments of Neurology and Neuroscience, Johns Hopkins School of Medicine, Baltimore, MD, USA.

Publikováno v: FASEB journal : official publication of the Federation of American Societies for Experimental Biology [FASEB J] 2021 Feb; Vol. 35 (2), pp. e21276.

Mss51 deletion enhances muscle metabolism and glucose homeostasis in mice.

Autor: Rovira Gonzalez YI; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.; Cellular and Molecular Medicine Graduate Program., Moyer AL; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.; Cellular and Molecular Medicine Graduate Program., LeTexier NJ; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA., Bratti AD; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA., Feng S; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA., Sun C; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.; Department of Neurology.; Department of Neuroscience, and., Liu T; Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA., Mula J; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA., Jha P; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA., Iyer SR; Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, Maryland, USA., Lovering RM; Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, Maryland, USA., O'Rourke B; Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA., Noh HL; Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA., Suk S; Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA., Kim JK; Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.; Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA., Essien Umanah GK; Department of Neurology.; Department of Neuroscience, and., Wagner KR; The Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.; Department of Neurology.; Department of Neuroscience, and.

Publikováno v: JCI insight [JCI Insight] 2019 Oct 17; Vol. 4 (20). Date of Electronic Publication: 2019 Oct 17.

Chromatin Changes at the PPAR-γ2 Promoter During Bone Marrow-Derived Multipotent Stromal Cell Culture Correlate With Loss of Gene Activation Potential.

Autor: Lynch PJ; Cellular and Tissue Therapies Branch, Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, Maryland, USA., Thompson EE; Cellular and Tissue Therapies Branch, Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, Maryland, USA., McGinnis K; Cellular and Tissue Therapies Branch, Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, Maryland, USA., Rovira Gonzalez YI; Cellular and Tissue Therapies Branch, Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, Maryland, USA., Lo Surdo J; Cellular and Tissue Therapies Branch, Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, Maryland, USA., Bauer SR; Cellular and Tissue Therapies Branch, Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, Maryland, USA., Hursh DA; Cellular and Tissue Therapies Branch, Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, Maryland, USA.

Publikováno v: Stem cells (Dayton, Ohio) [Stem Cells] 2015 Jul; Vol. 33 (7), pp. 2169-81. Date of Electronic Publication: 2015 May 26.