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Welcome to the Pubget Medical Subject Headings (MESH) browser. Click on a topic or subtopic below to explore related papers. In the gold box is the most recent paper about the current MESH term, and below are 20 related papers.
Dystrophin (0):
Recent article
Dystrophin
Molecular Therapy (18)11 2010
Abstract
We performed functional analyses of muscle in the exon 52-deleted mdx (mdx52) mouse, to predict the function of in-frame dystrophin following exon 51-skipping, which leads to a protein lacking most of hinge 3. A series of AOs based on phosphorodiamidate morpholino oligomers was screened by intramusc...
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PMID: 20823833
PDF is available here.
PDF is available here.
| < More recent | Older article > |
Circulation Journal (74)11 2010
Abstract
These results suggest that the inhibition of contractile activity during IPost prevents cardiomyocyte oncosis and enhances cardioprotection through PI3K-dependent restoration of sarcolemmal dystrophin....
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PMID: 20877127
PDF is available here.
PDF is available here.
Circulation Journal (74)11 2010
Abstract
New England Journal of Medicine (363)15 2010
Abstract
We report on delivery of a functional dystrophin transgene to skeletal muscle in six patients with Duchenne's muscular dystrophy. Dystrophin-specific T cells were detected after treatment, providing evidence of transgene expression even when the functional protein was not visualized in skeletal musc...
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PMID: 20925545
PDF is available here.
PDF is available here.
Abstract
Abstract
We investigated systemic gene delivery in 4-day-old GRMD dogs given a single intravenous injection of an AAV9 vector (1.5 x 10(14) vector genomes/kg) carrying a human codon-optimized human mini-dystrophin gene under control of the cytomegalovirus (CMV) promoter. One of the three treated dogs was eut...
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PMID: 20517298
PDF is available here.
PDF is available here.
Abstract
Neuromuscular Disorders (20)8 2010
Abstract
We review the clinical and genetic features in 15 manifesting carriers identified among 860 subjects within the United Dystrophinopathy Project, a large clinical dystrophinopathy cohort whose members undergo comprehensive DMD mutation analysis. We defined manifesting carriers as females with signifi...
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PMID: 20630757
PDF is available here.
PDF is available here.
Neuroreport (21)10 2010
Abstract
We have shown that localization of the scaffolding proteins gamma2-syntrophin, alpha-dystrobrevin-2, and dystrophin to glial endfeet is also dependent on the presence of alpha-syntrophin. In this study, we show that the expression levels of alpha-syntrophin, gamma2-syntrophin, and dystrophin at the...
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PMID: 20508543
PDF is available here.
PDF is available here.
Prenatal Diagnosis (30)7 2010
Abstract
We briefly review the history of molecular prenatal diagnostic testing, using Duchenne muscular dystrophy as an example, and describe how over the last 30 years we have moved from offering testing to a few affected individuals using techniques, such as Southern blotting to identify deletions, to mor...
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PMID: 20572117
PDF is available here.
PDF is available here.
Abstract
Gene Therapy (17)7 2010
Abstract
We inserted in a plasmid coding for the dog micro-dystrophin sequences containing a MGN target. The number of base pairs in these inserted sequences changed the reading frame. One of these modified target micro-dystrophin plasmids and an appropriate MGN were then transfected in 293FT cells. The MGN...
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PMID: 20393509
PDF is available here.
PDF is available here.
Abstract
We have performed a comparative proteomic study of the established mdx mouse model of x-linked muscular dystrophy. Fluorescence difference in-gel electrophoretic analysis of 9-week-old dystrophin-deficient versus age-matched normal extraocular muscle, using a pH 4-7 gel range, identified out of 1088...
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PMID: 20471957
PDF is available here.
PDF is available here.
Abstract
Recent developments in molecular therapies for Duchenne muscular dystrophy (DMD) demand accurate genetic diagnosis, because therapies are mutation specific. The KUCG (Kobe University Clinical Genetics) database for DMD and Becker muscular dystrophy is a hospital-based database comprising 442 cases....
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PMID: 20485447
PDF is available here.
PDF is available here.
Abstract
We engineered the K18N, L54R, D165V, A168D, L172H, and Y231N mutations into the full-length dystrophin cDNA and characterized the biochemical properties of each mutant protein. The K18N and L54R mutations are associated with the most severe diseases in humans and each caused a small but significant...
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PMID: 20457930
PDF is available here.
PDF is available here.
Neuromuscular Disorders (20)5 2010
Abstract
Duchenne muscular dystrophy (DMD) is characterised by the absence of dystrophin in muscle biopsies, although residual dystrophin can be present, either as dystrophin-positive (revertant) fibres or traces. As restoration of dystrophin expression is the end point of clinical trials, such residual dyst...
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PMID: 20395141
PDF is available here.
PDF is available here.
Neuromuscular Disorders (20)5 2010
Abstract
We demonstrate that reverse protein arrays are a novel and excellent material-saving method for the measurement and quantification of changes in protein expression between healthy and diseased muscle tissue as well as cultured primary myotubes. We evaluated a set of antibodies and found reproducible...
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PMID: 20304647
PDF is available here.
PDF is available here.
Abstract
We show long-term splice correction of the DMD gene in mdx mice following intramuscular PNA delivery and effective splice correction in aged mdx mice. Further, we report detailed optimization of systemic PNA delivery dose regimens and PNA AO lengths to yield splice correction, with 25-mer PNA AOs pr...
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PMID: 20068555
PDF is available here.
PDF is available here.
Abstract
We have developed a drug-screening system using C2C12 myoblasts expressing a reporter green fluorescent phosphate (GFP), with its reading frame disrupted by the insertion of a targeted dystrophin exon. A library of 2,000 compounds (Spectrum collection; Microsource Discovery System) was screened to i...
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PMID: 20087314
PDF is available here.
PDF is available here.
Journal of Biochemistry (147)4 2010
Abstract
We demonstrated that the skin permeability of gentamicin increased with the use of a thioglycolate-based depilatory agent. After transdermal administration, the readthrough activity in skeletal muscle, as determined using a lacZ/luc reporter system, was found to be equivalent to systemic administrat...
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PMID: 19910311
PDF is available here.
PDF is available here.
Brain Pathology (20)2 2010
Abstract
We generated Utrn-A and -B promoter-specific antibodies, Taqman Polymerase chain reaction (PCR)-based absolute copy number assays, and luciferase-reporter constructs to study CNS of normal and dystrophic mdx mice. Differential expression of Utrn-A and -B was noted in microdissected and capillary-enr...
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PMID: 19486009
PDF is available here.
PDF is available here.
Brain Pathology (20)2 2010
Abstract
We generated Utrn-A and -B promoter-specific antibodies, Taqman Polymerase chain reaction (PCR)-based absolute copy number assays, and luciferase-reporter constructs to study CNS of normal and dystrophic mdx mice. Differential expression of Utrn-A and -B was noted in microdissected and capillary-enr...
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PMID: 19486009
PDF is available here.
PDF is available here.
Brain Pathology (20)2 2010
Abstract
We generated Utrn-A and -B promoter-specific antibodies, Taqman Polymerase chain reaction (PCR)-based absolute copy number assays, and luciferase-reporter constructs to study CNS of normal and dystrophic mdx mice. Differential expression of Utrn-A and -B was noted in microdissected and capillary-enr...
|
PMID: 19486009
PDF is available here.
PDF is available here.
Brain Pathology (20)2 2010
Abstract
We generated Utrn-A and -B promoter-specific antibodies, Taqman Polymerase chain reaction (PCR)-based absolute copy number assays, and luciferase-reporter constructs to study CNS of normal and dystrophic mdx mice. Differential expression of Utrn-A and -B was noted in microdissected and capillary-enr...
|
PMID: 19486009
PDF is available here.
PDF is available here.
Brain Pathology (20)2 2010
Abstract
We generated Utrn-A and -B promoter-specific antibodies, Taqman Polymerase chain reaction (PCR)-based absolute copy number assays, and luciferase-reporter constructs to study CNS of normal and dystrophic mdx mice. Differential expression of Utrn-A and -B was noted in microdissected and capillary-enr...
|
PMID: 19486009
PDF is available here.
PDF is available here.
Brain Pathology (20)2 2010
Abstract
We generated Utrn-A and -B promoter-specific antibodies, Taqman Polymerase chain reaction (PCR)-based absolute copy number assays, and luciferase-reporter constructs to study CNS of normal and dystrophic mdx mice. Differential expression of Utrn-A and -B was noted in microdissected and capillary-enr...
|
PMID: 19486009
PDF is available here.
PDF is available here.
Brain Pathology (20)2 2010
Abstract
We generated Utrn-A and -B promoter-specific antibodies, Taqman Polymerase chain reaction (PCR)-based absolute copy number assays, and luciferase-reporter constructs to study CNS of normal and dystrophic mdx mice. Differential expression of Utrn-A and -B was noted in microdissected and capillary-enr...
|
PMID: 19486009
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
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PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Neurochemical Research (35)3 2010
Abstract
We have adopted the PC12 cell line as in vitro cell model for studying Dp71 function in neuronal cells. These cells express a cytoplasmic (Dp71f) and a nuclear (Dp71d) isoform of Dp71 as well as various dystrophin-associated proteins (DAPs). In this study, we revealed by confocal microscopy analysis...
|
PMID: 19784870
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.
Muscle & Nerve (41)3 2010
Abstract
We hypothesize that this enhancement of the late phase of homosynaptic LTD may be due to a disruption of Ca(2+) homeostasis associated with the absence of the protein dystrophin. These findings may explain some of the central nervous system deficiencies reported in DMD boys....
|
PMID: 19722255
PDF is available here.
PDF is available here.