Results 11 to 20 of about 7,799 (249)
Translational regulation of utrophin by miRNAs. [PDF]
PLoS ONE, 2011 BackgroundUtrophin is the autosomal homolog of dystrophin, the product of the Duchenne Muscular Dystrophy (DMD) locus. Its regulation is of therapeutic interest as its overexpression can compensate for dystrophin's absence in animal models of DMD.
Utpal Basu +5 more
doaj +4 more sources
Utrophin: A Structural and Functional Comparison to Dystrophin [PDF]
Brain Pathology, 1996 Utrophin is an autosomally‐encoded homologue of dystrophin, the protein product of the Duchenne muscular dystrophy (DMD) gene. Although, Utrophin is very similar in sequence to dystrophin and possesses many of the protein‐binding properties ascribed to dystrophin, both proteins are expressed in an apparently reciprocal manner and may be coordinately ...
Derek J. Blake +2 more
openalex +3 more sources
Correction: Dystrophin- and Utrophin-Based Therapeutic Approaches for Treatment of Duchenne Muscular Dystrophy: A Comparative Review. [PDF]
BioDrugsSzwec S +3 more
europepmc +3 more sources
Molecular and Functional Analysis of the Utrophin Promoter [PDF]
Nucleic Acids Research, 1996 Utrophin is a ubiquitously expressed cytoskeletal protein which is an important structural component of the mammalian neuromuscular junction. It shows extensive sequence similarity to dystrophin leading to postulation that utrophin may be able to compensate for the absence of dystrophin in Duchenne muscular dystrophy (DMD) patients.
Cindi L. Dennis +3 more
openalex +3 more sources
Fundamental Research, 2022 Duchenne muscular dystrophy (DMD) is a serious genetic neuromuscular rare disease that is prevalent and caused by the mutation/deletion of the X-linked DMD gene that encodes dystrophin.
Ruo Wu +3 more
doaj +1 more source
Cis-Acting Sequence Elements and Upstream Open Reading Frame in Mouse Utrophin-A 5'-UTR Repress Cap-Dependent Translation. [PDF]
PLoS ONE, 2015 Utrophin, the autosomal homologue of dystrophin can functionally compensate for dystrophin deficiency. Utrophin upregulation could therefore be a therapeutic strategy in Duchenne Muscular Dystrophy (DMD) that arises from mutation in dystrophin gene.
Trinath Ghosh, Utpal Basu
doaj +1 more source
Fatigue Resistance and Mitochondrial Adaptations to Isometric Interval Training in Dystrophin-Deficient Muscle: Role of Contractile Load. [PDF]
FASEB JHigh‐load, but not low‐load, isometric interval training (IT) increased mitochondrial content and muscle fatigue resistance in mdx52 mice, a model for Duchenne muscular dystrophy. High‐load isometric IT restored citrate synthase activity, peroxisome proliferator‐activated receptor γ coactivator 1 alpha (PGC‐1α) expression, and mitochondrial complex II ...
Yamauchi N +7 more
europepmc +2 more sources
Hepatology, EarlyView., 2022 Adaptive mitochondrial mechanisms allow mitochondrial resilience and prevent the worsening of fibrosis, while deregulation of these mechanisms promotes the progression from no/minimal‐mild (F0‐F2) fibrosis to advanced fibrosis and cirrhosis (F3‐F4). Abstract Background and Aims Hepatitis B virus (HBV) infection causes oxidative stress (OS) and alters ...
Dimitri Loureiro +17 more
wiley +1 more source
Functional improvement of dystrophic muscle by repression of utrophin: let-7c interaction. [PDF]
PLoS ONE, 2017 Duchenne muscular dystrophy (DMD) is a fatal genetic disease caused by an absence of the 427kD muscle-specific dystrophin isoform. Utrophin is the autosomal homolog of dystrophin and when overexpressed, can compensate for the absence of dystrophin and ...
Manoj K Mishra +4 more
doaj +1 more source
Drug discovery for Duchenne muscular dystrophy via utrophin promoter activation screening. [PDF]
PLoS ONE, 2011 Duchenne muscular dystrophy (DMD) is a devastating muscle wasting disease caused by mutations in dystrophin, a muscle cytoskeletal protein. Utrophin is a homologue of dystrophin that can functionally compensate for its absence when expressed at increased
Catherine Moorwood +5 more
doaj +1 more source