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utrophin gene expression was dominated by the full length transcript throughout embryogenesis.
Knockdown of UTRN expression by shRNA evidently inhibited cell proliferation and promoted cell apoptosis in glioma cells.
Correlation of Utrophin Levels with the Dystrophin (zeige DMD ELISA Kits) Protein Complex and Muscle Fibre Regeneration in Duchenne and Becker Muscular Dystrophy Muscle Biopsies.
there is an inverse correlation between the level of muscle fibrosis and the level of utrophin and that of the number of revertant myofibers in Duchenne muscular dystrophy (zeige DMD ELISA Kits)
probed the role of N-terminal CH1 (zeige SUCO ELISA Kits) and C-terminal CH2 (zeige Acyp1 ELISA Kits) domains in the structure and function of dystrophin (zeige DMD ELISA Kits) tandem CH domain and compared with earlier results on utrophin to understand the unifying principles of how tandem CH domains work
targeting Drp1 (zeige CRMP1 ELISA Kits)-dependent mitochondrial dynamics may provide a novel strategy to suppress breast cancer metastasis and improve the chemotherapeutic effect in the future
The actin binding affinity of the utrophin tandem calponin-homology domain (CH) is determined by its CH1 (zeige SUCO ELISA Kits) domain, when compared to its CH2 (zeige Acyp1 ELISA Kits) domain.
this study demonstrated a pathway for Drp1 (zeige CRMP1 ELISA Kits) autophagic degradation. Chemical inhibition of lysosomal degradation and ATG7 (zeige ATG7 ELISA Kits) knockdown increased Drp1 (zeige CRMP1 ELISA Kits) levels.
UtroUp recognises 18 base pairs of the utrophin promoter and efficiently drives utrophin upregulation.
This family study showed that the 6q24.2 mircoduplication of the utrophin gene is a potential risk factor for the development of annular pancreas.
The present findings demonstrate that genotoxic stress in neurons results in p53 (zeige TP53 ELISA Kits)-dependent declines in Drp1 (zeige CRMP1 ELISA Kits) and parkin (zeige PARK2 ELISA Kits) levels contribute to altered mitochondrial morphology and cell death.
The functional improvement of dystrophic muscle achieved using let7-SBOs suggests a novel utrophin upregulation-based therapeutic strategy for Duchenne muscular dystrophy (zeige DMD ELISA Kits).
Results support the hypothesis that utrophin is not involved in extraocular muscle sparing in mdx:utrophin(+/-) and mdx:utrophin(-/-) mice
This detailed evaluation of the SMT C1100 drug series strongly endorses the therapeutic potential of utrophin modulation as a disease modifying therapeutic strategy for all Duchenne muscular dystrophy (zeige DMD ELISA Kits) patients irrespective of their dystrophin (zeige DMD ELISA Kits) mutation.
cap-independent mode has significant contribution as cap-dependent translation is severely repressed with utrophin-A 5'-UTR (zeige UTS2R ELISA Kits)
Utrophin suppresses low frequency oscillations and coupled gating of mechanosensitive ion channels in dystrophic skeletal muscle
Sarcospan (zeige SSPN ELISA Kits)-mediated amelioration of muscular dystrophy in mouse model is dependent on the presence of both utrophin and alpha7beta1 integrin
Results showed that mdx (zeige DMD ELISA Kits)/utrn+/- mouse develops fibrosis in both hind limb and respiratory skeletal muscles at a young age while not being so affected such that it dies prematurely, this model may be an appropriate for Duchenne muscular dystrophy (zeige DMD ELISA Kits).
5-amino-4-imidazolecarboxamide riboside treatment increases utrophin A and beta-dystroglycan expression in mdx (zeige DMD ELISA Kits) mouse muscle.
utrophin depletion in dystrophin (zeige DMD ELISA Kits)-deficient mdx (zeige DMD ELISA Kits) muscle affects gating of mechanosensitive ion channels.
This gene shares both structural and functional similarities with the dystrophin gene. It contains an actin-binding N-terminus, a triple coiled-coil repeat central region, and a C-terminus that consists of protein-protein interaction motifs which interact with dystroglycan protein components. The protein encoded by this gene is located at the neuromuscular synapse and myotendinous junctions, where it participates in post-synaptic membrane maintenance and acetylcholine receptor clustering. Mouse studies suggest that this gene may serve as a functional substitute for the dystrophin gene and therefore, may serve as a potential therapeutic alternative to muscular dystrophy which is caused by mutations in the dystrophin gene. Alternative splicing of the utrophin gene has been described\; however, the full-length nature of these variants has not yet been determined.
, utrophin, or dystrophin-related protein 1
, dystrophin-related protein 1
, utrophin (homologous to dystrophin)