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utrophin gene expression was dominated by the full length transcript throughout embryogenesis.
clarify the role of Opa-1 and Drp-1 in mitochondrial dynamics and cell survival, a controversial alpha-synuclein research issue
In aortas of CKD rats and hippurate-treated rats, we observed an increase in Drp1 protein levels and mitochondrial fission. Inhibition of Drp1 improved endothelial function in both rat models. These results indicate that hippurate, by itself, can cause endothelial dysfunction. Increased mitochondrial fission plays an active role in hippurate-induced endothelial dysfunction via an increase in mitoROS
findings demonstrate that Drp1-mediated mitochondrial fission plays a critical role in the regulation of cell cycle progression and hepatocellular carcinoma cell proliferation
Knockdown of UTRN expression by shRNA evidently inhibited cell proliferation and promoted cell apoptosis in glioma cells.
Correlation of Utrophin Levels with the Dystrophin 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
probed the role of N-terminal CH1 and C-terminal CH2 domains in the structure and function of dystrophin tandem CH domain and compared with earlier results on utrophin to understand the unifying principles of how tandem CH domains work
targeting Drp1-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 domain, when compared to its CH2 domain.
this study demonstrated a pathway for Drp1 autophagic degradation. Chemical inhibition of lysosomal degradation and ATG7 knockdown increased Drp1 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-dependent declines in Drp1 and parkin levels contribute to altered mitochondrial morphology and cell death.
UAPC located in caveolae and non-caveolae lipid raft domains of HUVECs may have a mechanosensory function that could participate in the control of eNOS activity
Examined the thermodynamic stability and aggregation of utrophin N-ABD and compared with that of dystrophin. Utrophin N-ABD has decreased denaturant and thermal stability, unfolds faster, and is correspondingly more susceptible to proteolysis.
Homeobox protein engrailed-1 protein regulates transcription of the utrophin gene.
These results indicate that Drp1-dependent mitochondrial positioning and activity controls T-cell activation by fuelling central supramolecular activation cluster assembly at the immune synapse.
EN1 might be a negative regulatory factor for UTROPHIN.
The structural and functional properties of dystrophins and utrophins in brain, the consequences of dystrophins loss-of-function, are discussed.
Distribution of dystrophin- and utrophin-associated protein complexes during activation of human neutrophils.
This study demonstrates the contribution of Dp427 and utrophin in male fertility, suggesting a potential pathology in DMD patients.
Findings show that utrophin haploinsufficiency does not worsen the functional performance of mdx mice and the force production of EDL muscles suggest that the monoallelic expression level of utrophin is sufficient in mdx/utrn+/- mice to prevent further deterioration of the muscle.
Utrophin up-regulation by artificial transcription factors induces muscle rescue and impacts the neuromuscular junction in mdx mice.
Utrophin levels influence mitochondrial pathology and oxidative stress in mdx myofibers.
The functional improvement of dystrophic muscle achieved using let7-SBOs suggests a novel utrophin upregulation-based therapeutic strategy for Duchenne muscular dystrophy.
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 patients irrespective of their dystrophin mutation.
cap-independent mode has significant contribution as cap-dependent translation is severely repressed with utrophin-A 5'-UTR
Utrophin suppresses low frequency oscillations and coupled gating of mechanosensitive ion channels in dystrophic skeletal muscle
Sarcospan-mediated amelioration of muscular dystrophy in mouse model is dependent on the presence of both utrophin and alpha7beta1 integrin
Results showed that mdx/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.
5-amino-4-imidazolecarboxamide riboside treatment increases utrophin A and beta-dystroglycan expression in mdx mouse muscle.
utrophin depletion in dystrophin-deficient mdx muscle affects gating of mechanosensitive ion channels.
Dystrophin binds microtubules with high affinity and pauses microtubule polymerization, whereas utrophin does not.
at dystrophin levels < 4%, survival and motor function are greatly improved in a mdx/utrn-deficient model, which expresses a range of low dystrophin levels, depending on the degree of skewing of X inactivation in a utrophin-negative background
Data indicate that the functional benefits of TAT-muUtr replacement treatment extend to the dystrophin:utrophin(-/-) double-knockout mouse and support its development as a therapy to mitigate muscle weakness in patients with Duchenne muscular dystrophy.
utrophin expression require sarcospan
We report that dystrophin-utrophin double knockout mice exhibit a spectrum of degenerative changes, outside skeletal muscle, in bone, articular cartilage, and intervertebral discs.
Mice lacking utrophin and dystrophin (mdx/utrn -/-) are severely affected and die prematurely. Mice with one utrophin allele (mdx/utrn +/-) are more severely affected than mdx mice, but outlive mdx/utrn -/- mice.
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)