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Ordered disorder of the astrocytic dystrophin (zeige DMD Proteine)-associated protein complex in the norm and pathology.
Data indicate that alpha-syntrophin plays an important role in the regulation of oxidative stress from endogenously generated reactive oxygen species (ROS (zeige ROS1 Proteine)) during myoblast differentiation by modulating the protein stability of catalase (zeige CAT Proteine).
alpha-syntrophin plays a pivotal role in the survival pathway triggered by menadione-induced oxidative stress in cultured myoblasts.
Alpha-syntrophin deficiency markedly reduces astrocyte swelling during severe hypoosmotic stress/brain edema.
Isolated muscle bundles from SNTA1 mutant mice showed reduced force production after hypo-osmotic shock. In addition, the mutant muscle bundles showed delayed recovery of specific gravity after being exposed to hypo-osmotic conditions.
alpha-Syntrophin, which resides in nuclei of myocytes, functions as the upstream mediator of nuclear nNOS (zeige NOS1 Proteine) translocation and nNOS (zeige NOS1 Proteine)-dependent mitochondrial biogenesis.
the removal of the perivascular pool of AQP4 (zeige AQP4 Proteine) due to alpha-syntrophin deletion reduces edema formation, especially under pathological conditions and during states associated with elevated K+.
Scaffold proteins alpha-syntrophin and dystrophin (zeige DMD Proteine) exhibit lower densities in retinal microglia compared with brain astrocytes.
The interaction between the conserved COOH-terminal 125-amino acid domain (which is located in the light chains of MAP1A (zeige MAP1A Proteine), MAP1B (zeige MAP1B Proteine), and MAP1S (zeige MAP1S Proteine)) and alpha1-syntrophin is direct and occurs through the pleckstrin (zeige PLEK Proteine) homology domain 2 (PH2 (zeige PhC2 Proteine)).
Data show that in Dp71 (zeige DMD Proteine)-null mice, the levels of beta-dystroglycan (beta-DG) and alpha1-syntrophin (alpha1-Syn (zeige SYP Proteine)) were lower and utrophin expression did not change, and the neuronal nitric oxide synthase (nNOS (zeige NOS1 Proteine)) expression and activity were increased.
A novel SNTA1 variant is likely causative for drug induced long-QT syndrome by augmenting the late sodium current.
In a nonreferred nationwide Danish cohort of SIDS (zeige IDS Proteine) cases, up to 5/66 (7.5%) of SIDS (zeige IDS Proteine) cases can be explained by genetic variants in the sodium channel complex genes.
our results present a possible mechanism of Rac1 activation involving SNTA1 and emphasise its role in ROS (zeige ROS1 Proteine) generation, cell migration, and acquisition of malignancy.
Calcium homeostasis mishandling in Duchenne muscular dystrophy (zeige DMD Proteine) myotubes depends on store operated calcium entry under the influence alpha1-syntrophin regulation as well as TRPV2 (zeige TRPV2 Proteine)-dependant cation influx.
The combined mutations of A261V-SNTA1 plus R800L-SCN5A (zeige SCN5A Proteine) increase the INa (zeige INA Proteine) current late/peak ratio and time constants of current decay.
In contrast to stomach, lung, colon and rectal cancers, SNTA1 protein was found to be downregulated in esophageal cancers and upregulated in breast cancer.
alpha1D-adrenergic receptors are regulated by syntrophins through a PDZ domain-mediated interaction
These results establish an SNTA1-based nNOS (zeige NOS1 Proteine) complex attached to SCN5A (zeige SCN5A Proteine) as a key regulator of sodium current and suggest that SNTA1 be considered a rare long QT syndrome-susceptibility gene.
Syntrophins are cytoplasmic peripheral membrane scaffold proteins that are components of the dystrophin-associated protein complex. This gene is a member of the syntrophin gene family and encodes the most common syntrophin isoform found in cardiac tissues. The N-terminal PDZ domain of this syntrophin protein interacts with the C-terminus of the pore-forming alpha subunit (SCN5A) of the cardiac sodium channel Nav1.5. This protein also associates cardiac sodium channels with the nitric oxide synthase-PMCA4b (plasma membrane Ca-ATPase subtype 4b) complex in cardiomyocytes. This gene is a susceptibility locus for Long-QT syndrome (LQT) - an inherited disorder associated with sudden cardiac death from arrhythmia - and sudden infant death syndrome (SIDS). This protein also associates with dystrophin and dystrophin-related proteins at the neuromuscular junction and alters intracellular calcium ion levels in muscle tissue.
syntrophin, alpha 1 (dystrophin-associated protein A1, 59kDa, acidic component)
, 59 kDa dystrophin-associated protein A1 acidic component 1
, acidic alpha 1 syntrophin
, dystrophin-associated protein A1, 59kDa, acidic component
, pro-TGF-alpha cytoplasmic domain-interacting protein 1
, syntrophin, acidic 1
, 59-1 DAP