Anti-Syntrophin alpha 1 antibody [EPR14828] - BSA and Azide free

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

Syntrophin alpha 1 also known as SNTA1 or by its protein mass of about 53 kDa is an adaptor protein that plays an important role in linking the cytoskeleton to the cell membrane. It interacts with ion channels receptors and signaling proteins at the membrane. Syntrophin alpha 1 forms part of the dystrophin-associated protein complex important for structural integrity and signaling processes in muscle tissue. This protein sees expression mainly in skeletal and cardiac muscles as well as in the brain where it contributes to signal transduction and cellular architecture.

Biological function summary

Syntrophin alpha 1 contributes to maintaining muscular and neural function by organizing protein complexes at the cell membrane. It anchors various signaling molecules and is part of the dystrophin-glycoprotein complex. This involvement helps stabilize the muscle cell membrane during contraction and impact preventing damage. In neurons it modulates synaptic signaling and assists in maintaining cellular organization. The precise coordination of this protein with others in its complex ensures proper physiological responses to environmental stimuli.

Pathways

Syntrophin alpha 1 is a component of signaling pathways related to muscle contraction and neurological processes. It interfaces with the PI3K/AKT signaling pathway connected to cellular growth and the nitric oxide pathway that regulates muscle blood flow. Syntrophin alpha 1 is closely related to dystrophin in these pathways and together they interface with neuronal nitric oxide synthase (nNOS) modulating blood flow and synaptic activity. This partnership not only regulates physiological functions but also maintains cellular stability during stress.

Associated diseases and disorders

Alterations in syntrophin alpha 1 are associated with muscular dystrophies and cardiac conditions. Its malfunction contributes to disorders such as Duchenne muscular dystrophy where the absence of dystrophin disrupts the syntrophin-mediated membrane stability. Furthermore SNTA1 mutations can lead to long QT syndrome affecting cardiac electrical activity. In both cases the disturbance in syntrophin's interaction with dystrophin and nNOS contributes to disease progression leading to impaired muscle or cardiac function.