Anti-alpha smooth muscle Actin antibody [ACTA2/791]

Supplementary info

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

Activity summary

Alpha smooth muscle actin (α-SMA) also known as ACTA2 is an actin isoform with a specific role in the contractile function of smooth muscle cells. The molecular weight of α-SMA is approximately 42 kDa. This protein is expressed widely in vascular smooth muscle cells the peritoneal lining and myofibroblasts. It often serves as a marker for these cell types. The expression of α-SMA is critical for the mechanical attributes of cells contributing to the rigidity and contractility of tissues where it is present.

Biological function summary

Alpha smooth muscle actin aids in maintaining the structural integrity of tissues by forming part of the actin cytoskeleton an important element in cellular support. It exists in high concentration in stress fibers contributing to cellular movements and shape maintenance. These actions are essential in various dynamic cellular processes such as cell migration and adhesion. Alpha smooth muscle actin does not typically form complexes but it associates with other components of the actin cytoskeleton to ensure cell stability and function.

Pathways

Alpha smooth muscle actin functions significantly within the TGF-beta signaling pathway which influences cell proliferation differentiation and apoptosis. It interacts closely with proteins such as myosin to facilitate cellular contractility and motility. Additionally α-SMA plays a part in the RhoA/Rho kinase (ROCK) pathway connecting with regulators of actin filament organization. These pathways are essential for modulation of smooth muscle contraction and actin filament assembly contributing to vascular development and wound healing.

Associated diseases and disorders

Alpha smooth muscle actin is importantly involved in fibrotic diseases and vascular diseases like arteriosclerosis. Increased expression of α-SMA is often observed in fibrotic tissues contributing to pathogenesis due to excessive extracellular matrix deposition. In the context of vascular disorders overexpression of α-SMA can lead to abnormal vascular remodeling often seen in diseases like hypertension. Interactions with proteins such as fibronectin and collagens facilitate these pathological changes highlighting the importance of α-SMA in disease development.