Anti-TAGLN/Transgelin antibody [TAGLN/247] - BSA and Azide free

Supplementary info

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

Activity summary

TAGLN also known as Transgelin or SM22-alpha is a protein with a molecular weight of approximately 22 kDa. Structurally it belongs to the calponin family and contains an ACT domain which is critical for its actin-binding ability. It is expressed abundantly in smooth muscle cells where it stabilizes cytoskeletal dynamics by interacting with actin filaments. TAGLN also shows expression in fibroblasts and myofibroblasts supporting structural integrity and cellular movement.

Biological function summary

The regulatory involvement of TAGLN in smooth muscle contraction influences cellular activities essential for vascular function. This protein modulates remodeling and differentiation within smooth muscle cells. It can associate with actin and calponin to form complexes that regulate the stability of cytoskeletal structures ensuring effective cellular responses to mechanical stimuli. By linking signal transduction to cytoskeletal mechanics TAGLN facilitates the maintenance of cell shape and tension.

Pathways

TAGLN plays a role in the regulation of the RhoA/Rho kinase pathway contributing to actin cytoskeleton organization and smooth muscle contraction. Additionally it is involved in the WNT signaling pathway influencing cell proliferation and differentiation. In these pathways TAGLN works with proteins like RhoA and beta-catenin to transmit signals from the extracellular environment to the nucleus impacting gene expression and cellular responses.

Associated diseases and disorders

Disruptions in TAGLN expression associate with vascular diseases and certain cancers. Downregulation or altered expression patterns can lead to smooth muscle cell dysfunction contributing to atherosclerosis. Similarly TAGLN interacts with proteins such as fibronectin and MMP2 in cancer where its altered expression could promote metastasis and tumor progression. Understanding these connections highlights TAGLN's potential as a target for therapeutic interventions in these diseases.