Anti-Smad2 + Smad3 antibody

Supplementary info

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

Activity summary

Smad2 and Smad3 are intracellular proteins tightly involved in the TGF-β signaling pathway. These proteins also known as mothers against decapentaplegic homolog 2 and 3 play an important role in transmitting signals from the cell surface to the nucleus. Smad2 has a molecular weight of approximately 58 kDa while Smad3 is about 52 kDa. They are expressed in various tissues throughout the body including heart skin and immune cells. Upon activation Smad2 and Smad3 undergo phosphorylation a modification that is important for their function as signal transducers.

Biological function summary

The functions of Smad2 and Smad3 are critical in mediating cellular processes such as proliferation differentiation and apoptosis. These proteins often form complexes specifically oligomeric structures with other Smad proteins like co-Smad4 to exert their regulatory roles. The Smad2/3 complexes control the transcription of specific genes in response to TGF-β stimuli influencing cellular responses in a context-dependent manner.

Pathways

Smad2 and Smad3 are central to the TGF-β signaling pathway one significant pathway that affects cellular growth and differentiation. These proteins interact with TGF-β receptors on the cell surface to become phosphorylated forming a complex with Smad4 which then translocates to the nucleus. In the nucleus this complex regulates gene expression. Both Smad2 and Smad3 also engage with other signaling pathways such as the MAPK pathway further influencing cell behavior and cooperating with proteins like ERK.

Associated diseases and disorders

Smad2 and Smad3 have been linked to conditions like cancer and fibrosis. Dysregulation of Smad2/3 signaling often leads to unchecked cell proliferation a hallmark of tumorigenesis. In fibrosis excessive Smad2/3 activity contributes to tissue scarring due to increased extracellular matrix production. For instance their interaction with proteins like α-SMA (alpha-smooth muscle actin) in fibroblasts plays a role in cardiac and pulmonary fibrosis. Understanding their exact contribution provides insights into potential therapeutic targets for treating these diseases.