Anti-SLUG antibody

Supplementary info

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

Activity summary

SLUG also known as SNAI2 is a zinc finger transcription factor that plays a mechanical role in the regulation of genes implicated in cell differentiation and development. With an approximate mass of 29 kDa SLUG is expressed in various tissues particularly in the neural crest and epithelial-cell precursors. It acts as a repressor by binding to E-box motifs in the promoter regions of its target genes. SLUG functions in coordination with other cofactors to modulate gene expression that influences diverse biological processes including epithelial-mesenchymal transition (EMT).

Biological function summary

SLUG influences cell motility and invasion by controlling EMT a process critical for development and cancer metastasis. SLUG functions as a part of the Snail family of transcription factors and collaborates with other EMT-related molecules. It influences the expression of genes that maintain the epithelial phenotype facilitating the switch to a mesenchymal state required for increased cell mobility. Through these actions SLUG participates in the dynamic remodeling of tissues and is an important player during embryonic development and in certain pathological conditions.

Pathways

Researchers have associated SLUG with the TGF-beta and Wnt signaling pathways both essential for cell growth and differentiation. These pathways support SLUG's role in promoting EMT by modulating its transcriptional activity. SLUG often interacts with proteins such as TWIST1 and ZEB1 which synergistically act to downregulate epithelial markers and upregulate mesenchymal markers. This synergy highlights SLUG's significant role in facilitating changes in cellular architecture and function.

Associated diseases and disorders

SLUG shows a strong connection with the progression of cancers and fibrosis. It contributes to cancer metastasis through its competence in inducing EMT enabling tumor cells to invade and establish secondary tumors. In breast cancer SLUG correlates with increased invasiveness and poor prognosis. In fibrosis SLUG promotes tissue scarring by facilitating fibroblast activation and extracellular matrix deposition. SLUG has interactions with other proteins such as E-Cadherin where its repressing activity on E-Cadherin contributes to the disruption of cell-cell adhesion a hallmark of metastatic cells.