Anti-TLE3/ESG antibody [CL3573]

Supplementary info

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

Activity summary

TLE3 also known as ESG is a transcriptional corepressor with a molecular mass of around 80 kDa. It belongs to the transducin-like enhancer of split (TLE) family which interacts with DNA-binding proteins to modulate gene transcription. TLE3 is expressed mainly in the nucleus of cells and has notable expression in various tissues including the brain skeletal muscle and adipose tissues. Its mechanical role involves binding to nuclear receptors and influencing the transcriptional repression process by preventing the assembly of transcriptional activators on target genes.

Biological function summary

TLE3 serves as a critical modulator of differentiation pathways. It often functions as part of a broader repressor complex working closely with Groucho-related proteins. These complexes exert influence over cell lineage commitment and differentiation particularly in the context of adipogenesis and muscle development. TLE3 helps direct stem cell fate by repressing pro-differentiation signals maintaining cells in a less differentiated state until specific developmental cues trigger further differentiation.

Pathways

The function of TLE3 intersects with Wnt and Notch signaling pathways both essential for cellular growth and differentiation processes. TLE3 associates with proteins like TCF/LEF during Wnt signaling to suppress target gene activation therefore regulating cellular proliferation and differentiation. In the Notch pathway TLE3 interacts with the CSL transcription factor contributing to the repression of Notch-responsive genes which play a part in the maintenance of stem cell populations and tissue homeostasis.

Associated diseases and disorders

TLE3 shows a connection with cancer and metabolic syndromes. In cancer aberrant expression of TLE3 can lead to disrupted cell differentiation promoting oncogenesis. For example its interaction with TCF/LEF proteins in the Wnt pathway can affect tumor suppressor gene expression. In metabolic disorders TLE3 impacts adipogenesis contributing to obesity-linked insulin resistance. Dysregulation in these pathways linked to proteins like PPARγ highlights TLE3's role in disease pathophysiology and potential as a therapeutic target.