Recombinant Human CTNNBIP1/ICAT protein (His tag N-Terminus)

Supplementary information

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

The CTNNBIP1 protein also known as ICAT (Inhibitor of beta-catenin and TCF-4) is a small protein with a molecular mass of approximately 8 kDa. It is located mainly in the cytoplasm of cells. ICAT functions by interacting directly with beta-catenin which is an important component of the Wnt signaling pathway. CTNNBIP1 negatively regulates the signaling events by preventing the formation of the beta-catenin/TCF transcriptional complex. This inhibition plays a significant role in controlling the transcriptional activity mediated by beta-catenin influencing cell proliferation and differentiation.

Biological function summary

CTNNBIP1 affects the transcriptional regulation processes by its interaction with the beta-catenin and TCF-4 transcription factor complex. This interaction inhibits the association between beta-catenin and TCF-4 which in turn influences Wnt target gene expression. CTNNBIP1 as part of the beta-catenin regulatory complex modulates gene transcription that is important for developmental processes and maintenance of cell fate decisions. By preventing excessive beta-catenin transcriptional activity the protein contributes to maintaining cellular homeostasis.

Pathways

CTNNBIP1 is involved in the Wnt signaling pathway a critical pathway for regulating cell growth cell fate determination and embryonic development. The Wnt pathway contrasts between beta-catenin interactions with ICAT versus TCF/LEF family members which guide transcriptional changes. CTNNBIP1 balances beta-catenin availability competing with TCF/LEF for binding therefore modulating downstream effects. This regulation has impacts on other complexes such as GSK-3β which phosphorylates beta-catenin marking it for degradation and thereby influencing pathway flux.

CTNNBIP1 is linked to conditions like cancer and neurodevelopmental disorders. Dysregulation of the Wnt signaling often due to mutations or altered expression of CTNNBIP1 can contribute to oncogenesis particularly in colorectal cancer. Alterations in beta-catenin interactions are an important factor in tumor progression as abnormal signaling leads to uncontrolled cellular proliferation. Additionally disruption in CTNNBIP1 function or expression implicates neurological conditions through altered signaling balance with potential involvement in disorders such as schizophrenia. These conditions highlight the importance of CTNNBIP1 in maintaining normal cellular communication and genome regulation.