μ-protocadherin 抑制因子

Cadherin-dependent calcium-dependent cell adhesion is a crucial process in maintaining tissue structure and integrity in multicellular organisms. Cadherins, a class of transmembrane proteins, mediate this adhesion by forming homophilic interactions between adjacent cells in a calcium-dependent manner. The presence of calcium ions is essential for the structural stability of cadherins, as they promote the proper conformation for binding. These adhesion complexes are linked to the actin cytoskeleton via catenins, facilitating the transmission of intracellular signals that regulate cell behavior, morphology, and differentiation. The specificity and strength of cadherin-mediated adhesion play a vital role in processes like embryonic development, wound healing, and maintaining epithelial and endothelial barriers.

Targeting cadherins for disruption or inhibition involves intervening in the cadherin-mediated cell adhesion process, which can have significant implications in understanding cellular dynamics and disease processes. Small molecule inhibitors, peptides, or antibodies that specifically bind to cadherins can directly disrupt their adhesion function. Alternatively, modulation of the calcium levels in the cellular environment can indirectly impact cadherin stability and adhesion, as cadherins require calcium ions for their structural integrity and function. Targeting the post-translational modifications of cadherins, such as glycosylation, or interfering with the linkage between cadherins and catenins, can also disrupt cadherin-mediated adhesion. This targeted disruption of cadherins has been a focus in studies related to cancer metastasis, tissue development, and understanding the mechanisms of cell-cell interaction.