T1-cadherin inhibitors encompass a range of chemicals that target the adhesive functions of T1-cadherin directly or indirectly through associated pathways. Central to cadherins, including T1-cadherin, is their reliance on calcium for adhesive interactions. EGTA, a calcium chelator, directly impedes this calcium-dependent adhesive function by sequestering calcium ions. This disruption impacts the integrity of cadherin-mediated cell-cell junctions.
Alongside this direct approach, various compounds target pathways intertwined with cadherin-mediated signaling. The PI3K pathway is known to be an intersection for multiple cellular processes, including those mediated by cadherins. Compounds like LY294002 and Wortmannin inhibit the PI3K pathway, indirectly influencing T1-cadherin's functions. In the complex web of cellular signaling, T1-cadherin is also impacted by the Wnt/beta-catenin and TGF-beta pathways. Chemicals like XAV939, IWP-2, and SB431542 interfere with these pathways, thus wielding an indirect influence over T1-cadherin's role in cell adhesion and communication. Furthermore, the Notch signaling pathway, when modulated by DAPT, demonstrates the intricate network of pathways that have the capacity to impact T1-cadherin function.
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