Since the non-canonical NF-B was responsible for the SM-induced upregulation of cell adhesion molecules, we investigated cluster formation in NIK-deficient T SB H sb 17 cells. SMAC also increases the homotypic interactions of T SB H sb 17 cells through a non-canonical NF-B-and integrin-mediated mechanism resulting in increased ability of T SB H sb 17 cells to withstand shear stress. CIAP1/2 antagonization by SMAC mimetic induces non-canonical NF-B mediated T_H 17 cell homotypic interactions and increases their resistance to shear stress The upregulation of cell adhesion and cytoskeletal organization genes prompted us to follow the SM-induced morphological changes in T SB H sb 17 cells.[Extracted from the article]

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