Date published: 2025-9-14

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TNF-IP 8L2 Inhibitors

Chemical inhibitors of TNF-IP 8L2 can modulate various cellular processes by interfering with the protein's role in apoptosis, necroptosis, cytoskeletal remodeling, and cell survival pathways. Z-VAD-FMK is a broad-spectrum caspase inhibitor that can prevent apoptosis by blocking the caspase enzymes that TNF-IP 8L2 may regulate. Similarly, Necrostatin-1, by inhibiting RIPK1, can disrupt necroptosis, a programmed form of necrosis linked with TNF-IP 8L2. In the context of cellular architecture, NSC 23766 disrupts the interaction of Rac1 with its GEFs, potentially altering the cytoskeletal organization and cellular remodeling processes associated with TNF-IP 8L2's function. LY294002 and Wortmannin, both inhibitors of PI3K, can obstruct the PI3K signaling pathway, thereby affecting the role of TNF-IP 8L2 in cell proliferation and survival.

Further manipulation of signaling pathways relevant to TNF-IP 8L2's functional role includes the use of PD98059 and U0126, which are selective inhibitors of the MEK1/2 enzymes in the MAPK/ERK pathway, a pathway known to be involved in cell proliferation and survival. Inhibiting this pathway can alter the function of TNF-IP 8L2 in these processes. SB203580 and SP600125 target the p38 MAPK and JNK signaling pathways, respectively, both of which are involved in cellular stress responses. By inhibiting these kinases, the ability of TNF-IP 8L2 to influence stress response pathways is affected. BAY 11-7082 interferes with the NF-κB signaling pathway, which is central to inflammation and cell survival, and thus can alter TNF-IP 8L2's role in these processes. Lastly, Y-27632 inhibits ROCK, potentially affecting TNF-IP 8L2's involvement in actin cytoskeleton organization, while MG-132's inhibition of proteasome activity can prevent the degradation of proteins that interact with or regulate TNF-IP 8L2.

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