Date published: 2025-11-7

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MS4A4D Inhibitors

Chemical inhibitors of MS4A4D function through various mechanisms to impede its activity by targeting signaling pathways that are crucial for its activation. Genistein operates by obstructing tyrosine kinase-dependent signaling pathways, which are essential for phosphorylation events that activate MS4A4D. Similarly, PP2 contributes to the inhibition by selectively preventing Src family kinases from phosphorylating their substrates; this action is vital as these kinases are requisite for the activation of several proteins, including MS4A4D. LY294002 and Wortmannin both serve as PI3K inhibitors and impede the PI3K/Akt signaling pathway. By inhibiting this pathway, these chemicals lead to a decrease in the activation of downstream proteins such as MS4A4D, which require this route for proper function. Furthermore, PD98059 and U0126, both MEK inhibitors, inhibit the MAPK/ERK pathway. Disrupting this pathway is instrumental in precluding the necessary phosphorylation events that would otherwise facilitate MS4A4D activity.

Additional compounds like SB203580, a p38 MAPK inhibitor, and SP600125, a JNK inhibitor, obstruct their respective MAPK pathways, thereby inhibiting the functional activation of MS4A4D. This effect arises because MS4A4D is contingent on the signaling mediated by these kinases for its activity. Rapamycin, an mTOR inhibitor, inhibits the mTOR signaling pathway; this pathway is a central conduit for various cellular processes, and its inhibition results in reduced activity of proteins potentially regulated by mTOR, including MS4A4D. Y-27632 acts as a ROCK inhibitor, impeding the Rho/ROCK pathway and, consequently, the activity of MS4A4D which may be regulated by this route. ZM-447439 targets Aurora kinases, whose inhibition disrupts the associated kinase-dependent pathways that could regulate MS4A4D activity. Lastly, Bortezomib, by inhibiting the proteasome, prevents the degradation of regulatory proteins, thereby leading to an indirect inhibition of MS4A4D by stabilizing proteins that maintain MS4A4D in an inactive state.

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