IndraLab

Statements

NAC inhibits RIPK1. 10 / 10
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"In this study, the addition of NAC effectively reduced EtOH treatment necroptosis of the osteoblastic cells as NAC attenuated the upregulation of RIPK1 and RIPK3 (Figure 6(g))."
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"In our study, NAC and AAP inactivated RIPK1 and RIPK3 that led to the reduction of H 2 O 2 -induced necroptosis (XREF_FIG)."
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"We found that pretreatment with NAC attenuated the increase in RIPK1, RIPK3, and MLKL induced by shikonin treatment (Figure 3C and D)."
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"It has been reported that ROS promotes necroptosis by a positive feedback mechanism in osteoblastic cells, while ROS inhibitor N-acetylcysteine (NAC) attenuates the up-regulation of RIPK1, RIPK3 and MLKL, and the RIP1 inhibitor necrostatin-1 (Nec-1) reduced ROS generation [17]."
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"In TCMK-1 cells, Klotho and NAC attenuated the elevation in RIP1, RIP3, and LDH release induced by H/R or H2O2."
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"The current study showed that ASX-induced necroptosis was mediated via NADPH oxidase and ROS, as well as the activation of RIP1-RIP3, as Nec-1 (a specific inhibitor of RIP1), NAC (an antioxidant) and ML171 (an NADPH oxidase inhibitor) significantly suppressed the number of PI-positive AGS cells.RIP3 binds to the plasma membrane and induces the phosphorylation of MLKL, which induces the oligomerization of p-MLKL to induce plasma membrane rupture and necroptosis (49)."
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"As shown in Fig. 1 E, pretreatment with NAC significantly attenuated APAP-induced upregulation of hepatic RIP1."
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"NAC, a GSH precursor, almost completely inhibited APAP-induced elevation of hepatic RIP1 and its downstream molecule RIP3."
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"Necrostatin-1-mediated treatment effectively inhibits the RIPK1/RIPK3/MLKL-dependent signaling, and NAC partly prevents the production of ROS and decreases the activation of necroptosis through a positive feedback loop involving RIPK1/RIPK3 and finally ameliorates alcohol-induced osteopenia by reducing osteoblast necroptosis."
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"NAC (ROS inhibitor) inhibited RIP1, RIP3, and increased ATF4; however, necrostatin-1 (Nec-1) (RIP1 inhibitor) specifically inhibited the protein expression of RIP1 and RIP3 and had no influence on ATF4."
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