IndraLab
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"Additionally, while the effect of Y100 was abrogated by necrostatin-1 (an inhibitor of the necroptosis effector RIPK1), neither siRNA mediated knockdown of RIPK1 nor inhibition of RIPK3 with GSK ' 872 was sufficient to prevent Y100 mediated cell death (XREF_SUPPLEMENTARY and XREF_SUPPLEMENTARY)."
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"Treatment with RIPK1-specific inhibitors such as necrostatin-1 (Nec-1), GSK963 and 5-(3′,5 dimethoxybenzal)-2-thio-imidazole-4-ketone (DTIO) also reduced infarct volume and neurological deficit scores and significantly decreased ischemia-induced neuroinflammation and generation of reactive oxygen species (ROS) [15,25–27]."
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"Mechanistically, we show that inactivation of RIP1 by necrostatin-1 suppressed nuclear factor kappaB (NF-kappaB) cascade signals, including activation of IKKalpha, nuclear factor kappa B inhibitor protein alpha (IkappaBalpha), accumulation of nuclear p65 and NF-kappaB promoter activity."
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"By using a chemical approach, we showed that pretreatment of mice with Necrostatin-1 (Nec-1) (inhibitor of RIPK1) and/or PJ34 (inhibitor of PARP-1) significantly protected mice against concanavalin A (ConA) liver injury (aspartate amino-transferase (AST)/alanine amino-transferase (ALT)) associated with down-regulated hepatocyte specific IL-33 expression."
sparser
"Inhibition of RIP1 by necrostatin-1 did not inhibit A1-IRS activity, thereby excluding necroptosis ( xref ). xref We also looked for mitochondrial perturbation and did not observe any cytochrome C redistribution ( xref ) or ROS increase ( xref ) after incubation with A1-IRS, and mitochondria appeared normal when observed under electronic microscopy (data not shown)."
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"XREF_BIBR and XREF_BIBR Although inhibition of necroptosis by RIP3 deficiency, RIP1 blockade by necrostatin-1, or MLKL deficiency all reduce cell death at early time points, XREF_BIBR and XREF_BIBR RIP3 deficiency was unable to abrogate acetaminophen induced liver injury at 24 hours."
sparser
"Furthermore, necrostatin-1, which inhibits RIPK1, a central regulator of necroptosis ( xref ), did not improve cell viability after combination treatment with lapatinib and FTY720, although necrostatin-1 significantly improved cell viability after gefitinib treatment under starvation conditions that induce necroptosis. ( xref and xref )."
sparser
"In line with its essential role in programmed necrosis, pharmacological inhibition of RIPK1 by necrostatin-1 protected the same subset of sensitive tumor cell lines that we had used for analysis in Figure xref d (resistant KNS-62 cells were again included as control) from both TRAIL/zVAD/CHX- and TNF/zVAD/CHX-induced programmed necrosis (Figure xref a)."
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"Previous studies have reported that pharmacological inhibition of RIPK1 by necrostatin-1 (Nec-1) or Nec-1 stable (Nec-1s) showed neuroprotective effects in 6-hydroxydopamine (OHDA)-treated PC12 cells, neural cells derived from induced pluripotent stem cells of PD patients with OPA1 gene mutations, and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice ."
sparser
"However, it should be noted that, although inhibition of RIP1 kinase by necrostatin-1 did not have an effect on the cytotoxic activity of NaD1, the ability of NaD1 to effect the necroptotic pathway downstream of RIP1 kinase activity, such as via direct modulation of MLKL-mediated membrane disruption, xref not addressed in our current study should be determined to eliminate definitively necroptosis as having a role."
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"In line with its essential role in programmed necrosis, pharmacological inhibition of RIPK1 by necrostatin-1 protected the same subset of sensitive tumor cell lines that we had used for analysis in Figure XREF_FIG d (resistant KNS-62 cells were again included as control) from both TRAIL/zVAD/CHX- and TNF/zVAD/CHX induced programmed necrosis."
sparser
"Previous studies have reported that pharmacological inhibition of RIPK1 by necrostatin-1 (Nec-1) or Nec-1 stable (Nec-1s) showed neuroprotective effects in 6-hydroxydopamine (OHDA)-treated PC12 cells, neural cells derived from induced pluripotent stem cells of PD patients with OPA1 gene mutations, and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice xref , xref ."
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"Furthermore, necrostatin-1, which inhibits RIPK1, a central regulator of necroptosis (47), did not improve cell viability after combination treatment with lapatinib and FTY720, although necrostatin-1 significantly improved cell viability after gefitinib treatment under starvation conditions that induce necroptosis."