PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24799565-3 2014 We show that treatment of macrophages with the pan caspase inhibitor (zVAD-FMK) results in both increased phosphorylation and decreased cleavage of receptor interacting protein kinase-1 (Rip1), leading to necroptosis that is dependent on autocrine TNF signaling. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 70-78 receptor interacting serine/threonine kinase 1 Homo sapiens 148-185 26028172-8 2015 Of note, the Receptor-Interacting Protein (RIP)1 inhibitor necrostatin-1 (Nec-1) or the Mixed Lineage Kinase Domain-Like protein (MLKL) inhibitor necrosulfonamide (NSA) significantly reduce BV6/MS275-induced cell death in the presence of zVAD.fmk, suggesting that BV6/MS275 cotreatment triggers necroptosis when caspases are inhibited. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 238-242 receptor interacting serine/threonine kinase 1 Homo sapiens 13-48 26111062-4 2015 However, we found that RIP1 is ubiquitinated with K63 and linear polyubiquitin chains during TNFalpha, IAP antagonist BV6 and caspase inhibitor zVAD-fmk-induced necroptotic signaling. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 144-152 receptor interacting serine/threonine kinase 1 Homo sapiens 23-27 26111062-8 2015 Knockdown of the E3 ligase c-IAP1 decreased RIP1 ubiquitination, necrosome assembly and necroptosis induced by TNFalpha, BV6 and zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 129-137 receptor interacting serine/threonine kinase 1 Homo sapiens 44-48 24799565-3 2014 We show that treatment of macrophages with the pan caspase inhibitor (zVAD-FMK) results in both increased phosphorylation and decreased cleavage of receptor interacting protein kinase-1 (Rip1), leading to necroptosis that is dependent on autocrine TNF signaling. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 70-78 receptor interacting serine/threonine kinase 1 Homo sapiens 187-191 24799565-4 2014 Stimulation of cells with TLR agonists such as LPS in the presence of zVAD-FMK also induced Rip1-phosphorylation via a TNFR-independent mechanism. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 70-78 receptor interacting serine/threonine kinase 1 Homo sapiens 92-96 17062895-5 2006 The underlying mechanism of zVAD-fmk-mediated sensitization to necrotic cell death involves the inhibition of caspase-8-mediated proteolysis of RIP1 and disturbance of the ANT-CypD interaction. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 28-36 receptor interacting serine/threonine kinase 1 Homo sapiens 144-148 24030154-7 2013 Importantly, BV6/DAC-induced cell death in the presence of zVAD.fmk is significantly reduced by pharmacological inhibition of key components of necroptosis signaling, that is, receptor-interacting protein (RIP) 1 using necrostatin-1 or mixed lineage kinase domain-like protein (MLKL) using necrosulfonamide. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 59-63 receptor interacting serine/threonine kinase 1 Homo sapiens 176-212 23410748-7 2013 The cleavage of RIP1, which plays a crucial role in TNF-induced necroptosis and is cleaved by caspase-8, was completely inhibited by Z-VAD-fmk or Z-DEVD-fmk, whereas the partial degradation of RIP1 was detected in the presence of Z-Asp-CH2-DCB. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 133-142 receptor interacting serine/threonine kinase 1 Homo sapiens 16-20 21049020-2 2010 In the presence of zVAD-fmk, a broad-spectrum caspase inhibitor, Fas engagement can also trigger an alternative, non-apoptotic caspase-independent form of cell death, which is initiated by RIP1. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 19-27 receptor interacting serine/threonine kinase 1 Homo sapiens 189-193 21985437-0 2012 RIP1 mediates the protection of geldanamycin on neuronal injury induced by oxygen-glucose deprivation combined with zVAD in primary cortical neurons. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 116-120 receptor interacting serine/threonine kinase 1 Homo sapiens 0-4 21985437-5 2012 In this study, we showed that oxygen-glucose deprivation (OGD) combined with a caspase inhibitor zVAD (OGD/zVAD)-induced RIP1 protein expression in a time-dependent manner. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 97-101 receptor interacting serine/threonine kinase 1 Homo sapiens 121-125 21985437-5 2012 In this study, we showed that oxygen-glucose deprivation (OGD) combined with a caspase inhibitor zVAD (OGD/zVAD)-induced RIP1 protein expression in a time-dependent manner. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 107-111 receptor interacting serine/threonine kinase 1 Homo sapiens 121-125 21985437-9 2012 We concluded that the GA-mediated protection against OGD/zVAD-induced neuronal injury was associated with enhanced RIP1 protein instability by decreasing Hsp90 protein level. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 57-61 receptor interacting serine/threonine kinase 1 Homo sapiens 115-119 34949739-4 2022 We showed that LPS/zVAD- and poly I:C/zVAD-induced cell death in bone marrow-derived macrophages (BMDMs) was inhibited by receptor-interacting protein kinase 1 (RIP1) inhibitor necrostatin-1 and autophagy inhibitor 3-methyladenine. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 19-23 receptor interacting serine/threonine kinase 1 Homo sapiens 122-159 34949739-4 2022 We showed that LPS/zVAD- and poly I:C/zVAD-induced cell death in bone marrow-derived macrophages (BMDMs) was inhibited by receptor-interacting protein kinase 1 (RIP1) inhibitor necrostatin-1 and autophagy inhibitor 3-methyladenine. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 38-42 receptor interacting serine/threonine kinase 1 Homo sapiens 161-165 34949739-10 2022 We conclude that enhanced TRIF-RIP1-dependent autocrine action of IFNbeta, rather than inhibition of ERK or Akt, is involved in TLRs/zVAD-induced autophagic and necroptotic cell death via the JAK/STAT1/ROS pathway. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 133-137 receptor interacting serine/threonine kinase 1 Homo sapiens 31-35 34949739-4 2022 We showed that LPS/zVAD- and poly I:C/zVAD-induced cell death in bone marrow-derived macrophages (BMDMs) was inhibited by receptor-interacting protein kinase 1 (RIP1) inhibitor necrostatin-1 and autophagy inhibitor 3-methyladenine. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 19-23 receptor interacting serine/threonine kinase 1 Homo sapiens 161-165 34949739-4 2022 We showed that LPS/zVAD- and poly I:C/zVAD-induced cell death in bone marrow-derived macrophages (BMDMs) was inhibited by receptor-interacting protein kinase 1 (RIP1) inhibitor necrostatin-1 and autophagy inhibitor 3-methyladenine. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 38-42 receptor interacting serine/threonine kinase 1 Homo sapiens 122-159 34826043-7 2021 After treatment with bufalin, the expressions of tumor necrosis factor alpha, phospho-tumor necrosis factor receptor 1, phospho-receptor interacting protein 1 and c-caspase 3 increased (all P<0.01), the killing effect of bufalin could be mostly inhibited by NEC-1, and by z-VAD-fmk (both P<0.01). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 272-281 receptor interacting serine/threonine kinase 1 Homo sapiens 128-158 30206205-6 2018 Thus, treatment with TNFR2/ZVAD enables TNFR1 in macrophages to stimulate gene induction via a pathway requiring RIPK1 kinase activity. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 27-31 receptor interacting serine/threonine kinase 1 Homo sapiens 113-118 31416203-6 2019 GTN and z-VAD-fmk induced human breast cancer MDA-MB-231 cells to undergo necroptosis via endoplasmic reticulum (ER) and oxidative stresses, with increased expressions of necroptotic genes such as rip1, rip3, and mlkl. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 8-17 receptor interacting serine/threonine kinase 1 Homo sapiens 197-201 28810529-7 2017 SM in presence of zVAD and 3-MA significantly decreased viability and proliferation of HT-29 cells, and expression of RIPK1 and RIPK3 in compare to absence the inhibitors. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 18-22 receptor interacting serine/threonine kinase 1 Homo sapiens 118-123 28088644-8 2017 RIP1 inhibitor necrostatin-1 (Nec-1), MLKL inhibitor necrosulfonamide (NSA) and silencing RIP1, RIP3, and MLKL inhibited t-BHPH-induced cell death while pan-caspase inhibitor Z-VAD-FMK showed no effect. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 175-184 receptor interacting serine/threonine kinase 1 Homo sapiens 0-4 27456663-9 2017 However, in the zVAD pretreated cells, necroptotic cell death with a significant increase in expression of RIP1, RIP3, and MLKL genes was observed Conclusion: The novel hybrid benzoxazole-coumarins effectively induce Caspase-3 dependent apoptosis in HN-5 cancer cells, but also could circumvent the blockage of apoptotic cell death by induction of necroptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 16-20 receptor interacting serine/threonine kinase 1 Homo sapiens 107-111 27752362-8 2016 Regarding the inhibitors, z-VAD-fmk diminishes the cleaved caspase 8, RIP1, RIP3, and MLKL induced by Tan IIA, and reconstructs the ripoptosome complex, which marks cells moving from apoptosis to necroptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 26-35 receptor interacting serine/threonine kinase 1 Homo sapiens 70-74