PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24876379-3 2014 The ceramide-to-S1P pathway is also implicated in the development of pain, raising the intriguing possibility that these sphingolipids may contribute to chemotherapy- induced painful peripheral neuropathy, which can be a critical dose-limiting side effect of many widely used chemotherapeutic agents.We demonstrate that the development of paclitaxel-induced neuropathic pain was associated with ceramide and S1P formation in the spinal dorsal horn that corresponded with the engagement of S1P receptor subtype 1 (S1PR(1))- dependent neuroinflammatory processes as follows: activation of redox-sensitive transcription factors (NFkappaB) and MAPKs (ERK and p38) as well as enhanced formation of pro-inflammatory and neuroexcitatory cytokines (TNF-alpha and IL-1beta). Sphingolipids 121-134 tumor necrosis factor Homo sapiens 741-750 26189109-0 2015 Differential changes in sphingolipids between TNF-induced necroptosis and apoptosis in U937 cells and necroptosis-resistant sublines. Sphingolipids 24-37 tumor necrosis factor Homo sapiens 46-49 26189109-1 2015 Differential changes in various sphingolipids between TNF-induced necroptosis and apoptosis were investigated using liquid chromatography-tandem mass spectrometry. Sphingolipids 32-45 tumor necrosis factor Homo sapiens 54-57 22973882-0 2012 Ceramide sphingolipid signaling mediates Tumor Necrosis Factor (TNF)-dependent toxicity via caspase signaling in dopaminergic neurons. Sphingolipids 9-21 tumor necrosis factor Homo sapiens 64-67 25180167-1 2014 AIMS: Sphingolipid and oxidant signaling affect glucose uptake, atrophy, and force production of skeletal muscle similarly and both are stimulated by tumor necrosis factor (TNF), suggesting a connection between systems. Sphingolipids 6-18 tumor necrosis factor Homo sapiens 150-171 25180167-1 2014 AIMS: Sphingolipid and oxidant signaling affect glucose uptake, atrophy, and force production of skeletal muscle similarly and both are stimulated by tumor necrosis factor (TNF), suggesting a connection between systems. Sphingolipids 6-18 tumor necrosis factor Homo sapiens 173-176 25180167-13 2014 INNOVATION: These findings identify nSMase3 as an intermediate that links TNF receptor activation, sphingolipid signaling, and skeletal muscle oxidant production. Sphingolipids 99-111 tumor necrosis factor Homo sapiens 74-77 23789954-5 2014 Three pathways have been identified: estrogen signaling to Bcrp, vascular endothelial growth factor signaling to P-glycoprotein and TNFalpha/PKC/ sphingolipid signaling to P-glycoprotein. Sphingolipids 146-158 tumor necrosis factor Homo sapiens 132-140 22884781-7 2012 In contrast, the addition of Th1 cytokines (GM-CSF/IFN-gamma/TNF-alpha) at concentrations of 2.5 or 10nM resulted in a slight increase in SC ceramide levels, which were accompanied by no change or an increase in the expression of those genes encoding sphingolipid metabolic enzymes in the epidermis. Sphingolipids 251-263 tumor necrosis factor Homo sapiens 61-70 22973882-3 2012 Here we investigated the contribution of ceramide sphingolipid signaling in TNF-dependent toxicity. Sphingolipids 50-62 tumor necrosis factor Homo sapiens 76-79 22973882-7 2012 CONCLUSIONS: We conclude that TNF/TNFR1-dependent activation of SMases generates ceramide and sphingolipid species that promote degeneration and caspase-dependent cell death of DA neurons. Sphingolipids 94-106 tumor necrosis factor Homo sapiens 30-33 22964618-2 2012 This enzyme deficiency results in an accumulation of sphingolipids in the cells of GD patients, which may contribute to the dysregulation of the immune system, B-cell dysfunction and expression of specific cytokines such as interleukin (IL) -1, IL-6, IL-8, IL-10, and tumor necrosis factor (TNF). Sphingolipids 53-66 tumor necrosis factor Homo sapiens 268-289 22964618-2 2012 This enzyme deficiency results in an accumulation of sphingolipids in the cells of GD patients, which may contribute to the dysregulation of the immune system, B-cell dysfunction and expression of specific cytokines such as interleukin (IL) -1, IL-6, IL-8, IL-10, and tumor necrosis factor (TNF). Sphingolipids 53-66 tumor necrosis factor Homo sapiens 291-294 17306937-3 2007 Although sphingolipids such as ceramide and sphingosine 1-phosphate (S1-P) have been shown to serve as signaling molecules in the TNF-alpha inflammatory response, their role in the TNF-alpha induction of IL-8 gene expression in lung epithelial cells is not known. Sphingolipids 9-22 tumor necrosis factor Homo sapiens 130-139 17306937-4 2007 We investigated the role of sphingolipids in the TNF-alpha induction of IL-8 gene expression in H441 lung epithelial cells. Sphingolipids 28-41 tumor necrosis factor Homo sapiens 49-58 22257771-0 2012 TNF-alpha- and tumor-induced skeletal muscle atrophy involves sphingolipid metabolism. Sphingolipids 62-74 tumor necrosis factor Homo sapiens 0-9 19328962-1 2009 We investigated the effects of the sphingolipid FTY720 on tumor necrosis factor-alpha (TNF-alpha)-induced proliferation and signal transduction in human smooth muscle cells (SMC). Sphingolipids 35-47 tumor necrosis factor Homo sapiens 58-85 19328962-1 2009 We investigated the effects of the sphingolipid FTY720 on tumor necrosis factor-alpha (TNF-alpha)-induced proliferation and signal transduction in human smooth muscle cells (SMC). Sphingolipids 35-47 tumor necrosis factor Homo sapiens 87-96 16450077-7 2006 We conclude that the antiatherogenic/antiinflammatory effect of lysosphingolipids depends on a competitive interaction of EDG receptor-induced inhibition and TNF-alpha-initiated stimulation of NF-kappaB translocation into the cell nucleus thereby preventing or stimulating inflammatory events in atherogenesis. Sphingolipids 64-81 tumor necrosis factor Homo sapiens 158-167 12732456-1 2003 Previous studies have shown that tumor necrosis factor alpha (TNFalpha) is involved in the pathogenic events following exposure to fumonisin B(1) (FB(1)), a potent inhibitor of ceramide synthase and sphingolipid biosynthesis. Sphingolipids 199-211 tumor necrosis factor Homo sapiens 33-60 16787207-1 2006 Ceramide, a product of sphingolipid metabolism, is generated in response to various stress stimuli, such as tumor necrosis factor-alpha, CD95/Fas, chemotherapeutic agents, and irradiation. Sphingolipids 23-35 tumor necrosis factor Homo sapiens 108-135 14752919-0 2003 [Sphingolipid signaling: a potential pathway for TNF-alpha induced preconditioning]. Sphingolipids 1-13 tumor necrosis factor Homo sapiens 49-58 15817701-6 2005 The role of TNF-alpha-induced activation of the sphingolipid cascade in this pathway was examined. Sphingolipids 48-60 tumor necrosis factor Homo sapiens 12-21 12732456-1 2003 Previous studies have shown that tumor necrosis factor alpha (TNFalpha) is involved in the pathogenic events following exposure to fumonisin B(1) (FB(1)), a potent inhibitor of ceramide synthase and sphingolipid biosynthesis. Sphingolipids 199-211 tumor necrosis factor Homo sapiens 62-70 12732456-2 2003 The intimate role of sphingolipid mediators in TNFalpha signaling and cellular death suggests that FB(1) may alter the sensitivity of cells to TNFalpha-induced apoptosis. Sphingolipids 21-33 tumor necrosis factor Homo sapiens 47-55 12732456-2 2003 The intimate role of sphingolipid mediators in TNFalpha signaling and cellular death suggests that FB(1) may alter the sensitivity of cells to TNFalpha-induced apoptosis. Sphingolipids 21-33 tumor necrosis factor Homo sapiens 143-151 11404253-3 2001 In this paper, we explore the signaling pathway employed by TNF-alpha using C2 ceramide as a cell-penetrating sphingolipid representative of the metabolites induced by TNF-alpha. Sphingolipids 110-122 tumor necrosis factor Homo sapiens 60-69 12753742-2 2003 Here we show that upon TNFalpha binding, TNFR1 translocates to cholesterol- and sphingolipid-enriched membrane microdomains, termed lipid rafts, where it associates with the Ser/Thr kinase RIP and the adaptor proteins TRADD and TRAF2, forming a signaling complex. Sphingolipids 80-92 tumor necrosis factor Homo sapiens 23-31 15041894-6 2003 Key components of TNF signaling include sphingolipids, particularly ceramide generated from acidic sphingomyelinase activation serving as a source for gangliosides. Sphingolipids 40-53 tumor necrosis factor Homo sapiens 18-21 14987386-0 2002 Sphingolipid signalling: molecular basis and role in TNF-alpha-induced cell death. Sphingolipids 0-12 tumor necrosis factor Homo sapiens 53-62 14987386-4 2002 This review summarises current knowledge of the signalling functions of sphingolipids, especially in the regulation of tumour necrosis factor [alpha] (TNF-[alpha])-mediated cytotoxic effects. Sphingolipids 72-85 tumor necrosis factor Homo sapiens 151-162 14987386-6 2002 On the basis of recent observations, a working model is proposed for the molecular mechanisms underlying regulation of sphingolipid generation following TNF-[alpha] receptor 1 activation. Sphingolipids 119-131 tumor necrosis factor Homo sapiens 153-164 11815603-1 2002 In C6 glioma cells, the sphingolipid second messenger ceramide potentiates expression of inducible nitric-oxide synthase (iNOS) induced by tumor necrosis factor alpha (TNF-alpha) without affecting GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme in the biosynthesis of 6(R)-5,6,7,8-tetrahydrobiopterin (BH(4)), a cofactor required for iNOS activity. Sphingolipids 24-36 tumor necrosis factor Homo sapiens 139-166 11815603-1 2002 In C6 glioma cells, the sphingolipid second messenger ceramide potentiates expression of inducible nitric-oxide synthase (iNOS) induced by tumor necrosis factor alpha (TNF-alpha) without affecting GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme in the biosynthesis of 6(R)-5,6,7,8-tetrahydrobiopterin (BH(4)), a cofactor required for iNOS activity. Sphingolipids 24-36 tumor necrosis factor Homo sapiens 168-177 11823712-3 2002 Using cellular models of ischemic tolerance, we have demonstrated that an effector of TNF-alpha-induced preconditioning is ceramide, a sphingolipid messenger in TNF-alpha signaling. Sphingolipids 135-147 tumor necrosis factor Homo sapiens 86-95 11823712-3 2002 Using cellular models of ischemic tolerance, we have demonstrated that an effector of TNF-alpha-induced preconditioning is ceramide, a sphingolipid messenger in TNF-alpha signaling. Sphingolipids 135-147 tumor necrosis factor Homo sapiens 161-170 11404253-3 2001 In this paper, we explore the signaling pathway employed by TNF-alpha using C2 ceramide as a cell-penetrating sphingolipid representative of the metabolites induced by TNF-alpha. Sphingolipids 110-122 tumor necrosis factor Homo sapiens 168-177 32050431-8 2020 In hCMEC/D3 cells, exogenous tumor necrosis factor alpha (TNFalpha) potently regulated gene expression of pro-inflammatory cytokines and a set of genes involved in sphingolipid (SL) homeostasis. Sphingolipids 164-176 tumor necrosis factor Homo sapiens 29-56 32528400-6 2020 In Alzheimer"s disease sphingolipids are involved in the processing and aggregation of beta-amyloid and in the transmission of the cytotoxic signal beta-amyloid and TNFalpha-induced. Sphingolipids 23-36 tumor necrosis factor Homo sapiens 165-173 10788433-5 2000 Ceramide, a sphingolipid metabolite, may mediate some of the actions of TNF-alpha. Sphingolipids 12-24 tumor necrosis factor Homo sapiens 72-81 33574879-9 2021 GO and KEGG enrichment analysis suggested that the common targets participated in diverse biological processes and pathways, including cell proliferation and apoptosis, inflammatory response, signal transduction, and protein phosphorylation through cancer pathway, MAPK signaling pathway, PI3K-Akt signaling pathway, HIF-1 signaling pathway, sphingolipid signaling pathway, FoxO signaling pathway, and TNF signaling pathway. Sphingolipids 342-354 tumor necrosis factor Homo sapiens 402-405 32050431-8 2020 In hCMEC/D3 cells, exogenous tumor necrosis factor alpha (TNFalpha) potently regulated gene expression of pro-inflammatory cytokines and a set of genes involved in sphingolipid (SL) homeostasis. Sphingolipids 164-176 tumor necrosis factor Homo sapiens 58-66 32050431-8 2020 In hCMEC/D3 cells, exogenous tumor necrosis factor alpha (TNFalpha) potently regulated gene expression of pro-inflammatory cytokines and a set of genes involved in sphingolipid (SL) homeostasis. Sphingolipids 178-180 tumor necrosis factor Homo sapiens 29-56 32050431-8 2020 In hCMEC/D3 cells, exogenous tumor necrosis factor alpha (TNFalpha) potently regulated gene expression of pro-inflammatory cytokines and a set of genes involved in sphingolipid (SL) homeostasis. Sphingolipids 178-180 tumor necrosis factor Homo sapiens 58-66 32050431-10 2020 In summary, our in vivo and in vitro data revealed that inflammatory mediators including MPO, TNFalpha induce dysfunctional SL homeostasis in brain endothelial cells. Sphingolipids 124-126 tumor necrosis factor Homo sapiens 94-102 32085881-5 2020 Sphingolipid signaling was identified as one of the key mediators and regulators of pro-inflammatory conditions, and, specifically, TNF-alpha related signaling. Sphingolipids 0-12 tumor necrosis factor Homo sapiens 132-141 30471562-0 2019 Vitamin E delta-tocotrienol inhibits TNF-alpha-stimulated NF-kappaB activation by up-regulation of anti-inflammatory A20 via modulation of sphingolipid including elevation of intracellular dihydroceramides. Sphingolipids 139-151 tumor necrosis factor Homo sapiens 37-46