PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12063170-9 2002 It is known that Taxol, but not other microtubule-interacting agents, induces the production of cytokines, such as tumor necrosis factor alpha (TNF-alpha) in mouse macrophages. Paclitaxel 17-22 tumor necrosis factor Mus musculus 115-142 24853387-11 2015 Finally, both acute and chronic administration of AM1710 decreased messenger RNA levels of tumor necrosis factor-alpha and monocyte chemoattractant protein 1 in lumbar spinal cord of paclitaxel-treated WT mice. Paclitaxel 183-193 tumor necrosis factor Mus musculus 91-118 23318472-5 2013 The beneficial effects of paclitaxel were accompanied by the downregulation of tumor necrosis factor-alpha, interleukin-1, and interleukin-6 production. Paclitaxel 26-36 tumor necrosis factor Mus musculus 79-106 20434553-9 2010 Incubation of a murine macrophage-like cell line with paclitaxel significantly increased TNF-alpha and -10 released from the cells and expression of microRNAs such as miR-155, miR-147, miR-146a and miR-132. Paclitaxel 54-64 tumor necrosis factor Mus musculus 89-106 17463156-6 2007 Finally, there was a significant decrease in TNF-alpha and nitric oxide but not IL-12p40 when macrophages were cultured with lipopolysaccharide (LPS) and either paclitaxel or peloruside. Paclitaxel 161-171 tumor necrosis factor Mus musculus 45-54 25564714-12 2015 Of interest, prior TAX administration could also sensitize to TNF-induced apoptosis in the Yoshida AH-130 hepatoma transplanted in mice. Paclitaxel 19-22 tumor necrosis factor Mus musculus 62-65 18161023-3 2008 Compared with paclitaxel or MDP alone or with a mixture of paclitaxel + MDP, 2"- O -MTC-01 significantly increases the production and expression of TNF-alpha and IL-12 from mouse peritoneal macrophages, which demonstrates a synergism of MDP and paclitaxel in one conjugated molecule. Paclitaxel 59-69 tumor necrosis factor Mus musculus 148-157 18161023-3 2008 Compared with paclitaxel or MDP alone or with a mixture of paclitaxel + MDP, 2"- O -MTC-01 significantly increases the production and expression of TNF-alpha and IL-12 from mouse peritoneal macrophages, which demonstrates a synergism of MDP and paclitaxel in one conjugated molecule. Paclitaxel 59-69 tumor necrosis factor Mus musculus 148-157 17127735-8 2006 TNFalpha, IFNgamma, and IL-10 production were all significantly inhibited in the paclitaxel-treated mice. Paclitaxel 81-91 tumor necrosis factor Mus musculus 0-8 12063170-9 2002 It is known that Taxol, but not other microtubule-interacting agents, induces the production of cytokines, such as tumor necrosis factor alpha (TNF-alpha) in mouse macrophages. Paclitaxel 17-22 tumor necrosis factor Mus musculus 144-153 12063170-10 2002 The time course of Taxol-induced TNF-alpha expression coincides with that of Taxol-induced p66shc phosphorylation, and U0126 inhibits significantly Taxol-induced TNF-alpha expression in RAW 264.7 cells. Paclitaxel 19-24 tumor necrosis factor Mus musculus 33-42 12063170-11 2002 Our data indicate that the Taxol-induced serine phosphorylation of p66shc in RAW 264.7 cells is microtubule-independent and may be related to increased TNF-alpha expression after Taxol and LPS treatment. Paclitaxel 27-32 tumor necrosis factor Mus musculus 152-161 12063170-11 2002 Our data indicate that the Taxol-induced serine phosphorylation of p66shc in RAW 264.7 cells is microtubule-independent and may be related to increased TNF-alpha expression after Taxol and LPS treatment. Paclitaxel 179-184 tumor necrosis factor Mus musculus 152-161 9588177-0 1998 Structural significance of the benzoyl group at the C-3"-N position of paclitaxel for nitric oxide and tumor necrosis factor production by murine macrophages. Paclitaxel 71-81 tumor necrosis factor Mus musculus 103-124 11500829-4 2001 When stimulated with Taxol, macrophages from wild-type mice responded robustly by secreting both TNF and NO, while macrophages from either TLR4-deficient C57BL/10ScNCr mice or MyD88 knockout mice produced only minimal amounts of TNF and NO. Paclitaxel 21-26 tumor necrosis factor Mus musculus 97-100 11500829-4 2001 When stimulated with Taxol, macrophages from wild-type mice responded robustly by secreting both TNF and NO, while macrophages from either TLR4-deficient C57BL/10ScNCr mice or MyD88 knockout mice produced only minimal amounts of TNF and NO. Paclitaxel 21-26 tumor necrosis factor Mus musculus 229-232 10930572-0 2000 Structural significance of the acyl group at the C-10 position and the A ring of the taxane core of paclitaxel for inducing nitric oxide and tumor necrosis factor production by murine macrophages. Paclitaxel 100-110 tumor necrosis factor Mus musculus 141-162 10930572-2 2000 Various synthetic analogs of paclitaxel were examined for their potencies to induce nitric oxide (NO) and tumor necrosis factor (TNF) production by murine peritoneal Mphi, and by human peripheral blood cells. Paclitaxel 29-39 tumor necrosis factor Mus musculus 106-127 10930572-2 2000 Various synthetic analogs of paclitaxel were examined for their potencies to induce nitric oxide (NO) and tumor necrosis factor (TNF) production by murine peritoneal Mphi, and by human peripheral blood cells. Paclitaxel 29-39 tumor necrosis factor Mus musculus 129-132 9588177-2 1998 Recently, we have shown that the benzoyl group at the C-3" position of paclitaxel is the most important site to induce nitric oxide (NO) and tumor necrosis factor (TNF) production by C3H/HeN M phi (Biochem. Paclitaxel 71-81 tumor necrosis factor Mus musculus 141-162 9588177-2 1998 Recently, we have shown that the benzoyl group at the C-3" position of paclitaxel is the most important site to induce nitric oxide (NO) and tumor necrosis factor (TNF) production by C3H/HeN M phi (Biochem. Paclitaxel 71-81 tumor necrosis factor Mus musculus 164-167 9588177-7 1998 In the present study, synthetic analogs of paclitaxel with replacement of the C-3"-N position were examined for their potencies to induce NO and TNF production by peritoneal M phi of LPS-responsive C3H/HeN mice and LPS-hyporesponsive C3H/HeJ mice, by human blood cells and human M phi. Paclitaxel 43-53 tumor necrosis factor Mus musculus 145-148 9543698-1 1998 Taxol, an anticancer drug, has been known not only to block cell division by stabilizing microtubules but also to activate murine macrophages to express TNF-alpha, interleukin-1, and to produce nitric oxide (NO). Paclitaxel 0-5 tumor necrosis factor Mus musculus 153-162 9317152-1 1997 Activation of macrophages by LPS and taxol results in production of IL-1, IL-6, TNF-alpha, and granulocyte-macrophage CSF (GM-CSF), which are involved in regulating hemopoiesis, inflammation, and immune responses. Paclitaxel 37-42 tumor necrosis factor Mus musculus 80-89 9353423-3 1997 We reported that tumor-distal macrophages, which mediate immunosuppression through dysregulated nitric oxide (NO) and tumor necrosis factor alpha (TNF alpha) production, are differentially regulated by taxol. Paclitaxel 202-207 tumor necrosis factor Mus musculus 118-145 9353423-3 1997 We reported that tumor-distal macrophages, which mediate immunosuppression through dysregulated nitric oxide (NO) and tumor necrosis factor alpha (TNF alpha) production, are differentially regulated by taxol. Paclitaxel 202-207 tumor necrosis factor Mus musculus 147-156 9275183-5 1997 In an attempt to reconcile this apparent discrepancy, we examined the requirement for p53 in the cytotoxic effects of tumor necrosis factor alpha (TNF-alpha), a cytokine released from murine macrophages upon paclitaxel treatment. Paclitaxel 208-218 tumor necrosis factor Mus musculus 118-145 9275183-6 1997 Conditioned medium from paclitaxel-treated macrophages was capable of inducing p53-independent apoptosis when applied to transformed mouse embryonic fibroblasts and was inhibitable by antibodies against TNF-alpha. Paclitaxel 24-34 tumor necrosis factor Mus musculus 203-212 7583354-4 1995 Activation of NF-kappa B and accumulation of TNF-alpha mRNA correlated semiquantitatively under the following conditions: (1) inhibition of NF-kappa B by dithiocarbamates; (2) induction of TNF synthesis by taxol; (3) partial induction of TNF-alpha mRNA by various inducers in macrophages from lpsd mice; and (4) inhibition of NF-kappa B activation by a protease inhibitor. Paclitaxel 206-211 tumor necrosis factor Mus musculus 45-54 9127007-5 1997 However, at high concentrations of LPS or Taxol, a CD14-independent pathway of activation is observed: this pathway leads to minimal IP-10 gene induction, even though induction of TNF-alpha and IL-1beta occurs. Paclitaxel 42-47 tumor necrosis factor Mus musculus 180-189 9127007-7 1997 These data suggest the existence of two pathways of activation by both LPS and Taxol: one that is CD14 dependent and leads to induction of TNF-alpha, IL-1beta, and IP-10 gene induction, and a CD14-independent pathway that results in the induction of TNF-alpha and IL-1beta, with minimal induction of IP-10. Paclitaxel 79-84 tumor necrosis factor Mus musculus 139-148 9127007-7 1997 These data suggest the existence of two pathways of activation by both LPS and Taxol: one that is CD14 dependent and leads to induction of TNF-alpha, IL-1beta, and IP-10 gene induction, and a CD14-independent pathway that results in the induction of TNF-alpha and IL-1beta, with minimal induction of IP-10. Paclitaxel 79-84 tumor necrosis factor Mus musculus 250-259 9147616-0 1997 Potentiation of antitumor efficacy of paclitaxel by recombinant tumor necrosis factor-alpha. Paclitaxel 38-48 tumor necrosis factor Mus musculus 64-91 9147616-2 1997 Our aim was to determine whether TNF increases the antitumor efficacy of paclitaxel and if so whether the increase is mediated through the enhancement of apoptosis induction by paclitaxel. Paclitaxel 73-83 tumor necrosis factor Mus musculus 33-36 9147616-10 1997 Histological analysis of treated MCa-K tumors revealed that TNF alone did not induce apoptosis of tumor cells, but in the combination it enhanced the apoptotic response to paclitaxel. Paclitaxel 172-182 tumor necrosis factor Mus musculus 60-63 9147616-11 1997 Thus, TNF increased the antitumor efficacy of paclitaxel by enhancing cellular sensitivity to paclitaxel"s induction of apoptosis. Paclitaxel 46-56 tumor necrosis factor Mus musculus 6-9 9147616-11 1997 Thus, TNF increased the antitumor efficacy of paclitaxel by enhancing cellular sensitivity to paclitaxel"s induction of apoptosis. Paclitaxel 94-104 tumor necrosis factor Mus musculus 6-9 8858130-2 1996 In the present study, a variety of synthetic analogs of paclitaxel were examined for their potencies to induce nitric oxide (NO) and tumor necrosis factor (TNF) production by peritoneal M phi from LPS-responsive C3H/HeN, and LPS-hyporesponsive C3H/HeJ mice, and by M phi-like LPS-responsive J774.1 and its mutant LPS-hyporesponsive J7.DEF3 cells. Paclitaxel 56-66 tumor necrosis factor Mus musculus 133-154 8858130-2 1996 In the present study, a variety of synthetic analogs of paclitaxel were examined for their potencies to induce nitric oxide (NO) and tumor necrosis factor (TNF) production by peritoneal M phi from LPS-responsive C3H/HeN, and LPS-hyporesponsive C3H/HeJ mice, and by M phi-like LPS-responsive J774.1 and its mutant LPS-hyporesponsive J7.DEF3 cells. Paclitaxel 56-66 tumor necrosis factor Mus musculus 156-159 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 30-35 tumor necrosis factor Mus musculus 74-83 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 30-35 tumor necrosis factor Mus musculus 245-254 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 30-35 tumor necrosis factor Mus musculus 245-254 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 60-65 tumor necrosis factor Mus musculus 74-83 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 60-65 tumor necrosis factor Mus musculus 245-254 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 60-65 tumor necrosis factor Mus musculus 245-254 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 60-65 tumor necrosis factor Mus musculus 74-83 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 60-65 tumor necrosis factor Mus musculus 245-254 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 60-65 tumor necrosis factor Mus musculus 245-254 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 60-65 tumor necrosis factor Mus musculus 74-83 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 60-65 tumor necrosis factor Mus musculus 245-254 7759887-8 1995 Synergy between IFN-gamma and taxol was mainly dependent on taxol-induced TNF-alpha secretion because not only the increase of inducible NO synthase (iNOS) gene expression by rIFN-gamma plus taxol was associated with the increased expression of TNF-alpha gene but also taxol-induced NO production was decreased by the treatment of anti-murine TNF-alpha neutralizing Abs. Paclitaxel 60-65 tumor necrosis factor Mus musculus 245-254 7759887-9 1995 STSN and polymyxin B potently inhibited taxol-induced TNF-alpha secretion and TNF-alpha gene expression as well as iNOS gene expression by rIFN-gamma plus taxol. Paclitaxel 40-45 tumor necrosis factor Mus musculus 54-63 7759887-12 1995 In conclusion, the present results strongly suggest that the capacity of taxol to increase NO synthesis from rIFN-gamma-primed macrophages is the result of taxol-induced TNF-alpha secretion via the signal transduction pathway of PKC activation. Paclitaxel 73-78 tumor necrosis factor Mus musculus 170-179 7759887-12 1995 In conclusion, the present results strongly suggest that the capacity of taxol to increase NO synthesis from rIFN-gamma-primed macrophages is the result of taxol-induced TNF-alpha secretion via the signal transduction pathway of PKC activation. Paclitaxel 156-161 tumor necrosis factor Mus musculus 170-179 8521300-1 1995 BACKGROUND: The anti-tumor agent, Taxol, has been shown in murine macrophages to stimulate tumor necrosis factor (TNF), modulate TNF receptors, induce a large panel of immediate-early genes, and induce protein tyrosine phosphorylation indistinguishably from LPS. Paclitaxel 34-39 tumor necrosis factor Mus musculus 91-112 8521300-1 1995 BACKGROUND: The anti-tumor agent, Taxol, has been shown in murine macrophages to stimulate tumor necrosis factor (TNF), modulate TNF receptors, induce a large panel of immediate-early genes, and induce protein tyrosine phosphorylation indistinguishably from LPS. Paclitaxel 34-39 tumor necrosis factor Mus musculus 114-117 8521300-1 1995 BACKGROUND: The anti-tumor agent, Taxol, has been shown in murine macrophages to stimulate tumor necrosis factor (TNF), modulate TNF receptors, induce a large panel of immediate-early genes, and induce protein tyrosine phosphorylation indistinguishably from LPS. Paclitaxel 34-39 tumor necrosis factor Mus musculus 129-132 7529746-4 1995 Taxol alone induced murine C3H/He macrophages to secrete tumor necrosis factor alpha (TNF) and to produce nitric oxide (NO) with kinetics similar to that of LPS. Paclitaxel 0-5 tumor necrosis factor Mus musculus 57-84 7529746-4 1995 Taxol alone induced murine C3H/He macrophages to secrete tumor necrosis factor alpha (TNF) and to produce nitric oxide (NO) with kinetics similar to that of LPS. Paclitaxel 0-5 tumor necrosis factor Mus musculus 86-89 7529746-6 1995 RsDPLA inhibited taxol-induced TNF and NO production from C3H/He macrophages in a dose-dependent manner. Paclitaxel 17-22 tumor necrosis factor Mus musculus 31-34 7529746-8 1995 Polymyxin B blocked the inhibitory effect of RsDPLA on taxol-induced TNF production. Paclitaxel 55-60 tumor necrosis factor Mus musculus 69-72 7529746-9 1995 The inhibitory activity of RsDPLA appeared to be reversible since macrophages still responded to taxol in inducing TNF production after the RsDPLA was washed out with phosphate-buffered saline prior to the addition of taxol. Paclitaxel 97-102 tumor necrosis factor Mus musculus 115-118 7529746-10 1995 Taxol-induced TNF production was not inhibited by colchicine, vinblastine, or 10-deacetylbaccatine III. Paclitaxel 0-5 tumor necrosis factor Mus musculus 14-17 7529746-13 1995 Taxol-induced TNF production by the mutant cells was also inhibited by RsDPLA. Paclitaxel 0-5 tumor necrosis factor Mus musculus 14-17 7583354-4 1995 Activation of NF-kappa B and accumulation of TNF-alpha mRNA correlated semiquantitatively under the following conditions: (1) inhibition of NF-kappa B by dithiocarbamates; (2) induction of TNF synthesis by taxol; (3) partial induction of TNF-alpha mRNA by various inducers in macrophages from lpsd mice; and (4) inhibition of NF-kappa B activation by a protease inhibitor. Paclitaxel 206-211 tumor necrosis factor Mus musculus 45-48 7901279-2 1993 Three lines of evidence support this hypothesis: a) Taxol, a microtubule-binding diterpene, mimics the ability of LPS to induce cytokines and down-regulate receptors for TNF-alpha. Paclitaxel 52-57 tumor necrosis factor Mus musculus 170-179 8101863-5 1993 We report that RsDPLA and SDZ 880.431 potently inhibited taxol-induced TNF secretion, gene activation, and protein-tyrosine phosphorylation. Paclitaxel 57-62 tumor necrosis factor Mus musculus 71-74 7901310-1 1993 Taxol is a potent, microtubule-stabilizing, antineoplastic drug that induces interleukin-1-beta (IL-1-beta) and tumor necrosis factor-alpha (TNF-alpha) release by thioglycolate-elicited mouse peritoneal macrophages. Paclitaxel 0-5 tumor necrosis factor Mus musculus 112-139 7901310-1 1993 Taxol is a potent, microtubule-stabilizing, antineoplastic drug that induces interleukin-1-beta (IL-1-beta) and tumor necrosis factor-alpha (TNF-alpha) release by thioglycolate-elicited mouse peritoneal macrophages. Paclitaxel 0-5 tumor necrosis factor Mus musculus 141-150 1970196-2 1990 The microtubule stabilizer taxol shared two actions of LPS on macrophages: it rapidly decreased TNF-alpha receptors and triggered TNF-alpha release. Paclitaxel 27-32 tumor necrosis factor Mus musculus 96-105 1356126-4 1992 Toward this end, the ability of taxol to induce TNF-alpha mRNA and five other genes (IL-1 beta, IP-10, D3, D7, and D8) associated with LPS-activation of macrophages was examined by Northern blot analysis. Paclitaxel 32-37 tumor necrosis factor Mus musculus 48-57 1356126-5 1992 Taxol alone (1-30 microM) induced murine C3H/OuJ macrophages to secrete bioactive TNF-alpha and express increased levels of each of the six genes under investigation. Paclitaxel 0-5 tumor necrosis factor Mus musculus 82-91 1353517-0 1992 Taxol, a microtubule-stabilizing antineoplastic agent, induces expression of tumor necrosis factor alpha and interleukin-1 in macrophages. Paclitaxel 0-5 tumor necrosis factor Mus musculus 77-104 1353517-4 1992 In a dose-dependent manner, LPS-free taxol induced release of biologically active tumor necrosis factor alpha (TNF) by inflammatory murine macrophages. Paclitaxel 37-42 tumor necrosis factor Mus musculus 82-109 1353517-4 1992 In a dose-dependent manner, LPS-free taxol induced release of biologically active tumor necrosis factor alpha (TNF) by inflammatory murine macrophages. Paclitaxel 37-42 tumor necrosis factor Mus musculus 111-114 1353517-5 1992 Taxol-induced production of TNF was inhibitable by interleukin-10. Paclitaxel 0-5 tumor necrosis factor Mus musculus 28-31 1353517-6 1992 By Northern blot, taxol (10 and 1 microM) induced TNF mRNA expression to an extent similar to LPS. Paclitaxel 18-23 tumor necrosis factor Mus musculus 50-53 1353517-7 1992 Induction of TNF mRNA by 10 microM taxol was detectable at 45 min of stimulation, maximal at 90 min, and evident for at least 8 h. The same low concentration of taxol also induced interleukin 1 (IL-1) alpha and beta mRNA expression. Paclitaxel 35-40 tumor necrosis factor Mus musculus 13-16 1353517-7 1992 Induction of TNF mRNA by 10 microM taxol was detectable at 45 min of stimulation, maximal at 90 min, and evident for at least 8 h. The same low concentration of taxol also induced interleukin 1 (IL-1) alpha and beta mRNA expression. Paclitaxel 161-166 tumor necrosis factor Mus musculus 13-16 1353517-8 1992 We conclude that taxol triggers macrophages for TNF and IL-1 production. Paclitaxel 17-22 tumor necrosis factor Mus musculus 48-51 1350792-4 1992 Likewise, Taxol induced TNF alpha secretion. Paclitaxel 10-15 tumor necrosis factor Mus musculus 24-33 1970196-2 1990 The microtubule stabilizer taxol shared two actions of LPS on macrophages: it rapidly decreased TNF-alpha receptors and triggered TNF-alpha release. Paclitaxel 27-32 tumor necrosis factor Mus musculus 130-139 34566640-4 2021 Based on the results, PTX inhibited the migration of RA-FLS in a dose-dependent manner and significantly reduced the spontaneous expression of IL-6, IL-8, and RANKL mRNA and TNF-alpha-induced transcription of the IL-1 beta, IL-8, MMP-8, and MMP-9 genes. Paclitaxel 22-25 tumor necrosis factor Mus musculus 174-183 34904193-9 2022 PECS-101 also decreased PTX-induced increase in Tnf, Il6, and Aif1 (Iba-1) gene expression in the DRGs and the loss of intra-epidermal nerve fibers. Paclitaxel 24-27 tumor necrosis factor Mus musculus 48-51 34795003-12 2021 Finally, in an orthotopic murine metastatic OV model, sFIS assay predicted the higher capacity of chemo-immunotherapy (paclitaxel-carboplatin plus anti-TNF antibody combination) in achieving a pro-immunogenic peripheral milieu (si-IFN/ISG responseHIGHsi-NFkappaB responseLOW), which aligned with high antitumor efficacy. Paclitaxel 119-129 tumor necrosis factor Mus musculus 152-155 34566640-6 2021 Mechanistic studies revealed that PTX significantly inhibited the TNF-alpha-induced phosphorylation of ERK1/2 and JNK in the mitogen-activated protein kinase (MAPK) pathway and suppressed the TNF-alpha-induced activation of AKT, p70S6K, 4EBP1, and HIF-1alpha in the AKT/mTOR pathway. Paclitaxel 34-37 tumor necrosis factor Mus musculus 66-75 34566640-6 2021 Mechanistic studies revealed that PTX significantly inhibited the TNF-alpha-induced phosphorylation of ERK1/2 and JNK in the mitogen-activated protein kinase (MAPK) pathway and suppressed the TNF-alpha-induced activation of AKT, p70S6K, 4EBP1, and HIF-1alpha in the AKT/mTOR pathway. Paclitaxel 34-37 tumor necrosis factor Mus musculus 192-201 33323915-17 2020 The paclitaxel effects were accompanied by inhibition of the inflammatory cytokines, MCP-1, TNF-alpha, TNF-R2, and TLR4, as well as attenuation of the apoptosis markers, Bax, Bcl-2, and Caspase-3. Paclitaxel 4-14 tumor necrosis factor Mus musculus 92-101 35281908-12 2022 JG remarkably enhanced the anticancer effect of PTX by increasing the red blood cell and platelet counts; increasing hemoglobin, interleukin (IL)-2, and tumor necrosis factor-alpha levels; increasing CD4+T cells and the CD4+/CD8+ ratio; and decreasing IL-10 levels. Paclitaxel 48-51 tumor necrosis factor Mus musculus 153-180 31712703-4 2019 In paclitaxel-treated mice, increased fatigue and decreased cognitive performance occurred in parallel with reduced microglia immunoreactivity, increased circulating chemokine expression (CXCL1), as well as transient increases in pro-inflammatory cytokine/chemokine (Il-1beta, Tnfalpha, Il-6, and Cxcl1) gene expression in the brain. Paclitaxel 3-13 tumor necrosis factor Mus musculus 277-285 32401077-7 2020 PTX + SPS-NEs increased the release of NO, IL-6 and TNF-alpha, and the expression of p-p65 NF-kappaB, p-I-kappaB, TLR4. Paclitaxel 0-3 tumor necrosis factor Mus musculus 52-61 32401077-8 2020 In addition, PTX + SPS-NEs significantly inhibited tumor growth by 72.82% and increased the secretion of serum IL-2, TNF-alpha and IFN-gamma. Paclitaxel 13-16 tumor necrosis factor Mus musculus 117-126 31270160-9 2019 Paclitaxel treatment also upregulated TNF and CXCL1 in macrophage cultures and DRG tissues in both sexes, but these changes were compromised by Tlr9 mutation in male animals. Paclitaxel 0-10 tumor necrosis factor Mus musculus 38-41 31707979-0 2019 Paclitaxel-activated astrocytes produce mechanical allodynia in mice by releasing tumor necrosis factor-alpha and stromal-derived cell factor 1. Paclitaxel 0-10 tumor necrosis factor Mus musculus 82-109 31707979-8 2019 Cultured astrocytes were activated by paclitaxel with significant increases in protein levels for tumor necrosis factor-alpha (TNF-alpha) and stromal-derived cell factor 1 (SDF-1). Paclitaxel 38-48 tumor necrosis factor Mus musculus 98-125 31707979-8 2019 Cultured astrocytes were activated by paclitaxel with significant increases in protein levels for tumor necrosis factor-alpha (TNF-alpha) and stromal-derived cell factor 1 (SDF-1). Paclitaxel 38-48 tumor necrosis factor Mus musculus 127-136 31707979-9 2019 Importantly, intrathecal injection of paclitaxel-activated astrocytes produced mechanical allodynia that was reversed by TNF-alpha and SDF-1 neutralizing antibodies. Paclitaxel 38-48 tumor necrosis factor Mus musculus 121-130 31707979-10 2019 CONCLUSION: Our results suggest for the first time that paclitaxel can directly activate astrocytes, which are sufficient to produce acute pain by releasing TNF-alpha and SDF-1. Paclitaxel 56-66 tumor necrosis factor Mus musculus 157-166 29620264-0 2018 Pegylated liposomal-paclitaxel induces ovarian cancer cell apoptosis via TNF-induced ERK/AKT signaling pathway. Paclitaxel 20-30 tumor necrosis factor Mus musculus 73-76 28950656-8 2017 Mechanistically, the combination treatment was more efficient than paclitaxel monotherapy in reducing ATP, MDA, TNF-alpha and Il-17 contents in SEC. Paclitaxel 67-77 tumor necrosis factor Mus musculus 112-121 28125674-11 2017 We also found that PTX induced up-regulation of several inflammatory cytokines and chemokines (TNF-alpha, IFN-gamma, CCL11, CCL4, CCL3, IL-12p70 and GM-CSF) in the spinal cord. Paclitaxel 19-22 tumor necrosis factor Mus musculus 95-104