PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17804813-9 2007 Furthermore, inhibition of ATF-2 expression prevented the increased resistance of polyamine-deficient cells to apoptosis induced by treatment with tumor necrosis factor-alpha and cycloheximide. Polyamines 82-91 tumor necrosis factor Homo sapiens 147-174 22555848-6 2012 Polyamine-deficient cells also exhibited an increase in resistance to tumor necrosis factor-alpha/cycloheximide-induced apoptosis, which was prevented by inhibiting SG formation with silencing SG resident proteins Sort1 and TIA-1. Polyamines 0-9 tumor necrosis factor Homo sapiens 70-97 21506109-5 2011 However it decreased cell death in C-28/I2 chondrocytes exposed to stimuli previously reported to promptly trigger apoptosis, that is, the cytokine tumor necrosis factor-alpha (TNF) plus cycloheximide (CHX) or the polyamine analogue N(1),N(11)-diethylnorspermine (DENSPM) plus CHX. Polyamines 214-223 tumor necrosis factor Homo sapiens 177-180 17354225-8 2007 In summary, high levels of AS expression, which may be required for several arginine-dependent processes in cancer, including the production of nitric oxide, proline, pyrimidines and polyamines, is regulated by TNF-alpha and may provide an important molecular pathway linking inflammation and metabolism to ovarian tumorigenesis. Polyamines 183-193 tumor necrosis factor Homo sapiens 211-220 15965903-0 2006 Polyamine depletion inhibits apoptosis following blocking of survival pathways in human chondrocytes stimulated by tumor necrosis factor-alpha. Polyamines 0-9 tumor necrosis factor Homo sapiens 115-142 16048438-5 2005 Sustained phosphorylation of STAT3 at tyrosine residues was observed in polyamine-depleted cells after exposure to TNF-alpha. Polyamines 72-81 tumor necrosis factor Homo sapiens 115-124 16048438-9 2005 Significantly higher levels of Bcl-2 and c-IAP2 proteins were observed in polyamine-depleted cells before and after 9 h of TNF-alpha treatment. Polyamines 74-83 tumor necrosis factor Homo sapiens 123-132 16048438-14 2005 These results suggest that activation of STAT3 in response to polyamine depletion increases the transcription and subsequent expression of anti-apoptotic Bcl-2 and IAP family proteins and thereby promotes survival of cells against TNF-alpha-induced apoptosis. Polyamines 62-71 tumor necrosis factor Homo sapiens 231-240 15828019-0 2005 Polyamine depletion inhibits NF-kappaB binding to DNA and interleukin-8 production in human chondrocytes stimulated by tumor necrosis factor-alpha. Polyamines 0-9 tumor necrosis factor Homo sapiens 119-146 16048438-2 2005 The aim of the present study was to clarify the role of STAT3 signalling in the protection of polyamine-depleted intestinal epithelial cells against TNF-alpha (tumour necrosis factor-alpha)-induced apoptosis. Polyamines 94-103 tumor necrosis factor Homo sapiens 149-158 15994315-7 2005 Inhibition of PP2A by okadaic acid and fostriecin or PP2A small interfering RNA transfection significantly decreased TNF-alpha-induced apoptosis in control and polyamine-depleted cells. Polyamines 160-169 tumor necrosis factor Homo sapiens 117-126 15828019-2 2005 To search for new approaches to limit cartilage damage, we investigated the requirement of polyamines for NF-kappaB activation by TNFalpha in human C-28/I2 chondrocytes, using alpha-difluoromethylornithine (DFMO), a specific polyamine biosynthesis inhibitor. Polyamines 91-101 tumor necrosis factor Homo sapiens 130-138 15828019-2 2005 To search for new approaches to limit cartilage damage, we investigated the requirement of polyamines for NF-kappaB activation by TNFalpha in human C-28/I2 chondrocytes, using alpha-difluoromethylornithine (DFMO), a specific polyamine biosynthesis inhibitor. Polyamines 91-100 tumor necrosis factor Homo sapiens 130-138 15828019-9 2005 Our results show that the intracellular depletion of polyamines inhibits the response of chondrocytes to TNFalpha by interfering with the DNA binding activity of NF-kappaB. Polyamines 53-63 tumor necrosis factor Homo sapiens 105-113 26680812-8 2001 Polyamines, especially spermine suppressed TNFalpha-induced ROS generation in MCF-7 cells. Polyamines 0-10 tumor necrosis factor Homo sapiens 43-51 15941855-0 2005 Polyamine depletion reduces TNFalpha/MG132-induced apoptosis in bone marrow stromal cells. Polyamines 0-9 tumor necrosis factor Homo sapiens 28-36 15941855-9 2005 The effect of DFMO on TNFalpha/MG132-induced upregulation of caspase-3 activity was reversed by the addition of 100 microM putrescine, confirming that polyamines were really involved in the apoptotic process. Polyamines 151-161 tumor necrosis factor Homo sapiens 22-30 15941855-10 2005 Also, the number of apoptotic BMSCs after TNFalpha/MG132 treatment, as determined by terminal transferase-mediated dUTP nick end-labeling (TUNEL) assay, were threefold reduced after polyamine depletion (p<.05). Polyamines 182-191 tumor necrosis factor Homo sapiens 42-50 26680812-0 2001 Effects of Polyamines on TNFalpha- or Tamoxifen-induced Apoptosis in Human Breast Cancer Cells. Polyamines 11-21 tumor necrosis factor Homo sapiens 25-33 26680812-1 2001 PURPOSE: To investigate the effects of polyamines on tumor necrosis factor alpha (TNFalpha)-or tamoxifen (TAM)-induced apoptosis in estrogen receptor (ER)-positive MCF- 7 and ER-negative MDA-MB-231 human breast cancer cells. Polyamines 39-49 tumor necrosis factor Homo sapiens 53-80 26680812-1 2001 PURPOSE: To investigate the effects of polyamines on tumor necrosis factor alpha (TNFalpha)-or tamoxifen (TAM)-induced apoptosis in estrogen receptor (ER)-positive MCF- 7 and ER-negative MDA-MB-231 human breast cancer cells. Polyamines 39-49 tumor necrosis factor Homo sapiens 82-90 26680812-12 2001 CONCLUSION: These results suggest that polyamines may prevent TNFalpha or TAM-induced apoptosis in MCF-7 human breast cancer cells. Polyamines 39-49 tumor necrosis factor Homo sapiens 62-70 8439287-5 1993 A decrease in the proliferation rate of TNF-sensitive cells induced by either alpha-difluoromethylornithine treatment (resulting in polyamine depletion) or serum starvation rendered the cells insensitive to TNF-induced cytotoxicity, further suggesting a role for mitogenic signals and cell division in TNF-mediated cytotoxicity. Polyamines 132-141 tumor necrosis factor Homo sapiens 40-43 10652573-4 1999 Subcutaneously growing tumors were injected with pGL1-TNF-alpha complexed with a cationic polyamine and radiation, singly and in combination, over an 8-day period. Polyamines 90-99 tumor necrosis factor Homo sapiens 54-63 10652573-5 1999 The maximum antitumor effect was achieved with the combination of polyamine-pGL1-TNF-alpha and radiation. Polyamines 66-75 tumor necrosis factor Homo sapiens 81-90 10652573-8 1999 The results demonstrate that polyamine-pGL1-TNF-alpha can be safely and effectively administered together with radiation under the conditions used. Polyamines 29-38 tumor necrosis factor Homo sapiens 44-53 10199820-0 1999 Regulation of intracellular polyamine biosynthesis and transport by NO and cytokines TNF-alpha and IFN-gamma. Polyamines 28-37 tumor necrosis factor Homo sapiens 85-94 10199820-4 1999 This study was undertaken to determine the effects NO and the NO synthase (NOS)-inducing cytokines, tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), exert on polyamine regulation. Polyamines 183-192 tumor necrosis factor Homo sapiens 100-127 10199820-4 1999 This study was undertaken to determine the effects NO and the NO synthase (NOS)-inducing cytokines, tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), exert on polyamine regulation. Polyamines 183-192 tumor necrosis factor Homo sapiens 129-138 10199820-10 1999 Administration of NO donors, or TNF-alpha and IFN-gamma, suppressed [3H]putrescine uptake, thereby preventing transport-mediated reestablishment of intracellular polyamine levels. Polyamines 162-171 tumor necrosis factor Homo sapiens 32-41 10102555-2 1999 Previous studies suggest that polyamines are involved in priming of the PMN respiratory burst by tumor necrosis factor-alpha (TNF-alpha) and can stabilize DNA against degradation. Polyamines 30-40 tumor necrosis factor Homo sapiens 97-124 10102555-2 1999 Previous studies suggest that polyamines are involved in priming of the PMN respiratory burst by tumor necrosis factor-alpha (TNF-alpha) and can stabilize DNA against degradation. Polyamines 30-40 tumor necrosis factor Homo sapiens 126-135 10102555-3 1999 The purpose of this study was to determine whether exogenous polyamines can modulate priming by TNF-alpha or delay nuclear changes associated with PMN apoptosis (programmed cell death). Polyamines 61-71 tumor necrosis factor Homo sapiens 96-105 10102555-12 1999 CONCLUSIONS: Polyamines could potentially impair the priming of PMN oxidative function by TNF-alpha at sites where this cytokine is present. Polyamines 13-23 tumor necrosis factor Homo sapiens 90-99 9368191-1 1998 Tumor necrosis factor-alpha (TNF-alpha) induces a rapid increase in polymorphonuclear leukocyte (PMN) polyamine content which appears to be required for optimal priming of the respiratory burst. Polyamines 102-111 tumor necrosis factor Homo sapiens 0-27 9368191-1 1998 Tumor necrosis factor-alpha (TNF-alpha) induces a rapid increase in polymorphonuclear leukocyte (PMN) polyamine content which appears to be required for optimal priming of the respiratory burst. Polyamines 102-111 tumor necrosis factor Homo sapiens 29-38 9632528-0 1998 Sensitization of tnf-induced apoptosis with polyamine synthesis inhibitors in different human and murine tumour cell lines. Polyamines 44-53 tumor necrosis factor Homo sapiens 17-20 9632528-4 1998 TNF decreased the intracellular levels of the three polyamines Spm, spermidine (Spd) and putrescine (Put). Polyamines 52-62 tumor necrosis factor Homo sapiens 0-3 7852843-0 1995 An inhibitor of polyamine biosynthesis impairs human polymorphonuclear leukocyte priming by tumor necrosis factor alpha. Polyamines 16-25 tumor necrosis factor Homo sapiens 92-119 7852843-2 1995 Previous reports suggest that polyamine biosynthesis by ornithine decarboxylase (ODC) has an essential role in macrophage activation by TNF. Polyamines 30-39 tumor necrosis factor Homo sapiens 136-139 7852843-7 1995 Thus, polyamine biosynthesis plays an important role in priming by TNF, but is not involved in all PMN responses to this cytokine. Polyamines 6-15 tumor necrosis factor Homo sapiens 67-70 1912611-1 1991 These experiments were designed to test polyamine (PA) involvement in the secretion and action of transforming growth factor alpha (TGF-alpha) in hormone responsive MCF-7 breast cancer cells in liquid culture. Polyamines 40-49 tumor necrosis factor Homo sapiens 98-130 1312903-0 1992 Inhibitors of polyamine biosynthesis block tumor necrosis factor-induced activation of macrophages. Polyamines 14-23 tumor necrosis factor Homo sapiens 43-64 1312903-5 1992 The data presented in this paper suggest that polyamines may play a functional role in tumor necrosis factor-driven macrophage activation, and they are discussed in the context of their possible use as inhibitors of polyamine metabolism in tumor chemotherapy. Polyamines 46-56 tumor necrosis factor Homo sapiens 87-108 1312903-5 1992 The data presented in this paper suggest that polyamines may play a functional role in tumor necrosis factor-driven macrophage activation, and they are discussed in the context of their possible use as inhibitors of polyamine metabolism in tumor chemotherapy. Polyamines 46-55 tumor necrosis factor Homo sapiens 87-108 1912611-1 1991 These experiments were designed to test polyamine (PA) involvement in the secretion and action of transforming growth factor alpha (TGF-alpha) in hormone responsive MCF-7 breast cancer cells in liquid culture. Polyamines 51-53 tumor necrosis factor Homo sapiens 98-130