• Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is known to cause apoptosis in several types of malignant tumor cells through its interaction with the death domain-containing receptor, death receptor 5 (DR5). (nih.gov)
  • In the present study, we showed that co-treatment with troglitazone (TGZ), a synthetic ligand of peroxisome proliferator-activated receptor γ (PPARγ), and TRAIL synergistically induced apoptosis through DR5 upregulation in human colon cancer DLD-1 cells. (nih.gov)
  • TNF-related apoptosis inducing ligand (TRAIL) induces apoptosis through its death receptors (DRs) 4 and/or 5 expressed on the surface of target cells. (oncotarget.com)
  • Tumor necrosis element (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. (opioid-receptors.com)
  • member of the tumor necrosis factor superfamily known as TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) (16). (opioid-receptors.com)
  • Lymphocyte inhibitor of TRAIL (TNF-related apoptosis-inducing ligand): a new receptor protecting lymphocytes from the death ligand TRAIL. (ox.ac.uk)
  • These include Fas, TNF-R1, lymphocyte-associated receptor of death (LARD), DR4, and TNF-related apoptosis-inducing ligand receptor inducer of cell killing-2 (TRICK2). (ox.ac.uk)
  • The latter two are receptors for the cytotoxic ligand TNF-related apoptosis-inducing ligand (TRAIL), and one of the paradoxes raised by the cloning of these molecules was why do most cells not die upon contact with the widely expressed TRAIL molecule? (ox.ac.uk)
  • The apoptotic response of cells can be induced by the intrinsic and the extrinsic pathway, the former being mediated by the mitochondria and the latter activated by ligand stimulation of death receptors at the cell surface [ 1 ]. (biomedcentral.com)
  • The antitumor effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in gliomas has thus far only been thoroughly established in tumor cell lines. (aacrjournals.org)
  • Circulating osteoprotegerin (OPG), a member of the receptor activator of nuclear factor kappa-B (RANK) axis, may influence breast cancer risk via its role as the decoy receptor for both the RANK ligand (RANKL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). (biomedcentral.com)
  • Bone homeostasis is maintained by the interplay between the receptor activator of nuclear factor kappa-B (RANK), its soluble activation ligand (RANKL), and OPG. (biomedcentral.com)
  • 5% false discovery rate) between risk of MACE and eight proteins: matrix metalloproteinase (MMP)-12, IL-27 subunit α (IL-27a), kidney injury molecule (KIM)-1, fibroblast growth factor (FGF)-23, protein S100-A12, TNF receptor (TNFR)-1, TNFR-2 and TNF-related apoptosis-inducing ligand receptor (TRAIL-R)2. (springer.com)
  • Involvement of Up-regulation of Death Receptors and Bim in Hispolon-mediated TNF-related Apoptosis-inducing Ligand Sensitization in Human Renal Carcinoma. (greenmedinfo.com)
  • In this study, we evaluated the sensitizing effect of hispolon on TNF-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in human renal carcinoma cells. (greenmedinfo.com)
  • In a second project we are investigating the induction of apoptosis by activation of death receptors for the ligand TRAIL in breast and ovarian cancer cells. (cancer.gov)
  • We have shown that most breast and ovarian cancer cell lines are resistant to the induction of apoptosis by TRAIL, the ligand for the death receptors DR4 and DR5. (cancer.gov)
  • Our current work utilizes biochemical and genetic approaches to identify mechanisms that regulate the induction of death by TRAIL ligand in breast and ovarian cancer cells. (cancer.gov)
  • Once ceramide-enriched microdomains are formed, Fas/FasL and DR5/TRAIL as well as other signaling mediators become clustered and can be activated in either a ligand-dependent or -independent manner [ 4 - 6 ]. (biomedcentral.com)
  • TNF , TNF-related apoptosis-inducing ligand ( TRAIL ), and Fas ligand ( FasL ). (massgenomics.org)
  • Among these associations, we found KIM-1 (kidney injury molecule-1), TNFR (TNF [tumor necrosis factor] receptor) 1 and 2, TRAIL-R2 (TRAIL [TNF-related apoptosis-inducing ligand] receptor 2), and RETN (resistin) to be associated with all 4 lipid fractions. (lu.se)
  • The extrinsic pathway is mediated by a variety of death receptor ligands, including tumor necrosis factor (TNF) and Fas ligand (FaSL), that trigger apoptosis by binding to cell surface receptors. (cdc.gov)
  • Designed tumor necrosis factor-related apoptosis-inducing ligand variants initiating apoptosis exclusively via the DR5 receptor. (crg.eu)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential anticancer drug that selectively induces apoptosis in a variety of cancer cells by interacting with death receptors DR4 and DR5. (crg.eu)
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a cytokine with potential therapeutic value against cancers because of its selective cytotoxicity to many transformed, but not normal, cells. (lonza.com)
  • The "decoy receptors" TRAIL-R3 (TR3) and TRAIL-R4 (TR4) were believed to negatively regulate TRAIL-induced cytotoxicity by competing for ligand binding with TRAIL-R1 (TR1) and TRAIL-R2 (TR2). (lonza.com)
  • By contrast, ligand binding by TR4 is dispensable for its apoptosis inhibitory function, thereby excluding the possibility that TR4 was a "decoy" to inhibit apoptosis by binding up TRAIL. (lonza.com)
  • In primary CD8(+) T cells, which express only TR2 and TR4 and are resistant to TRAIL-induced apoptosis, stimulation with phorbol myristate acetate abrogated the ligand-independent interaction between TR2 and TR4 and enhanced their sensitivity to TRAIL-induced apoptosis. (lonza.com)
  • We propose that TR4 is a "regulatory" rather than "decoy" receptor that inhibits apoptosis signaling by TRAIL through this previously uncharacterized ligand-independent mechanism. (lonza.com)
  • Association between endometriosis and polymorphisms in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), TRAIL receptor and osteoprotegerin genes and their serum levels. (cdc.gov)
  • Leptin and adiponectin can augment the oxidation of fatty acid in liver by activating the nuclear receptor super-family of transcription factors, namely peroxisome proliferator-activated receptor (PPAR)-α. (wjgnet.com)
  • Results DIM, but not I3C, increased adipocyte differentiation through upregulation of peroxisome proliferator‐activated receptor γ and CCAAT/enhancer‐binding protein α. (researchgate.net)
  • Apoptosis can be triggered by the engagement of cell surface receptors by their ligands. (ox.ac.uk)
  • 2013). Apoptosis is induced intrinsically by the release of pro-apoptotic proteins from the inter-membrane space of the mitochondrion (eg. (uni-muenchen.de)
  • In separate work, my team identified a set of secreted proteins overexpressed in the tumor microenvironment, and developed antibodies to block their cognate receptors for therapeutic gain. (gene.com)
  • 1) We study Cbl proteins, a family of ubiquitin ligases that negatively regulate signaling by receptor tyrosine kinases. (cancer.gov)
  • Numerous cellular proteins detect DNA damage and induce senescence , a permanent change of state characterized by morphological and gene expression changes. (massgenomics.org)
  • In the current study, we demonstrate that DcR1 and DcR2 inhibit TRAIL-induced apoptosis by distinct mechanisms. (opioid-receptors.com)
  • LIT is expressed predominantly on PBL, where it can competitively inhibit TRAIL-induced apoptosis through DR4/TRICK2, and may function to modulate lymphocyte sensitivity to TRAIL. (ox.ac.uk)
  • doxorubicin) or via activation of death receptors on the surface of the cell (eg. (uni-muenchen.de)
  • With great interest we discovered that the replacement of wildtype p53 by mutant p53 did not disturb the extrinsic apoptosis inducing capacity. (uni-muenchen.de)
  • The extrinsic apoptosis by TRAIL was increased in senescent tumor cells. (uni-muenchen.de)
  • α-TEA induces apoptosis via activation of extrinsic death receptors Fas (CD95) and DR5, JNK/p73/Noxa pathways, and suppression of anti-apoptotic mediators Akt, ERK, c-FLIP and survivin in breast, ovarian and prostate cancer cells. (biomedcentral.com)
  • Casticin-induced DR5 upregulation and apoptosis potentiation are ROS-dependent in BGC-823 cells We recently demonstrated that 5, 7-dimethoxyflavone selectively enhances TRAIL-induced apoptosis by ROS stimulated ER-stress triggering CHOP-mediated DR5 upregulation in hepatocellular carcinoma cells [15]. (nos-nop.org)
  • We have cloned LIT (lymphocyte inhibitor of TRAIL), which lacks a death domain. (ox.ac.uk)
  • MUC16 knockdown decreases caspase-8 inhibitor cFLIP mRNA levels, increases cFLIP degradation, and consequently increases TRAIL-induced apoptosis. (biomedcentral.com)
  • Regardless of the tumor heterogeneity, cotreatment with the proteasome inhibitor bortezomib efficiently sensitized all primary glioma samples for TRAIL-induced apoptosis and tremendously reduced their clonogenic survival. (aacrjournals.org)
  • Functional knockdown of ASMase with either the chemical inhibitor, desipramine, or siRNA markedly reduces α-TEA-induced cell surface membrane accumulation of ceramide and its co-localization with Fas, DR5, and FADD, cleavage of caspases-8 and -9 and apoptosis, suggesting an early and critical role for ASMase in α-TEA-induced apoptosis. (biomedcentral.com)
  • The presence of necrostatin-1, an inhibitor of receptor-interacting serine/threonine-protein kinase 1 (RIPK‑1), but not that of Z-VAD-fmk, attenuated the cytotoxic effects of GEF under AAS culture conditions. (spandidos-publications.com)
  • In this study, we demonstrate that α-TEA induces the accumulation of cell surface membrane ceramide, leading to co-localization with Fas, DR5, and FADD, followed by activation of caspases-8 and -9 and apoptosis in human MDA-MB-231 breast cancer cells. (biomedcentral.com)
  • TRAIL triggers apoptosis upon engagement of one of its two agonistic receptors, named DR4 (death receptor 4) (33) and DR5 (death receptor 5) (7, 46). (opioid-receptors.com)
  • In response to TRAIL, these receptors recruit the adaptor protein FADD (Fas-associated death domain), through death domain homophilic interactions (5), and the initiators procaspase-8 and -10, through death effector domain interactions with FADD, hence forming the macromolecular complex called DISC (death-inducing signaling complex). (opioid-receptors.com)
  • Transient overexpression of DcR1 or DcR2 in TRAIL-sensitive Sav1 tumor cells prevents cell death triggering by TRAIL (10, 11), and recent evidence indicates that tumor and normal cells can acquire resistance to TRAIL-induced killing by up-regulating TRAIL antagonistic receptors (6, 8, 9, 34). (opioid-receptors.com)
  • A growing number of receptors belonging to the TNF receptor family have been identified that contain a conserved cytoplasmic death domain. (ox.ac.uk)
  • MUC16 decreases TRAIL receptor R2 (DR5) expression and inhibits pro-caspase-8 activation at the death-inducing signaling complex (DISC). (biomedcentral.com)
  • RT-induced damage to cancer cells leads to different outcomes, such as survival, senescence, or death. (nature.com)
  • RT can directly induce cancer cell death through various mechanisms, such as apoptosis, necrosis, and autophagy. (nature.com)
  • Of note, an increased carbohydrate uptake and/or induction of death receptors of cancer cells was exploited to develop glycoconjugates that potentially induce cellular stress, ROS and apoptosis. (degruyter.com)
  • A review on therapeutic targeting of cancer via death receptors dissects this topic comprehensively and is therefore subtly discussed in this minireview which focuses on ROS cancer therapeutics [ 22 ]. (degruyter.com)
  • In the 1990's, the Human Genome Project inspired my team to discover several novel members of the TNF cytokine superfamily, most notably, Apo2L/TRAIL and its "death" and "decoy" receptors. (gene.com)
  • Hispolon induced up-regulation of Bim and death receptors expression at the post-translational level. (greenmedinfo.com)
  • Mechanistically, TSC2 inactivation caused elevation of TRAIL receptor expression, cooperating with mTORC1-S6 signaling to induce tumor cell death. (nki.nl)
  • Prevention of raft reorganization into larger platforms by inactivation of acid sphingomyelinase (ASMase), renders cells resistant to Fas clustering and apoptosis [ 9 ], indicating that ASMase/ceramide plays an important role in death receptor-mediated apoptosis. (biomedcentral.com)
  • Therapeutic intervention aims to reverse tumor-induced NK cell suppression and sustain NK cells' tumorlytic capacities. (frontiersin.org)
  • Here, we review tumor-NK cell interactions, discuss the mechanisms by which NK cells generate an antitumor immune response, and discuss NK cell-based therapeutic strategies targeting activating, inhibitory, and co-stimulatory receptors. (frontiersin.org)
  • In the present study, we investigated the therapeutic potential of TRAIL in primary human glioma cells. (aacrjournals.org)
  • Our study uncovers a pivotal role for TSC2 in the cancer immune response by governing crosstalk between TSC2-mTOR and TRAIL signaling, aiding future therapeutic exploration of this pathway in immuno-oncology. (nki.nl)
  • Novel H(3) receptor antagonists such as GSK207040 and GSK334429 may therefore have therapeutic potential not only in dementia but also in neuropathic pain. (ox.ac.uk)
  • MUC16 expression in EOC cells is associated with increased tumorigenesis and inhibiton of genotoxic drug-induced apoptosis. (biomedcentral.com)
  • However, CD56 dim NK cells can produce cytokines, specifically IFN-γ, after cell triggering via NKp46 of NKp30 activating receptors or after stimulation with combinations of IL-2, IL-12, and IL-15 ( 7 ). (frontiersin.org)
  • The RhoAGTP mediated repression of mTORC1 signaling occurred independent of leucine or insulin induced stimulation. (nos-nop.org)
  • The selectivity of TRAIL towards cancer cells has promoted clinical evaluation of recombinant human TRAIL (rhTRAIL) and its agonistic antibodies in treating several major human cancers including colon and non-Hodgkin's lymphoma. (oncotarget.com)
  • We have demonstrated that resistance to TRAIL-induced apoptosis can be overcome by co-incubation of the cells with chemotherapeutic agents, semi-synthetic retinoids (such as 4HPR), or molecularly targeted agents (such as anti-ErbB-2 antibodies). (cancer.gov)
  • SARS-CoV-2 genome, 15 of which are within the receptor binding domain, which allow Omicron to be more infectious and transmissible than a Delta variant and also resist neutralization by vaccine and infection-induced antibodies. (cdc.gov)
  • Second, T cell therapies using Tregs (either polyclonal, antigen-specific, or genetically engineered to express chimeric antigen receptors) to establish active dominant immune tolerance or T cells (engineered to express chimeric antigen receptors) to delete pathogenic immune cells. (frontiersin.org)
  • Upon TRAIL binding, DcR1 and DcR2 fail to recruit FADD and, consequently, fail to induce downstream cell signaling events leading to apoptosis (10, 32). (opioid-receptors.com)
  • Fas, DR5 and their adaptor FADD, as an essential early event in α-TEA induced Fas and DR5 dependent apoptosis. (biomedcentral.com)
  • In addition to the agonistic TRAIL receptors DR4 and DR5, TRAIL can bind to related but antagonistic receptors, including TRID or TRAIL-R3 (11, 27, 32) and TRUNDD or TRAIL-R4 (10), also coined DcR1 (decoy receptor 1) and DcR2 (decoy receptor 2), respectively. (opioid-receptors.com)
  • OPG binds RANKL as a decoy receptor, inhibiting the activation of RANK by RANKL and preventing the differentiation of bone marrow precursor (monocyte/macrophage) cells to osteoclasts - cells that are central in the process of bone resorption [ 2 ]. (biomedcentral.com)
  • These results suggest that combined treatment with TGZ and TRAIL may be promising as a new therapy against malignant tumors. (nih.gov)
  • Our findings could have implications for the use of TRAIL receptor targeted therapies in the treatment of human OSCC tumors particularly the ones harboring constitutively active Ras mutant. (oncotarget.com)
  • Breast cancer tumors that do not express hormone receptors or have amplification of Her2/Neu (so called triple-negative tumors) have a poor prognosis and no validated molecular targets. (cancer.gov)
  • SCR-6852, an oral and highly brain-penetrating estrogen receptor degrader (SERD), effectively shrinks tumors both in intracranial and subcutaneous ER + breast cancer models. (medscape.com)
  • Here, we show that inhibition of TRAIL-induced apoptosis by TR4 critically depends on its association with TR2 via the NH(2)-terminal preligand assembly domain overlapping the first partial cysteine-rich domain of both receptors. (lonza.com)
  • Publisher Correction: RAGE inhibition blunts insulin-induced oncogenic signals in breast cancer. (medscape.com)
  • Initial binding experiments suggested that TRAIL binding affinities to TRAIL agonistic and antagonistic receptors were similar (11, Laropiprant 24), but subsequent studies demonstrated that DcR1 and Laropiprant DcR2 affinities to TRAIL were lower than that of DR4 or DR5 (8). (opioid-receptors.com)
  • To date, the molecular mechanisms by which DcR1 and DcR2 confer resistance to TRAIL-induced apoptosis remain unclear (1, 6, 9, 13). (opioid-receptors.com)
  • DcR1 acts merely as a competitor for TRAIL binding, preventing DR5-associated DISC assembly, while DcR2 impairs TRAIL DISC processing and initiator caspase activation. (opioid-receptors.com)
  • The five disorders have similar pathophysiologies, i.e. disease-causing mechanisms, for which new strategies are in use or development to identify individuals predisposed to develop the SCARs-inducing effects of specific drugs and thereby avoid treatment with them. (wikipedia.org)
  • In the present study, we investigated the mechanisms by which MUC16 attenuates TRAIL-induced apoptosis. (biomedcentral.com)
  • These findings indicate that MUC16 protects EOC cells against TRAIL-induced apoptosis through multiple mechanisms including the blockade of TRAIL R2 expression and the regulation of cFLIP expression at both the transcriptional and the protein level. (biomedcentral.com)
  • Our contributions to elucidating the mechanisms of apoptosis led to clinical investigation of a novel class of molecules called Pro-Apoptotic Receptor Agonists, and aided in the advancement of apoptosis-promoting cancer medicines such as venclexta. (gene.com)
  • However, mechanisms involved in α-TEA induced Fas- and DR5-dependent apoptotic signaling are not fully understood. (biomedcentral.com)
  • The field of danger signal induced inflammation has revealed a common set of inflammatory mechanisms that underlie a wide variety of diseases, both induced by environmental factors, like pathogens, and by abnormal endogenous inflammatory response. (ntnu.edu)
  • Down-regulation of cFLIP following treatment of MUC16-expressing OVCAR3 cells with cFLIP siRNA also increases TRAIL-induced apoptosis. (biomedcentral.com)
  • The knockdown of L-type amino acid transporter 1 (LAT-1) by siRNA also enhanced GEF-induced cytotoxicity. (spandidos-publications.com)
  • Due to the pleiotropic effect of bortezomibenhanced TRAIL DISC formation upon TRAIL triggering, down-regulation of cFLIP L and activation of the intrinsic apoptosis pathway seem to cooperatively contribute to the antitumor effect of bortezomib/TRAIL cotreatment. (aacrjournals.org)
  • or with 20 ng/ml of recombinant human TRAIL and 10 µg/ml anti-histidine antibody preincubated with mIgG1 antibody (negative control) (far right/fourth panel). (bdbiosciences.com)
  • Cells induced to undergo apoptosis by treatment with recombinant human TRAIL gave a population of cells that was Annexin V-FITC positive (second panel, M2). (bdbiosciences.com)
  • Annexin V-FITC staining was blocked when cells were incubated with a mixture of recombinant human TRAIL and RIK-2 antibody (third panel, M2). (bdbiosciences.com)
  • The results indicate that clone RIK-2 can block cell mediated killing induced by recombinant human TRAIL as measured by Annexin V-FITC staining of Jurkat cells. (bdbiosciences.com)
  • PH24-EVs induced hepatocyte proliferation in a dose-dependent manner in vitro, whereas sham-Evs showed no significant difference compared to the controls. (bvsalud.org)
  • DcR2 interacts with DR5 in the native DISC in a TRAIL-dependent manner and prevents DR4 corecruitment to DR5. (opioid-receptors.com)
  • 2) We investigate induction of apoptosis in breast cancer cells by TRAIL receptor agonists. (cancer.gov)
  • We show that MUC16 attenuates apoptosis, activation of caspase-8 and mitochondria activation in EOC cells in response to TRAIL. (biomedcentral.com)
  • Pro-caspase-8 activation can directly result in cleavage of caspase-3 to execute apoptosis (type I cells) or cleave Bid to produce a truncated form (tBid), which induces the release of cytochrome c from the mitochondria leading to caspase-9 and subsequent caspase-3 activation (type II cells) as it is the case for EOC cells. (biomedcentral.com)
  • We isolated primary tumor cells from 13 astrocytoma and oligoastrocytoma patients of all four WHO grades of malignancy and compared the levels of TRAIL-induced apoptosis induction, long-term tumor cell survival, caspase, and caspase target cleavage. (aacrjournals.org)
  • Expression of a constitutively active Ras mutant (RasV12) in OSCC3 cells selectively upregulated surface expression of DR5, but not DR4, and restored TRAIL sensitivity. (oncotarget.com)
  • Notably, the overall TRAIL sensitivity correlated well with the levels of endogenous active Ras in the cell lines tested. (oncotarget.com)
  • As a next step we studied the influence of cell cycle arrest induced by p53 activation on TRAIL apoptosis sensitivity (Ehrhardt/Wachter et al. (uni-muenchen.de)
  • Since epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors, including gefitinib (GEF) have been reported to induce the apoptosis of several cancer cell lines, in the present study, we examined whether the cytotoxic effects of GEF are further enhanced under amino acid starvation (AAS) culture conditions. (spandidos-publications.com)
  • TRAIL has gained considerable interest in oncology since it displays specific antitumoral activity against a wide range of tumor cells (14, 41, 47) without significant side effects, at least in mice and monkeys (3, 21, 22). (opioid-receptors.com)
  • In contrast to cell lines, isolated primary tumor cells from all investigated glioma patients were highly TRAIL resistant. (aacrjournals.org)
  • Consequently, ROS-modulation has emerged as an anticancer strategy with synthesis of various ROS-inducing or responsive agents that target cancer cells. (degruyter.com)
  • Hispolon enhanced TRAIL-mediated apoptosis in renal carcinoma cells. (greenmedinfo.com)
  • Co-Treatment of Prostate Cancer Cells with Mscs Expressing Trail and Iap Inhibitors Reduce Trail Resistance and Production of Trail-Induced Cytokines. (essex.ac.uk)
  • Cells treated with the mixture of recombinant TRAIL and mIgG1 antibody could not block the killing (far right/fourth panel). (bdbiosciences.com)
  • Alpha-tocopherol ether-linked acetic acid (α-TEA), an analog of vitamin E (RRR-alpha-tocopherol), is a potent and selective apoptosis-inducing agent for human cancer cells in vivo and in vitro . (biomedcentral.com)
  • The occurrence of DR5-responsive tumor cells indicates that a DR5 receptor-specific TRAIL variant will permit tumor-selective therapies. (crg.eu)
  • Dendritic cells display a large amount of MHC-peptide complexes at their surface and can increase the expression of costimulatory receptors and migrate to the lymph nodes, spleen, and other lymphoid tissues, where they activate specific T cells. (medscape.com)
  • We also showed that DR5 was expressed on the surface of the tested cell lines which correlated with the cellular susceptibility to apoptosis induced by rhTRAIL and anti-DR5 antibody. (oncotarget.com)
  • NK cell activation and the triggering of effector functions is governed by a complex set of activating and inhibitory receptors. (frontiersin.org)
  • 2013). Cell cycle arrest was induced in tumor cell lines and patient samples in G0, G1 or G2 with cytostatic drugs, phase-specific inhibitors or RNA interference against cyclinB and E. Molecular or biochemical arrest at any point of the cell cycle augmented the rate of apoptosis by TRAIL. (uni-muenchen.de)
  • Consequently, when cell cycle arrest was deactivated by adding caffeine, the antitumor activity of TRAIL was decreased. (uni-muenchen.de)
  • While it is well understood that doxorubicin activates p53 and induces cell-cycle arrest, we observed that cell-cycle arrest disabled inactivation of anti-apoptotic Bcl-2-family members by vincristine. (uni-muenchen.de)
  • My postdoc studies on neurotransmitter receptors led to papers in Science, Nature and Cell, and earned the 1988 Boeringer Ingelheim Award. (gene.com)
  • Res effectively suppress the cardiomyocytes hypertrophy and apoptosis induced by ISO, characterized by the reduction of the myocardial cell surface area, the ANP gene expression, the LDH and MDA leakage amount and the rate of cell apoptosis, while decrease of the protein expression of GRP78, GRP94 and CHOP, and reverse the expression of Bcl-2 and Bax. (karger.com)
  • However, one pitfall observed throughout the years in in vitro and in in a multitude of human trials in vivo , is the resistance of cancer cell lines to hTRAIL-induced apoptosis. (csuohio.edu)
  • We have recently demonstrated convincingly in melanoma and triple negative breast cancer cell lines that recombinant (r) hTRAIL together with several natural compounds (Quercetin, Silibinin, Ursolic Acid) are efficient in inducing apoptosis in previously described TRAIL-resistant cancer cell lines. (csuohio.edu)
  • These variants do not induce apoptosis in DR4-responsive cell lines but show a large increase in biological activity in DR5-responsive cancer cell lines. (crg.eu)
  • Even wild-type TRAIL-insensitive ovarian cancer cell lines could be brought into apoptosis. (crg.eu)
  • The first signal may involve interaction between an MHC I-bound and/or MHC II-bound peptide on an APC with the T-cell receptor (TCRs) on the effector lymphocytes. (medscape.com)
  • VM), showed that the recovery of motor functions induced implanted either (1) as a solid piece in the lateral ven- by the grafted fetal dopamine neurons was well cor- tricle6 or a cortical cavity8 adjacent to the denervated related with the extent of graft-derived reinnervation caudate-putamen, or (2) as a crude cell suspension of the host caudate-putamen. (lu.se)
  • MUC16CTD expression is sufficient to attenuate the TRAIL signaling cascade. (biomedcentral.com)
  • Clinically, we found a negative correlation between TSC2 expression and TRAIL signaling in TCGA patient cohorts. (nki.nl)
  • She is currently a Senior Investigator leading the Chromosome Structure and Epigenetics Mechanism Unit within the Laboratory of Receptor Biology and Gene Expression at the Center for Cancer Research of the NCI/NIH in Bethesda. (elifesciences.org)
  • Correction: Expression of hormone receptors is associated with specific immunological profiles of the breast cancer microenvironment. (medscape.com)
  • This study provides the first prospective data on OPG and breast cancer risk by hormone receptor subtype. (biomedcentral.com)
  • We provide the first prospective data on OPG and breast cancer risk by hormone receptor status, in a large nested case-control study in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. (biomedcentral.com)
  • Structurally novel histamine H3 receptor antagonists GSK207040 and GSK334429 improve scopolamine-induced memory impairment and capsaicin-induced secondary allodynia in rats. (ox.ac.uk)
  • Functional antagonism of central H(3) receptors was demonstrated by blockade of R-alpha-methylhistamine-induced dipsogenia in rats (ID(50)=0.02 and 0.11 mg/kg p.o. for GSK207040 and GSK334429, respectively). (ox.ac.uk)
  • This study was undertaken to investigate whether Res can protect the heart suffering from hypertrophy injuries induced by isoproterenol (ISO), and whether the protective effect is mediated by endoplasmic reticulum (ER) stress. (karger.com)
  • These NFPs are a chemoattractant for host phagocytes and can be recognised by formyl peptide receptors on the plasma membrane [ 8 , 9 ]. (nature.com)
  • Due to its bacterial ancestry, mitochondrial formylation of methionine is required for translation initiation of mtDNA-derived mRNA [ 7 ] and will therefore be recognised by the same formyl peptide receptors. (nature.com)
  • Synthetic peptide corresponding to aa 427-445 of human TRAIL-R1. (enzolifesciences.com)
  • Consequently, cFLIP isoforms are potent negative regulators of the TRAIL signaling cascade. (biomedcentral.com)
  • This was associated with DIM‐enhanced phosphorylation of the signaling intermediates Akt, insulin receptor substrate‐1, and insulin receptor early in differentiation. (researchgate.net)
  • Genetic contribution of tumor necrosis factor (TNF)-alpha gene promoter (-1031, -863 and -857) and TNF receptor 2 gene polymorphisms in endometriosis susceptibility. (cdc.gov)
  • At the human recombinant H(3) receptor, GSK207040 and GSK334429 were potent functional antagonists (pA(2)=9.26+/-0.04 and 8.84+/-0.04, respectively versus H(3) agonist-induced changes in cAMP) and exhibited inverse agonist properties (pIC(50)=9.20+/-0.36 and 8.59+/-0.04 versus basal GTPgammaS binding). (ox.ac.uk)