• 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • In the current study, we demonstrate that DcR1 and DcR2 inhibit TRAIL-induced apoptosis by distinct mechanisms. (opioid-receptors.com)
  • In the field of cell biology, TNF-related apoptosis-inducing ligand (TRAIL), is a protein functioning as a ligand that induces the process of cell death called apoptosis. (wikipedia.org)
  • TRAIL has also been designated CD253 (cluster of differentiation 253) and TNFSF10 (tumor necrosis factor (ligand) superfamily, member 10). (wikipedia.org)
  • In humans, the gene that encodes TRAIL is located at chromosome 3q26, which is not close to other TNF family members. (wikipedia.org)
  • TRAIL shows homology to other members of the tumor necrosis factor superfamily. (wikipedia.org)
  • These artificial TRAIL mimics bind to DR4/DR5 on cancer cells and induce cell death via both apoptosis and necrosis, which makes them a potential candidate for anticancer drug development. (wikipedia.org)
  • Flow Cytometric Analysis of TRAIL-induced Killing and RIK-2 Blocking using FITC Annexin V staining. (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)
  • 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)
  • Apo-2L oder „tumor necrosis factor (TNF)-related apoptosis ligand" (TRAIL), TRAIL, ist ein Mitglied der TNF-Familie und ein vielversprechendes Protein für die Krebs. (uni-marburg.de)
  • Apo-2L or tumor necrosis factor (TNF)-related apoptosis ligand, TRAIL, is one of several members of the TNF family and due its selectivity towards transformed versus normal cells it bears the potential as a cancer therapeutic agent. (uni-marburg.de)
  • Furthermore, the TRAIL system seems to circumvent the resistance of tumors induced by treatment with chemo- and radiotherapie. (uni-marburg.de)
  • Besides the high apoptosis-inducing activity on cancer cells, no toxicity in mice and on freshly isolated human hepatocytes of either IZ-TRAIL alone or in combination with diverse chemotherapeutic drugs was observed. (uni-marburg.de)
  • TNF superfamily member (TRAIL) is a type II transmembrane protein and is responsible for initiating apoptosis. (ekb.eg)
  • Hispolon enhanced TRAIL-mediated apoptosis in renal carcinoma cells. (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)
  • Background: TNF-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily that can either induce cell death or activate survival pathways after binding to death receptors (DRs) DR4 or DR5. (ebsco.com)
  • INTRODUCTION: Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is a tumour necrosis factor (TNF) family member capable of inducing apoptosis in many cell types. (ox.ac.uk)
  • Among new therapeutic strategies, the efficacy of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), a member of the TNF superfamily with strong antitumoral activity and minimal toxicity to most normal cells and tissues, was investigated by complementary approaches both in vitro and in preclinical models. (hal.science)
  • EXPERIMENTAL DESIGN: The sensitivity of osteosarcoma and Ewing's sarcoma cell lines to TRAIL was investigated in vitro by determining TRAIL receptor expression together with TRAIL effects on cell viability and apoptosis. (hal.science)
  • RESULTS: In vitro, both osteosarcoma and Ewing's sarcoma cells that express the TRAIL death receptors were highly sensitive to TRAIL-induced caspase-8-mediated apoptosis. (hal.science)
  • TRAIL administered in vivo by nonviral gene therapy inhibited primary bone tumor incidence and growth by 87% and prevented tumor-induced osteolysis, leading to a significant 2-fold increase in animal survival 40 days after tumor induction. (hal.science)
  • TRAIL = Tumour necrosis-factor Related Apoptosis-Inducing Ligand. (goconqr.com)
  • TRAIL is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. (thermofisher.cn)
  • TRAIL preferentially induces apoptosis in transformed and tumor cells, but does not appear to kill normal cells although it is expressed at a significant level in most normal tissues. (thermofisher.cn)
  • Like TNF and Fas ligand, TRAIL induces apoptosis and NF-kB activation in many tissues and cells. (thermofisher.cn)
  • TNFRSF10B is the receptor for the cytotoxic ligand TNFSF10/TRAIL. (elabscience.com)
  • Another regulatory factor, tumor necrosis factor (TNF)Crelated apoptosis-inducing ligand (TRAIL) is also implicated in the induction of caspase activity, autophagy, and, potentially, autophagic PCD, during lumen formation in an epithelial cell line (6). (scienceexhibitions.org)
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) binds to death receptors and induces apoptosis in various cancer cell lines while sparing normal cells. (oncotarget.com)
  • ADI downregulates survivin, upregulates DR5 receptor and sensitizes cancer cells to TRAIL induced apoptosis. (oncotarget.com)
  • In an HCT116 xenograft model ADI-TRAIL localized to the tumor and induced dose-dependent tumor regression, the fusion protein was superior to rhTRAIL administered at the same molar amounts. (oncotarget.com)
  • TRAIL (also known as Apo2 ligand), is a trimeric protein, a TNF superfamily member, expressed as a type-II transmembrane protein and plays a physiological role in anti-tumor immune surveillance [ 1 - 6 ]. (oncotarget.com)
  • TRAIL induces apoptosis after binding to death receptor 4 (DR4 or TRAIL-R1) and/or death receptor 5 (DR5 or TRAIL-R2) [ 1 , 2 , 4 - 7 ]. (oncotarget.com)
  • Many cancer cells are intrinsically resistant to TRAIL-induced apoptosis. (oncotarget.com)
  • The mammalian extrinsic apoptosis pathway is triggered by Fas ligand (FasL) and Apo2 ligand/tumor necrosis factor (TNF)-related apoptosis-inducing ligand (Apo2L/TRAIL). (deathbase.org)
  • Thus, the extrinsic apoptosis pathway in zebrafish closely resembles its mammalian counterpart and cooperates with the intrinsic pathway to trigger tissue-specific apoptosis during embryogenesis in response to ectopic Apo2L/TRAIL expression. (deathbase.org)
  • A zebrafish cDNA presumably coding for a 214 amino acid protein with sequence similarity to mammalian TRAIL (TNF-related apoptosis inducing ligand), was also isolated. (deathbase.org)
  • A small cluster of genes were identified whose expression was enhanced after co-treatment including BclG (Bcl-2 family protein G), XAF1 (X-linked inhibitor of apoptosis associated factor-1), TRAIL (TNF-related apoptosis inducing ligand) and TAP1 (transporter 1). (mpeg3.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)
  • recruits CD8+ T cells, granulocytes, and macrophages to the infection area and induces the release of TNF-related apoptosis-inducing ligand (TRAIL) from neutrophils. (metabiom.org)
  • It causes apoptosis primarily in tumor cells, by binding to certain death receptors. (wikipedia.org)
  • Application of engineered ligands that have variable affinity for different death (DR4 and DR5) and decoy receptors (DCR1 and DCR2) may allow selective targeting of cancer cells by controlling activation of Type 1/Type 2 pathways of cell death and single cell fluctuations. (wikipedia.org)
  • Involvement of Up-regulation of Death Receptors and Bim in Hispolon-mediated TNF-related Apoptosis-inducing Ligand Sensitization in Human Renal Carcinoma. (greenmedinfo.com)
  • Hispolon induced up-regulation of Bim and death receptors expression at the post-translational level. (greenmedinfo.com)
  • Shikonin derivatives cause apoptosis and cell cycle arrest in human chondrosarcoma cells via death receptors and MAPK regulation. (ebsco.com)
  • The activity of this protein may be modulated by binding to the decoy receptors TNFRSF10C/TRAILR3, TNFRSF10D/TRAILR4, and TNFRSF11B/OPG that cannot induce apoptosis. (thermofisher.cn)
  • The conserved domain is referred to as a death domain due to the fact that many of these receptors are involved in signaling APOPTOSIS. (reference.md)
  • Ligand binding to cognate receptors activates initiator caspases directly in a death-inducing signaling complex. (deathbase.org)
  • Many key regulators of immune cell function belong to the so-called tumor necrosis factor superfamily (TNFSF) and their cognate receptors, the so-called TNF receptor superfamily. (apogenix.com)
  • The interaction of trimeric TNFSF ligands with their specific cell surface receptors leads to clustering of these receptors, followed by intracellular signal transduction. (apogenix.com)
  • Apogenix' TNF receptor agonists mimic natural trimeric ligands, thus inducing optimal trimeric assembly of the TNF receptors. (apogenix.com)
  • In contrast to agonistic antibodies, the clustering mediated by Apogenix' TNF receptor agonists is independent of additional cross-linking via Fcγ receptors. (apogenix.com)
  • The integration of pathogen-associated molecular patterns (PAMPs) from microorganisms with their surface receptors in the immune cells, induces the production of several cytokines and chemokines that presents either a pro- and/or anti-inflammatory role by stimulating the secretion of a great variety of antibody subtypes and the activation of mechanisms of controlling the disease, such as the regulatory T cells. (bvsalud.org)
  • RgpA, a cystein proteinase, although activating T cells through the protease-activated receptors (PARs), degradates CD27 and counteracts T cell activation mediated by CD27 and its ligand CD70. (thermofisher.com)
  • This protein was shown to activate antiapoptotic kinase AKT/PKB through a signaling complex involving SRC kinase and tumor necrosis factor receptor-associated factor (TRAF) 6, which indicated this protein may have a role in the regulation of cell apoptosis. (nih.gov)
  • Higher levels of survivin and x-linked inhibitor of apoptosis protein (xIAP) were expressed in active RA synovial tissues compared with inactive RA observed at both the protein and mRNA levels. (ox.ac.uk)
  • Two key molecules that control PCD are order PU-H71 members of the death-associated protein kinase (DAPk) family. (scienceexhibitions.org)
  • Both DAPk and DAPk-related protein kinase-1 (DRP-1) promote death in a way that depends on their kinase order PU-H71 activities. (scienceexhibitions.org)
  • Finally, a full-length brook trout cDNA, that presumably codes for a 255 amino acid protein with sequence similarity to mammalian TNF-alpha and lymphotoxin-alpha, was isolated. (deathbase.org)
  • However, in certain cell types, the extrinsic pathway also induces mitochondrial damage by cleaving the pro-apoptotic Bcl-2 family protein Bid to its activated truncated form (tBid), which leads to Bak and Bax activation. (biologists.com)
  • CD27-binding protein (SIVA), a proapoptotic protein, can bind to this receptor and is thought to play an important role in the apoptosis induced by this receptor. (thermofisher.com)
  • The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
  • Deciphering these mechanisms will make substantial contributions to our understanding of the cellular strategies and genetic pathways used to maintain tissue homeostasis in response to apoptosis. (birmingham.ac.uk)
  • Many key molecules involved in these pathways belong to the TNF receptor superfamily. (apogenix.com)
  • These outcomes present sturdy proof that Cu-NPs can set off each intrinsic and extrinsic apoptotic pathways to mediate uterine harm, leading to oxidative stress-related modifications in gene expression. (caspase-14.com)
  • Recent reports have shown that inflammatory pathways are the main offender for cisplatin induced nephrotoxicity. (biomedcentral.com)
  • The CD56 bright population produces immunoregulatory cytokines, including interferon-γ (IFN-γ), tumor necrosis factor-beta (TNF-B), tumor necrosis factor-α (TNF-α), granulocyte macrophage-colony stimulating factor (GMCSF), IL-10, and IL-13 ( 4 ). (frontiersin.org)
  • Tumor necrosis factor-related apoptosis- inducing ligand polymorphism. (ekb.eg)
  • This gene encodes a member of the tumor necrosis factor (TNF) cytokine family which is a ligand for osteoprotegerin and functions as a key factor for osteoclast differentiation and activation. (nih.gov)
  • Chicken Tumor necrosis factor related apoptosis inducing ligand ELISA kit is suitable for the detection of samples from chicken species. (elisakit.cc)
  • Mouse tumor necrosis factor receptor superfamily member 10B (TNFRSF10B) is a member of the TNFR family which contains 1 death domain and 3 TNFR-Cys repeats. (elabscience.com)
  • Using degenerative primers, partial cDNAs of a TNF (tumor necrosis factor) receptor and two TNF ligands were obtained by PCR of zebrafish and trout cDNAs, or cDNA libraries. (deathbase.org)
  • In addition to apoptosis, necrosis is another type of cell death that frequently occurs in response to stresses. (birmingham.ac.uk)
  • Unlike apoptosis, necrosis has long been considered to be passive and uncontrolled. (birmingham.ac.uk)
  • Once in the tumor, S. typhimurium continues to proliferate and directly kills cancer cells by triggering of apoptosis, necrosis, and cell rupture. (metabiom.org)
  • CD27 is a 50 kDa member of the tumor necrosis factor (TNF) receptor superfamily that includes CD40 and CD30. (thermofisher.com)
  • CONCLUSIONS: This study indicates that the induction of apoptosis in active RA synovial tissues is inhibited despite stimulation of the intracellular pathway(s) that lead to apoptosis. (ox.ac.uk)
  • DAPk predominantly activates apoptosis through a caspase-dependent pathway (4). (scienceexhibitions.org)
  • Delineation of the cell-extrinsic apoptosis pathway in the zebrafish. (deathbase.org)
  • Although the core apoptosis pathway has been well studied, it is not yet clear how cells modulate their susceptibilities toward apoptosis. (birmingham.ac.uk)
  • Genetic epistasis and biochemical analyses revealed that Senju regulates the Toll signaling pathway at a step that converts Toll ligand Spatzle to its active form. (sdbonline.org)
  • Toll pathway modulates TNF-induced JNK-dependent cell death in Drosophila . (sdbonline.org)
  • Furthermore, the Spätzle (Spz) family ligands for the Toll receptor are transcriptionally upregulated by activated JNK signalling in a non-cell-autonomous manner, providing a molecular mechanism for JNK-induced Toll pathway activation. (sdbonline.org)
  • Robust activation of wound-induced transcription from ple and Ddc requires Toll pathway components ranging from the extracellular ligand Spatzle to the Dif transcription factor. (sdbonline.org)
  • However, even though EX incontestably leads to beneficial processes through BDNF expression, cellular sources and molecular mechanisms underlying EX-induced cerebral BDNF overproduction are still being elucidated. (bvsalud.org)
  • It aims to provide a cohesive overview of the three main mechanisms leading to EX-induced brain BDNF production: the neuronal-dependent overexpression, the elevation of cerebral blood flow (hemodynamic hypothesis), and the exerkine signaling emanating from peripheral tissues (humoral response). (bvsalud.org)
  • Several mechanisms participate in the drug and apoptosis resistance phenotype in CSCs in various cancers. (oaepublish.com)
  • This article will review the CSCs drug and apoptosis resistance mechanisms and how to target CSCs. (oaepublish.com)
  • We have discovered that apoptosis can induce cell proliferation through distinct mechanisms in a context-dependent manner, e.g. in proliferating versus differentiating tissues ( Fan and Bergmann, Dev Cell 14: 339 ). (birmingham.ac.uk)
  • However, our understanding of the molecular mechanisms underlying apoptosis-induced proliferation is far from complete. (birmingham.ac.uk)
  • Their mechanisms include maintaining physicochemical conditions in the colon (e.g., pH and bile acid profile), balancing the quantity of beneficial gut microbiota members through the production of short-chain fatty acids, reducing the abundance of putrefactive bacteria producing enzymes such as azoreductase, β-glucosidase, β-glucuronidase, and nitroreductase, binding and degrading mutagenic compounds, as well as performing immunomodulatory activities. (metabiom.org)
  • Inhalation of agents in the workplace can induce asthma in a mechanisms involved in asthma. (cdc.gov)
  • Within this complex, procaspase-8 and -10 are activated by autoproteolytic cleavage and initiate the caspase cascade leading to apoptosis (42). (opioid-receptors.com)
  • The process of apoptosis is caspase-8-dependent. (wikipedia.org)
  • Elevated expression of caspase-3 inhibitors, survivin and xIAP correlates with low levels of apoptosis in active rheumatoid synovium. (ox.ac.uk)
  • This inhibition of apoptosis was observed downstream of caspase-3 and may involve the caspase-3 inhibitors, survivin and xIAP. (ox.ac.uk)
  • The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases mediating apoptosis. (elabscience.com)
  • in this full case, inhibition of certain caspase actions might induce autophagy. (scienceexhibitions.org)
  • Inhibition of zHDR, zOTR, the adaptor zFADD, or caspase-8-like proteases blocked ligand-induced apoptosis, as did antiapoptotic Bcl-2 family members. (deathbase.org)
  • Conserved function of caspase-8 in apoptosis during bony fish evolution. (deathbase.org)
  • Caspase-8, a member of the caspase family, plays an important role in apoptotic signal transduction in mammals. (deathbase.org)
  • The endotoxin-induced myocardial dysfunction probably depends on the toll-like receptor (TLR) 4-induced cytokines release as a delay in onset of myocardial depression after endotoxin administration ( 10 ). (frontiersin.org)
  • Recent reports have shown that cisplatin induced nephrotoxicity is characterized by activation of pro-inflammatory cytokines and chemokines. (biomedcentral.com)
  • TNF-α appears to play a central role in the cisplatin induced renal injury by activation of a large network of chemokines and cytokines in the kidney following cisplatin injection. (biomedcentral.com)
  • Instead, they release diffusable cytokines, which mediate the inflammatory reaction and resultant apoptosis of epithelial cells. (medscape.com)
  • The TNFSF consists of 19 structurally related ligands, each binding to one or more of the 29 members of the TNF receptor superfamily. (apogenix.com)
  • Peroxisome proliferator-activated receptor-γ(PPARγ) is a member of the nuclear receptor superfamily of ligand-activated transcription factors [ 10 ]. (biomedcentral.com)
  • Therapeutic intervention aims to reverse tumor-induced NK cell suppression and sustain NK cells' tumorlytic capacities. (frontiersin.org)
  • A small number of Annexin-V positive cells in the untreated population represents a basal level of apoptosis (far left/first panel). (bdbiosciences.com)
  • Human mast cells induce osteoclastogenesis through cell surface RANKL. (nih.gov)
  • Also, the activation of autophagic cell death or its obstruction when autophagy genes are suppressed typically takes place in cells where apoptosis has been blocked through the use of inhibitors. (scienceexhibitions.org)
  • Ectopic expression of these ligands during embryogenesis induced apoptosis in erythroblasts and notochord cells. (deathbase.org)
  • In addition, this molecule was capable of transmitting apoptotic signals mediated through not only Fas but also the TNF receptor in mouse Casp8-deficient cells. (deathbase.org)
  • Substantial data have provided convincing evidence establishing that human cancers emerge from cancer stem cells (CSCs), which display self-renewal and are resistant to anticancer drugs, radiation, and apoptosis, and express enhanced epithelial to mesenchymal progression. (oaepublish.com)
  • In response to stresses such as radiation and toxins, cells can get damaged and are removed primarily by apoptosis, a major form of programmed cell death. (birmingham.ac.uk)
  • Work by us and others has revealed that, surprisingly, stress-induced apoptotic cells can actively induce proliferation of their neighbouring cells to compensate for the cell loss. (birmingham.ac.uk)
  • Several years later, Kerr and co-workers 2 defined the morphological changes in cells undergoing this process, also known as apoptosis. (nature.com)
  • Upregulation of PD-1 on T cells as well as the PD-ligand (L) 1 on monocytes in individuals with septic surprise in addition has been noticed [8] and it's been demonstrated that PD-1 amounts correlate with an increase of mortality nosocomial attacks and immune system dysfunction in individuals with septic surprise [9]. (bioxorio.com)
  • The RANKL inhibitor denosumab acts to reduce skeletal-related events in patients with bone metastases. (biomedcentral.com)
  • The outcomes indicated that publicity to Cu-NPs led to vital decreases within the relative uterine weight coefficients and will increase in inflammatory cell infiltration, mitochondrial swelling and vacuolization, shortened and lowered endometrial epithelial cell microvilli, and apoptosis. (caspase-14.com)
  • The N-terminal cytoplasmic domain is not conserved across family members, however, the C-terminal extracellular domain is conserved and can be proteolytically cleaved from the cell surface. (wikipedia.org)
  • It's a member of the [blank_start]__________[blank_end] ligand family. (goconqr.com)
  • TLR4 is the most studied member in the SIC study among the TLRs family. (frontiersin.org)
  • A zebrafish cDNA was obtained that presumably codes for a 438 amino acid ovarian TNF receptor (OTR) that was identified as a death-domain-containing member of the TNF receptor family. (deathbase.org)
  • however, the pore complexes that are formed by Bak and Bax remain poorly defined in terms of their composition, size, number and structure, as well as the mechanism by which they are regulated by other Bcl-2 family members. (biologists.com)
  • The BH3:groove interaction within Bak homodimers supports a general model to explain the associations between Bcl-2 family members. (biologists.com)
  • Galectin-9 (Gal-9) can be a member from the galectin family members that selectively binds to β-galactoside [13]. (bioxorio.com)
  • In contrast to the expression of other TNFR/TNF family members, expression of CD27 and its ligand CD70 is predominantly confined to lymphocytes. (thermofisher.com)
  • A recent addition to the list of immune checkpoint inhibitors is the CD95 ligand (CD95L). (apogenix.com)
  • Macrophages and monocytes are members of the mononuclear phagocyte system. (medscape.com)
  • LPS stimulates macrophages Cefdinir to release large amounts of TNFα and IL-1β that can precipitate tissue damage and lethal surprise. (bioxorio.com)
  • He subsequently worked at the University of Texas MD Anderson Cancer Center and the University of Massachusetts Medical School in the United States during which time his research focused on regulation of program cell death (apoptosis) and its related compensatory cell proliferation. (birmingham.ac.uk)
  • This evolutionarily conserved phenomenon has been termed apoptosis-induced compensatory cell proliferation (apoptosis-induced proliferation or AiP). (birmingham.ac.uk)
  • Under pathological conditions, uncontrolled apoptosis-induced proliferation contributes to tumour development and recurrence. (birmingham.ac.uk)
  • TNFSF-mediated signaling induces a wide range of biological effects, including programmed cell death (i.e., apoptosis), proliferation, differentiation, and tumor growth. (apogenix.com)
  • The TNF superfamily members are known for the regulation of cell proliferation and death. (thermofisher.com)
  • The pathophysiology of sepsis includes inflammation, immune dysfunction, and dysfunction of coagulation, while sepsis-induced cardiomyopathy ( SIC ), defined as a global but reversible dysfunction of both sides of the heart induced by sepsis, plays a significant role in all of the aspects above in the pathogenesis of sepsis. (frontiersin.org)
  • Two types of pet sepsis model have already been established: the lipopolysaccharide(LPS)-induced inflammation and the cecal ligation and puncture (CLP) model of microbial sepsis. (bioxorio.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)
  • RÉSUMÉ L'objectif de l'étude était d'évaler l'importance clinique du ligand de CD40 soluble (sCD40L) chez des patients atteints d'un carcinome hépatocellulaire (CHC) associé au virus de l'hépatite C (VHC). (who.int)
  • However, clinical success has been limited due to poor PK and development of resistance to death receptor-induced apoptosis. (oncotarget.com)
  • Resistance to anticancer agents and apoptosis results in cancer relapse and is associated with cancer mortality. (oaepublish.com)
  • Circulating Pneumolysin, another common PAMP produced by Streptococcus pneumoniae , induced cardiomyocyte injury through triggering profound calcium influx during pneumococcal infection ( 11 ). (frontiersin.org)
  • Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related mortality in the USA and throughout the world. (asu.edu)
  • The present study was undertaken to assess the effect of rosiglitazone, a PPARγ agonist and an anti-inflammatory agent, on cisplatin induced nephrotoxicity, and its anticancer activity in DMBA induced breast cancer rats. (biomedcentral.com)
  • To best of our knowledge this is the first report which shows that pre-treatment of rosiglitazone synergizes the anticancer activity of cisplatin and minimizes cisplatin induced nephrotoxicity in DMBA induced breast cancer. (biomedcentral.com)
  • About 212,930 new cases of breast cancer were diagnosed every year, of which 40,840 were related to deaths in the United States alone [ 1 ]. (biomedcentral.com)
  • ARG81958 Rat sRANK Ligand / TNFSF11 / TRANCE ELISA Kit is an Enzyme Immunoassay kit for the quantification of Rat sRANK Ligand / TNFSF11 / TRANCE in serum, plasma (heparin, EDTA) and cell culture supernatants. (arigobio.com)
  • ARG81958 Rat RANK Ligand / TNFSF11 / TRANCE ELISA Kit results of a typical standard run with optical density reading at 450 nm. (arigobio.com)
  • 2 (Bcl-2) expression, and elevated the expression of apoptotic peptidase activating issue 1 (Apaf-1), BCL2-associated X, apoptosis regulator (Bax), and cytochrome c. (caspase-14.com)
  • however, the septic shock in the early onset of sepsis, which induced by cytokine storm and cardiac dysfunction, is also an important cause of death for septic patients, especially for the young patients with toxic shock syndrome or meningococcemia ( 2 ). (frontiersin.org)
  • Other TLR-related genes (TLR2, 3, and 9) were demonstrated to be involved in sepsis-induced cardiac dysfunction from recent studies. (frontiersin.org)
  • Targeted disruption of the related gene in mice led to severe osteopetrosis and a lack of osteoclasts. (nih.gov)
  • Administration of HMGB1-particular neutralizing antibodies starting 24 hours following the starting point of sepsis induced by CLP was proven to result in a dose-dependent save of mice from lethal sepsis [4-6]. (bioxorio.com)
  • Therefore, unveiling the related novel molecular targets and networks participating in triggering and resisting the pathobiology of MIRI is a promising and valuable frontier. (hindawi.com)
  • HIF-1 alpha as a key factor in bile duct ligation-induced liver fibrosis in rats. (edu.pl)
  • Copper nanoparticle-induced uterine injury in female rats. (caspase-14.com)
  • Mammary tumours were induced in female Sprague-Dawley rats by feeding orally with dimethylbenz [a]anthracene (DMBA) (60 mg/kg). (biomedcentral.com)
  • T cell activation was reported to induce expression of this gene and lead to an increase of osteoclastogenesis and bone loss. (nih.gov)