• Activation of caspase-11 by LPS is known to cause the activation of other caspase proteins, leading to septic shock, pyroptosis, and often organismal death. (wikipedia.org)
  • These bacteria activate IFN-induced guanylate binding proteins, which are thought to mediate caspase-11 activation by promoting vacuolar lysis and release of bacteria and the LPS they produce into the cytoplasm. (wikipedia.org)
  • The formation of necrosome, a multiprotein complex that stimulates necroptosis, is tightly regulated by proteins downstream of the receptor and can be the deciding factor in inducing necroptosis. (news-medical.net)
  • Cell death by necroptosis involves membrane breakage, which leaks intracellular molecules such as heat shock proteins. (news-medical.net)
  • Viral proteins (v-FLIPS) which inhibit recruitment and activation of caspase-8 have been isolated. (bdbiosciences.com)
  • 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)
  • DEATH domain, found in proteins involved in cell death (apoptosis). (embl-heidelberg.de)
  • Other DD-containing proteins, such as ankyrin, MyD88 and pelle, are probably not directly involved in cell death signalling. (embl-heidelberg.de)
  • There are 10756 DEATH domains in 10503 proteins in SMART's nrdb database. (embl-heidelberg.de)
  • Taxonomic distribution of proteins containing DEATH domain. (embl-heidelberg.de)
  • The complete taxonomic breakdown of all proteins with DEATH domain is also avaliable . (embl-heidelberg.de)
  • Click on the protein counts, or double click on taxonomic names to display all proteins containing DEATH domain in the selected taxonomic class. (embl-heidelberg.de)
  • The most important enzymes involved in apoptosis are caspases, which hydrolyze important structural and functional proteins of the cell, ultimately leading to apoptosis. (spandidos-publications.com)
  • Once activated by their respective upstream signals, caspase-8 and -9 may cleave and activate downstream executioner caspases -3 and -7, which, in turn, cleave a plethora of target proteins, resulting in apoptotic death ( 6 - 8 ). (spandidos-publications.com)
  • The inhibitor of apoptosis proteins (IAPs) inhibit apoptosis by interacting with and then regulating the functions of caspase-8 or caspase-9, -3 and -7 ( 9 , 11 , 12 ). (spandidos-publications.com)
  • Caspases are essential in cells for apoptosis , one of the main types of programmed cell death in development and most other stages of adult life, and have been termed "executioner" proteins for their roles in the cell. (wikidoc.org)
  • They are called cysteine proteases , because they use a cysteine residue to cut those proteins, and are called caspases because the cysteine residue cleaves their substrate proteins at specific asparagine residues. (wikidoc.org)
  • Glycans, either alone or complexed with glycan-binding proteins, can deliver intracellular signals or control extracellular processes that promote initiation, execution and resolution of cell death programs. (nature.com)
  • Herein, we review the role of glycans and glycan-binding proteins as essential components of the cell death machinery during physiologic and pathologic settings. (nature.com)
  • At that time, glycobiology, which is the study of carbohydrates and their recognition by motif-specific carbohydrate-binding proteins or lectins, lagged far behind the studies that defined the structural and cellular biology of cell death. (nature.com)
  • Caspases are so-called executioner enzymes, that when activated, destroy the cancer cell from within, by chopping up proteins left and right-kind of "death by a thousand cuts. (nutritionfacts.org)
  • C1QBP significantly increased ROS level, apoptosis, and the expression of apoptotic proteins such as cleaved caspase-3 and bax/bcl2 via regulating XDH. (medsci.org)
  • However, since proteins with similar activities are present in mammals and since their mechanisms are likely to be conserved even if true sequence homologues are not identified, understanding how Rpr, Hid, and Grim act to bring about death is an important area of research. (caltech.edu)
  • BACKGROUND AND PURPOSE: The cannabinoid CB(1) receptor is primarily thought to be functionally coupled to the G(i) form of G proteins, through which it negatively regulates cAMP accumulation. (bvsalud.org)
  • Several DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS can bind to the death domains of the activated receptors and through a complex series of interactions activate apoptotic mediators such as CASPASES. (bvsalud.org)
  • Consistent with the results using c-Flip −/− MEFs, we found that TNF α stimulation induced caspase-dependent prolonged JNK activation and ROS accumulation, followed by apoptotic and necrotic cell death in various tumor cells. (nature.com)
  • They found that TNF induced both apoptotic and necrotic cell death. (news-medical.net)
  • Resistance to these treatments are due to the cells resisting apoptotic death. (news-medical.net)
  • 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)
  • Radiation and other agents induce caspase activation fundamentally via the mitochondrial pathway, which includes mitochondrial integration of apoptotic signals and the subsequent release of cytochrome c into the cytosol ( 5 , 9 , 10 ). (spandidos-publications.com)
  • The cleavage and inactivation of ICAD/DFF45 by a caspase allows CAD to enter the nucleus and fragment the DNA, causing the characteristic 'DNA ladder' seen in apoptotic cells. (wikidoc.org)
  • In all cases, apoptosis is mediated by caspases, although it is unclear how these diverse apoptotic stimuli cause protease activation. (diva-portal.org)
  • The other pathway is controlled by the release of cytochrome c from mitochondria and the subsequent ATP-dependent activation of the death regulator apoptotic protease-activating factor 1 (Apaf-1). (diva-portal.org)
  • Apoptotic adaptor molecule specific for caspase-2 and FASL/TNF receptor-interacting protein RIP. (joplink.net)
  • Apoptotic cell death is characterized by DNA fragmentation, membrane blebbing, and the formation of apoptotic bodies. (invivogen.com)
  • Two decades later, pioneering studies suggested that lectin-like molecules constitutively expressed on the surface of macrophages can selectively recognize changes on glycans decorating the surface of apoptotic thymocytes, 4 , 5 although these studies likewise did not provide substantial insight into the mechanisms by which lectin-glycan interactions regulate cell death. (nature.com)
  • The expression of wild-type arrestin-2 or its cleavage product arrestin-2-(1-380), but not of its caspase-resistant mutant, restores cell sensitivity to apoptotic stimuli. (bvsalud.org)
  • Caspase-8 (FLICE/MACH-1) is a 55 kDa cytosolic protein with homology to the CD95/Fas-associated signal transducer, FADD/MORT-1, as well as to other caspase (ICE/Ced-3) cysteine proteases. (bdbiosciences.com)
  • The N-terminal region of caspase-8 contains an amino acid sequence, termed the death domain, that facilitates caspase-8-FADD direct interaction. (bdbiosciences.com)
  • FADD therefore acts as an adapter molecule, allowing caspase-8 to become recruited to the cytoplasmic region of Fas following receptor activation. (bdbiosciences.com)
  • TNF-mediated apoptosis is initiated by ligand-induced recruitment of TNF receptor-associated death domain (TRADD), Fas-associated death domain (FADD), and caspase-8 to the death domain of TNF receptor 1 (TNFR1), thereby establishing the death-inducing signaling complex (DISC). (jci.org)
  • FADD then activates caspase-8, which ignites the death machine, and kills the cell. (nutritionfacts.org)
  • The adaptor molecule FADD recruits Caspase-8 to the activated receptor. (lu.se)
  • Instead, they react to signals that are sent from the toll-like receptors 7 and 9. (medscape.com)
  • Caspases are a family of calcium -dependent cysteine proteases , which play essential roles in apoptosis (programmed cell death), necrosis and inflammation . (wikidoc.org)
  • Caspase-1 is the prototypical member of the caspase family of cysteine proteases. (enzolifesciences.com)
  • The resulting death-inducing signaling complex performs Caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. (lu.se)
  • Murine caspase-11, and its human homologs caspase-4 and caspase-5, are mammalian intracellular receptor proteases activated by TLR4 and TLR3 signaling during the innate immune response. (wikipedia.org)
  • The proteases involved are of different origins and types: (i) present as precursor in plasma, (ii) secreted into the plasma by activated platelets or other blood cells, or (iii) intracellularly activated and cleaving cytosolic receptor domains. (frontiersin.org)
  • Although these platelet activation processes are relatively well-studied as a function of the platelet environment, only since recently it is becoming clear that a multitude of proteases present in plasma or produced by platelets themselves are important for the distinct properties of platelet populations, often by cleaving specific receptors. (frontiersin.org)
  • Here, we review current knowledge how proteases act on platelet receptors and the platelet membrane surface. (frontiersin.org)
  • Production of IL-1β downstream of caspase-11 requires another canonical inflammasome, called the NLRP3 inflammasome, that activates caspase-1. (wikipedia.org)
  • The DD mediates self-association of these receptors, thus giving the signal to downstream events that lead to apoptosis. (embl-heidelberg.de)
  • The intracellular domain of the p75 neurotrophin receptor (p75ICD) lacks catalytic activity but contains a motif similar to death domains found in the cytoplasmic regions of members of the tumor necrosis factor receptor family and their downstream targets. (embl-heidelberg.de)
  • Although some aspects of the signaling pathways downstream of p75 have been elucidated recently, mechanisms of receptor activation and proximal signaling events are unknown. (embl-heidelberg.de)
  • A surface area devoid of charged residues in the p75ICD death domain may indicate a potential site of interaction with downstream targets. (embl-heidelberg.de)
  • Our findings suggest that KTC could inhibit the growth of ectopic endometrial tissue through upregulating the level of TNF- α and its downstream signaling, including caspases and cytochrome c. (hindawi.com)
  • Processing of caspases is required for activation of downstream signaling and dsRNA stimulation inducese the processing of these caspases. (reactome.org)
  • Epistasis analysis suggests that the Toll pathway acts as a downstream modulator for JNK-dependent cell death. (sdbonline.org)
  • Caspase-11 was subsequently shown to be a cytosolic protein that responds solely to intracellular, cytosolic LPS. (wikipedia.org)
  • This mechanism contrasts to that of the canonical inflammasome, in which a bacterial ligand activates caspase-1 through an upstream sensor protein, and this is the reason why caspase-11 is often referred to as the non-canonical inflammasome. (wikipedia.org)
  • We have recently shown that tumor necrosis factor (TNF) α induces caspase-dependent and -independent JNK activation and ROS accumulation in cellular FLICE-inhibitory protein (c-Flip) −/− murine embryonic fibroblasts (MEFs). (nature.com)
  • The inhibitor of death receptor signaling, FLICE-inhibitory protein defines a new class of tumor progression factors. (nature.com)
  • Full-length recombinant human caspase-8 protein was used as immunogen. (bdbiosciences.com)
  • The death domain (DD) is a homotypic protein interaction module composed of a bundle of six alpha-helices. (embl-heidelberg.de)
  • TRAIL, also called Apo2L, is a cytotoxic protein that induces apoptosis of many transformed cell lines but not of normal tissues, even though its death domain-containing receptor, DR4, is expressed on both cell types. (embl-heidelberg.de)
  • Protein levels of caspases 8, 9, and 3 and cytochrome c in the ectopic and eutopic endometrium were measured by western blotting. (hindawi.com)
  • TUNEL and western blot assay showed that KTC could induce apoptosis of endometriotic tissues, accompanied with the increased protein expression of caspases 8 and 9, activated caspase-3, and cytochrome c in a dose-dependent manner. (hindawi.com)
  • Horvitz and his colleague Junying Yuan [2] found in 1993 that the protein encoded by the ced-3 gene was a cysteine protease with similar properties to the mammalian interleukin-1-beta converting enzyme (ICE) (now known as caspase 1) which at the time was the only known caspase. (wikidoc.org)
  • These include members of the Bcl-2 protein family, course, and extent of programmed cell death will aid man- which have both proapoptotic and antiapoptotic activity agement of patients with severe infections. (cdc.gov)
  • CusabioAlternative Name(s): Caspase and RIP adapter with death domain RIP-associated protein with a death domainGene. (joplink.net)
  • Their assembly leads to the activation of proinflammatory caspases (Caspase-1 or Caspase-4/5/11) and cytokines (interleukin (IL)-1 and IL-18) and the pore-forming protein, Gasdermin-D. Pyroptosis is characterized by nuclear condensation, cell swelling, and the formation of plasma membrane pores leading to cell lysis and release of cellular contents such as HMGB1, a DAMP of large size. (invivogen.com)
  • In contrast, 14.7K did not affect TNF-induced NF-κB activation via recruitment of receptor-interacting protein 1 (RIP-1) and TNF receptor-associated factor 2 (TRAF-2). (jci.org)
  • Arrestins are best known for their role in homologous desensitization of G protein-coupled receptors (GPCRs). (bvsalud.org)
  • G protein-coupled receptor kinases (GRKs) and arrestins terminate signaling by G protein-coupled receptors exerting a powerful influence on receptor functions. (bvsalud.org)
  • These include production of homologues of mammalian tumor necrosis factor receptor, interleukin-1beta receptor, interleukin 18-binding protein, interferon-alpha/beta receptor, and interferon-gamma receptor, as well as a complement-binding protein and a caspase inhibitor. (medscape.com)
  • An antagonist decoy receptor (designated as TRID for TRAIL receptor without an intracellular domain) that may explain the resistant phenotype of normal tissues was identified. (embl-heidelberg.de)
  • The intrinsic pathway is engaged by a variety of intracellular signals and leads to the activation of Caspase-9. (invivogen.com)
  • Necroptosis is a form of RCD initiated by extracellular or intracellular perturbations detected by death receptors, such as FAS and TNFR1, or pathogen recognition receptors (PRRs), including TLR3, TLR4, and DAI/ ZBP1. (invivogen.com)
  • Necroptotic cell death causes ion influx, cell swelling, and membrane lysis followed by the uncontrollable release of intracellular contents including pro-inflammatory cytokines and danger-associated molecular patterns (DAMPs). (invivogen.com)
  • What is the precise role of intracellular and extracellular galectins in the control of cell death programs? (nature.com)
  • Using CB(1)/CB(2) chimeric receptors, the second intracellular loop (ICL2) of the CB(1) receptor was identified as primarily responsible for mediating G(s) and G(i) coupling specificity. (bvsalud.org)
  • Radiation induces caspase activation fundamentally via the mitochondrial pathway. (spandidos-publications.com)
  • In contrast, the extrinsic pathway is initiated by extracellular perturbations, through death receptors, and induces the activation of Caspase-8. (invivogen.com)
  • Following this discovery, the other mammalian caspases, in addition to caspases in other organisms such as the fruit fly Drosophila melanogaster , were soon identified and characterised. (wikidoc.org)
  • Following completion of the Drosophila genome sequence, we carried out comprehensive BLAST searches to annotate it with respect to apoptosis, and found sequence homologues of virtually all mammalian cell death genes with the exception of death receptors. (caltech.edu)
  • The only Drosophila cell death genes for which mammalian homologues have not been identified are the cell death activators Rpr, Hid, and Grim. (caltech.edu)
  • 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)
  • This is because they are inflammatory caspases, which in concert with CASP1 , are involved in cytokine maturation. (wikidoc.org)
  • first focus on transcription factors and other parameters, such as cytokine receptor signaling. (scielo.br)
  • As Dörner emphasized, these cells are not under the command of the B-cell receptor and are independent of the cytokine BAFF (B-cell activating factor). (medscape.com)
  • MCF-7) and this phenotype is blocked by overexpression of the caspase-3 protease inhibitor, CrmA. (bdbiosciences.com)
  • Healthy male Sprague‑Dawley rats were used in the present study to examine the radioprotective effect of a type of pan-caspase inhibitor, z-VAD-fmk, following radiation, to investigate the effects of caspase blockade in a model of the nucleus of the abducens nerve. (spandidos-publications.com)
  • z-VAD-fmk ( N -benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone) is a powerful, irreversible and cell permeable inhibitor of caspases, and has been demonstrated to directly block the activity of caspases ( 13 ). (spandidos-publications.com)
  • Surprisingly, it has recently been shown that LPS activates caspase-11 not through a receptor/scaffold mediator, but through direct LPS binding to the caspase-11 CARD domain. (wikipedia.org)
  • the apoptosome (regulated by cytochrome c and the Bcl-2 family ) which activates caspase-9 . (wikidoc.org)
  • FAS is a so-called death receptor, which activates the FAS-associated death domain, along with death receptor five, and death receptor four. (nutritionfacts.org)
  • In cancer cells, curcumin, the pigment in the spice turmeric that makes curry powder yellow, upregulates and activates death receptors-as has been demonstrated in human kidney cancer cells, as well as skin cancer, and nose and throat cancer. (nutritionfacts.org)
  • Studies show that necrotic death is induced by a ligand binding to a receptor, such as when apoptosis is initiated. (news-medical.net)
  • As compared to passage-matched control cells, SWCNT-transformed BEAS-2B cells exhibited resistance to apoptosis induced by death ligands, e.g., tumor necrosis factor-a and Fas ligand, but not by inducers of mitochondria-mediated apoptosis, e.g., antimycin A and cisplatin, suggesting death receptor pathway as the primary pathway of defective apoptosis in SWCNT-transformed cells. (cdc.gov)
  • A closer look at Drosophila male testes revealed the surprising observation that high levels of caspases are present in wild type testes, along with the caspase activator Ark. (caltech.edu)
  • For bacteria that do not typically access the host cytosol, caspase-11 is activated with delayed kinetics if Gram-negative bacteria aberrantly escape the vacuole and enter into the cytoplasm. (wikipedia.org)
  • Viral particles bind to plasma membrane receptors on host cells and then enter into the cytoplasm, where the viral genome is replicated and viral progeny are assembled. (medscape.com)
  • Given that ROS accumulation and necrotic cell death enhance inflammation followed by compensatory proliferation of tumor cells, selective suppression of caspase-dependent ROS accumulation will be an alternative strategy to protect cells from ROS-dependent DNA damage and compensatory tumor progression. (nature.com)
  • The induced necrotic cell death by virial agents is important for virus-induced inflammation, and blockage of necroptosis is a primary concern for controlling certain viral diseases. (news-medical.net)
  • Unlike inflammation, apoptosis is a 'programmed cell death' mechanism, whereby enzymatic reactions lead to cell apoptosis and phagocytes remove the debris without stimulating an inflammatory response. (spandidos-publications.com)
  • Though caspase-11 was thought to be activated only by TLR4, these experiments showed that it was in fact activated by TRIF signaling, mediated by both TLR4 and TLR3 stimulation. (wikipedia.org)
  • 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)
  • T cells co-stimulation requires receptor CD28/B7 and B cell co-stimulation requires receptor CD40. (tutorialspoint.com)
  • Here, decreasing stimulation via the B-cell receptor by aging T-lymphocytes makes a difference. (medscape.com)
  • My postdoc studies on neurotransmitter receptors led to papers in Science, Nature and Cell, and earned the 1988 Boeringer Ingelheim Award. (gene.com)
  • Caspase-11 has been shown in vitro to be activated by Shigella flexneri infection, while a guinea pig model of Shigella infection has been shown to activate the human homolog of caspase-11, caspase-4. (wikipedia.org)
  • This allows them to autoactivate, so that they can then proceed to activate the effector caspases. (wikidoc.org)
  • It can also activate the death machine directly-as has been shown in lung cancer and colon cancer. (nutritionfacts.org)
  • 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)
  • The antibody recognizes both the proform of human caspase-8 (55/50 kDa doublet) as well as the cleaved form (40/36 kDa doublet) on SDS/PAGE. (bdbiosciences.com)
  • To determine the therapeutic efficacy and immunomodulatory effect of an anti-human death receptor 5 (DR5) antibody, TRA-8, in eliminating macrophage subsets in a mouse model of type II collagen-induced arthritis (CIA). (nih.gov)
  • TRIF activation is necessary for the upregulation of pro-caspase-11 (an inactive precursor to active caspase-11) expression and caspase-11-mediated pyroptosis. (wikipedia.org)
  • Caspase-11 activation by direct binding to LPS represents a novel and unprecedented mechanism for caspase activation. (wikipedia.org)
  • Caspase-11 activation results in pyroptosis, a form of lytic cell death that releases inflammatory molecules such as ATP, HMGB1 and IL-1α from the cytosol. (wikipedia.org)
  • NK cell activation and the triggering of effector functions is governed by a complex set of activating and inhibitory receptors. (frontiersin.org)
  • 2006). The E3 Ubiquitin Ligase Itch Couples JNK Activation to TNF α -induced Cell Death by Inducing c-FLIP(L) Turnover. (nature.com)
  • Reactive oxygen species promote TNF α -induced death and sustained JNK activation by inhibiting MAP kinase phosphatases. (nature.com)
  • The flow-dependent adhesion of platelets to those and other extracellular matrix components is stabilized by a panel of integrins, including integrin α 2 β 1 , α IIb β 3 , and α 6 β 1 (adhesive platelet population), while the initial activation of platelets is achieved by signaling via the collagen/laminin receptor, glycoprotein VI (GPVI). (frontiersin.org)
  • several of these TNF receptors use caspase activation as a signalling mechanism. (embl-heidelberg.de)
  • The prodomain of the initiator caspases contain domains such as a CARD domain (e.g. caspases-2 and -9) or a death effector domain (DED) (caspases-8 and -10) that enables the caspases to interact with other molecules that regulate their activation. (wikidoc.org)
  • Prevention of ATP production completely inhibited caspase activation and apoptosis in response to chemotherapeutic drugs and staurosporine. (diva-portal.org)
  • In contrast, inhibition of ATP production did not affect caspase activation after triggering of CD95. (diva-portal.org)
  • These results suggest that chemotherapeutic drug-induced caspase activation is entirely controlled by a receptor-independent mitochondrial pathway, whereas CD95-induced apoptosis can be regulated by a separate pathway not requiring Apaf-1 function. (diva-portal.org)
  • Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. (cancerindex.org)
  • To date the mechanism of regulation of caspase-1 activation is complex and poorly understood. (enzolifesciences.com)
  • The nonapoptotic caspase function of both caspase-8 and -10 does not require the protease activity and the DED-containing prodomains are sufficient for NF-kB activation. (reactome.org)
  • Depending on the cell context, ligation of DR3 by TL1A can trigger one of two signaling pathways, activation of the transcription factor NF-kB, or activation of caspases and apoptosis. (novusbio.com)
  • 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)
  • Apoptosis is programmed cell death triggered by activation of death receptors or cellular stress. (bvsalud.org)
  • Activation of caspases is the hallmark of apoptosis. (bvsalud.org)
  • Here we demonstrate that arrestin-2 isoform is cleaved by caspases during apoptosis induced via death receptor activation or by DNA damage at evolutionarily conserved sites in the C-terminus. (bvsalud.org)
  • KEY RESULTS: CB(1) receptors could couple to both G(s)-mediated cAMP accumulation and G(i)-induced activation of ERK1/2 and Ca(2+) mobilization, whereas CB(2) receptors selectively coupled to G(i) and inhibited cAMP production. (bvsalud.org)
  • Organic solvent-induced proximal tubular cell toxicity via caspase-3 activation. (cdc.gov)
  • It has been consequently hypothesized that the Fas-FasL death complex may play a role upon maintaining the immune privilege of the disc. (medsci.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)
  • 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)
  • Studies on the molecular mechanism of neuronal cell apoptosis following radiation have enriched the number of protective therapeutic strategies against radiation-induced neuronal cell death ( 2 ). (spandidos-publications.com)
  • this coupled with the unwanted apoptosis that occurs with ischaemia or Alzheimer's disease , has boomed the interest in caspases as potential therapeutic targets since they were discovered in the mid 1990s. (wikidoc.org)
  • Understanding the function of lectin-glycan recognition systems in cell death will facilitate the implementation of novel therapeutic strategies aimed at controlling unbalanced cell proliferation and survival in several pathologic conditions. (nature.com)
  • The mechanism linking caspase-11 to NLRP3 is not currently known. (wikipedia.org)
  • This mechanism produces the less reactive auto receptors with a moderate affinity for self-antigens that would lead to disease allowing the cells to survive. (tutorialspoint.com)
  • Therefore, the anorexigenic effect exerted by the CBD could be the result of a multitarget mechanism, involving the whole endocannabinoid receptor system, particularly in the hypothalamus. (researchgate.net)
  • [ 8 ] Caspase inhibition in clonal striatal cells showed no correlation between the reduction of aggregates in the cells and increased survival. (medscape.com)
  • Caspase-generated arrestin-2-(1-380) fragment translocates to mitochondria increasing cytochrome C release, which is the key checkpoint in cell death. (bvsalud.org)
  • Arrestin-2-(1-380) does not facilitate apoptosis in BID knockout cells, whereas its ability to increase caspase-3 activity and facilitate cytochrome C release is rescued when BID expression is restored. (bvsalud.org)
  • There is increasing evidence that neuronal cell death occurs via extrinsic (death receptors) and intrinsic (mitochondria) pathways. (spandidos-publications.com)
  • [ 7 ] More recent data from striatal neuronal cultures transfected with mutant huntingtin and transgenic mice carrying the spinocerebellar ataxia-1 (SCA-1) gene (another CAG repeat disorder) suggest that NIIs may not be necessary or sufficient to cause neuronal cell death, but translocation into the nucleus is sufficient to cause neuronal cell death. (medscape.com)
  • CB(1)/CB(2) receptor chimeras and site-directed mutagenesis combined with functional assays and computer modelling were used to determine the structural determinants mediating selective coupling to G(s) and G(i). (bvsalud.org)
  • One is mediated by recruitment of the proximal regulator caspase-8 to the death receptor complex. (diva-portal.org)
  • While caspase-11-mediated pyroptosis provides defense against pathogens, it has also been shown to cause damage to the host as well. (wikipedia.org)
  • An antagonist decoy receptor and a death domain-containing receptor for TRAIL. (embl-heidelberg.de)
  • We applied the McPhail model which is a traditional classical method to assessment of the progesterone receptor agonist and antagonist activity of a compound. (hindawi.com)
  • These molecules respond to stimuli which cause the clustering of the initiator caspases. (wikidoc.org)
  • Jawed vertebrates (gnathostomes) generate a diverse repertoire of B and T cell antigen receptors through the rearrangement of immunoglobulin V, D, and J gene fragments, whereas jawless fish (agnathans) assemble diverse lymphocyte antigen receptor genes through the genomic rearrangement of leucine-rich repeat (LRR) - encoding molecules. (scielo.br)
  • Caspase-11 appears to provide immune defense against bacteria that enter or access the host cell cytosol. (wikipedia.org)
  • Some caspases are also required in the immune system for the maturation of cytokines . (wikidoc.org)
  • Due to random genetic recombinations, immune cells genetically express receptors for the specific self and foreign antigens in the central lymphoid organs. (tutorialspoint.com)
  • An important way of regulation is provided by proteolytic cleavage of several of these receptors, leading to either a gain or a loss of platelet function. (frontiersin.org)
  • Caspases exist as inactive proenzymes which undergo proteolytic processing at conserved aspartic residues to produce two subunits, large and small, that dimerize to form the active enzyme. (cancerindex.org)
  • These data, combined with the inability of dBruce to block death induced by the apical caspase Dronc or the proapoptotic Bcl-2 family member Debcl/Drob-1/dBorg-1/Dbok, suggest that dBruce regulates cell death at a novel point. (caltech.edu)
  • Extracellular LPS binds specifically to the cell surface receptor TLR4. (wikipedia.org)
  • Once expressed, caspase-11 is only able to bind cytosolic LPS and cannot respond to extracellular LPS. (wikipedia.org)
  • Caspase-11 (EC 3.4.22.64, CASP-11) is an protease enzyme that has a preferred cleavage sequence of (Ile/Leu/Val/Phe)-Gly-His-Asp, with a strict requirement for Asp at the P1 position. (wikipedia.org)
  • The exact contribution that the cleavage of many caspase substrates makes to the biochemistry and morphology of apoptosis is unclear. (wikidoc.org)
  • Upon caspase-3/7 cleavage, Ac-DEVD-AFC generates the AFC fluorophore which has bright blue fluorescence and can be detected at Ex/Em=380 nm/500 nm. (eurogentec.com)
  • CASP2 , CASP8 , CASP9 and CASP10 ) cleave inactive pro-forms of effector caspases, thereby activating them. (wikidoc.org)
  • The conserved domain is referred to as a DEATH DOMAIN due to the fact that many of these receptors are involved in APOPTOSIS signaling pathways. (bvsalud.org)
  • A family of cell surface receptors that signal via a conserved domain that extends into the cell CYTOPLASM. (bvsalud.org)
  • Caspases are synthesized in the cell as inactive zymogens and require to be activated to be functional. (spandidos-publications.com)
  • They are first synthesized as inactive pro-caspases , that consist of a prodomain, a small subunit and a large subunit. (wikidoc.org)
  • Caspase-1 exists in cells as an inactive 45kDa pro-enzyme. (enzolifesciences.com)
  • In THP-1 cells, a large proportion of the caspase-1 is present in the inactive pro-enzyme form. (enzolifesciences.com)
  • To suppress this antiapoptotic function of NF- κ B might be a promising strategy to increase susceptibility of tumor cells to stress-induced cell death. (nature.com)
  • This result sparked further interest in how necrotic cell death occurs. (news-medical.net)
  • The "death receptors", which typically cause cell death by apoptosis, can be activated by ligands, such as TNF. (news-medical.net)
  • Necroptosis can therefore start in an apoptosis-like manner, but result in necrotic-like cell death. (news-medical.net)
  • Viral infections can induce different kinds of cell death. (news-medical.net)
  • Cell death before the viral replication cycle is complete can limit disease progression. (news-medical.net)
  • In such cases, alternate mechanisms of cell death, such as necroptosis can be successfully induced. (news-medical.net)
  • The importance of caspases to apoptosis and programmed cell death was originally established by Robert Horvitz and colleagues who found that the ced-3 gene was required for the cell death that took place during the development of the nematode C. elegans . (wikidoc.org)
  • Some labile cell types whose numbers are normally or all severe infections that could be targets for pharmaco- controlled through programmed cell death are subject to logic intervention. (cdc.gov)
  • Extensive lymphocyte severe infections is a massive loss of lymphocytes, den- apoptosis has also occurred in humans and animals infect- dritic cells, gastrointestial epithelial cells, and other cell ed with several exotic agents, including Bacillus anthracis , types through apoptosis, or programmed cell death. (cdc.gov)
  • Fortunately, because programmed cell death is pathogens and bioterrorism agents. (cdc.gov)
  • acquired defects in the control of apoptosis may lead to a Apoptosis, or programmed cell death, is the method variety of disease states. (cdc.gov)
  • Regulated cell death (RCD) plays an essential role in cell homeostasis, tissue remodeling, and diseases. (invivogen.com)
  • In contrast to accidental cell death (ACD), a biologically uncontrolled process, RCD relies on dedicated molecular machinery. (invivogen.com)
  • Its function is the elimination of unwanted cells during physiological conditions such as embryonal development (in these conditions RCD is known as "programmed" cell death) or pathological conditions such as infection. (invivogen.com)
  • Apoptosis is thus considered a "silent" form of cell death. (invivogen.com)
  • Cell Death Dis. (enzolifesciences.com)
  • Although one typically thinks of carbohydrates as associated with cell growth and viability, glycosylation also has an integral role in many processes leading to cell death. (nature.com)
  • Glycosylation of classical death receptors fine-tunes cell death programs. (nature.com)
  • Endogenous lectins and glycans are critical signals in the resolution of cell death. (nature.com)
  • Is there a hallmark 'glycosylation signature' that characterizes the initiation, execution and resolution of cell death programs in physiologic and pathologic settings? (nature.com)
  • The emergence of functional studies on animal lectins during the 1990s has provided the appropriate framework to better understand their roles in cell death. (nature.com)
  • We discuss here the contribution of glycan-lectin interactions to the initiation, execution and resolution of apoptosis and their emerging roles in other cell death programs including autophagy. (nature.com)
  • The anticancer effects of curcumin mainly result from the multitude of ways it regulates "programmed cell death. (nutritionfacts.org)
  • We do that primarily through a process called apoptosis-pre-programmed cell death, from the Greek ptosis , meaning falling, and apo , meaning away from. (nutritionfacts.org)
  • And, it's because curcumin can affect numerous mechanisms of cell death at the same time, it's "possible that cancer cells may not [easily] develop resistance to curcumin-induced cell death," like they do to most chemotherapy. (nutritionfacts.org)
  • Loss of Toll signalling suppresses ectopically and physiologically activated JNK signalling-induced cell death. (sdbonline.org)
  • Finally, gain of Toll signalling exacerbates JNK-mediated cell death and promotes cell death independent of caspases. (sdbonline.org)
  • This provokes speculation that core components of the cell death machinery can function to regulate processes other than apoptosis, such as spermatogenesis. (caltech.edu)
  • Thus, arrestin-2-(1-380) cooperates with another product of caspase activity, tBID, and their concerted action significantly contributes to cell death. (bvsalud.org)
  • Caspase-11, also termed the non-canonical inflammasome, is activated by TLR3/TLR4-TRIF signaling and directly binds cytosolic lipopolysaccharide (LPS), a major structural element of Gram-negative bacterial cell walls. (wikipedia.org)
  • Caspase-11 can therefore mediate host LPS sensing even in the absence of TLR4, provided an alternative TRIF-dependent signal (e.g., by TLR3) is provided. (wikipedia.org)
  • This selection removes the T or B cell clones before they attain maturation if they possess receptors that recognize self-antigens and bind to them with strong affinity. (tutorialspoint.com)
  • Triple point mutants, unable to bind caspase 9, caspase 3, and DIABLO/HtrA2/Omi, were completely ineffectual in inhibiting apoptosis. (rupress.org)
  • Here, we investigated the dual coupling properties of CB(1) receptors and characterized the structural determinants that mediate selective coupling to G(s) and G(i). (bvsalud.org)
  • Interestingly, dBruce mutant males are sterile, but a lack of increased caspase activity in these mutants suggests that dBruce may also play nonapoptotic roles. (caltech.edu)