Relevant bibliographies by topics / “don't eat me” signal

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic '“don't eat me” signal'

Author: Grafiati
Published: 24 May 2023

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Journal articles on the topic "“don't eat me” signal"

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Grimsley, C. "Cues for apoptotic cell engulfment: eat-me, don't eat-me and come-get-me signals." Trends in Cell Biology 13, no. 12 (December 2003): 648–56. http://dx.doi.org/10.1016/j.tcb.2003.10.004.

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Bradley, Conor A. "CD24 — a novel ‘don’t eat me’ signal." Nature Reviews Cancer 19, no. 10 (August 12, 2019): 541. http://dx.doi.org/10.1038/s41568-019-0193-x.

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Bradley, Conor A. "CD24 — a novel ‘don’t eat me’ signal." Nature Reviews Drug Discovery 18, no. 10 (August 21, 2019): 747. http://dx.doi.org/10.1038/d41573-019-00146-0.

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Majeti, R., C. Jamieson, W. W. Pang, S. Jaiswal, N. J. Leeper, G. Wernig, and I. L. Weissman. "Clonal Expansion of Stem/Progenitor Cells in Cancer, Fibrotic Diseases, and Atherosclerosis, and CD47 Protection of Pathogenic Cells." Annual Review of Medicine 73, no. 1 (January 27, 2022): 307–20. http://dx.doi.org/10.1146/annurev-med-042420-104436.

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We proposed and demonstrated that myelogenous leukemia has a preleukemic phase. In the premalignant phase, normal hematopoietic stem cells (HSCs) gradually accumulate mutations leading to HSC clonal expansion, resulting in the emergence of leukemic stem cells (LSCs). Here, we show that preleukemic HSCs are the basis of clonal hematopoiesis, as well as late-onset blood diseases (chronic-phase chronic myeloid leukemia, myeloproliferative neoplasms, and myelodysplastic disease). The clones at some point each trigger surface expression of “eat me” signals for macrophages, and in the clones and their LSC progeny, this is countered by upregulation of “don't eat me” signals for macrophages such as CD47,opening the possibility of CD47-based therapies. We include evidence that similar processes result in fibroblast expansion in a variety of fibrotic diseases, and arterial smooth muscle clonal expansion is a basis of atherosclerosis, including upregulation of both “eat me” and “don't eat me” molecules on the pathogenic cells.
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Brightwell, R. M., K. S. Grzankowski, S. Lele, K. Eng, M. Arshad, H. Chen, and K. Odunsi. "The CD47 “don't eat me signal” is highly expressed in human ovarian cancer." Gynecologic Oncology 143, no. 2 (November 2016): 393–97. http://dx.doi.org/10.1016/j.ygyno.2016.08.325.

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Feng, Mingye, James Y. Chen, Rachel Weissman-Tsukamoto, Jens-Peter Volkmer, Po Yi Ho, Kelly M. McKenna, Samuel Cheshier, et al. "Macrophages eat cancer cells using their own calreticulin as a guide: Roles of TLR and Btk." Proceedings of the National Academy of Sciences 112, no. 7 (February 2, 2015): 2145–50. http://dx.doi.org/10.1073/pnas.1424907112.

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Macrophage-mediated programmed cell removal (PrCR) is an important mechanism of eliminating diseased and damaged cells before programmed cell death. The induction of PrCR by eat-me signals on tumor cells is countered by don’t-eat-me signals such as CD47, which binds macrophage signal-regulatory protein α to inhibit phagocytosis. Blockade of CD47 on tumor cells leads to phagocytosis by macrophages. Here we demonstrate that the activation of Toll-like receptor (TLR) signaling pathways in macrophages synergizes with blocking CD47 on tumor cells to enhance PrCR. Bruton’s tyrosine kinase (Btk) mediates TLR signaling in macrophages. Calreticulin, previously shown to be an eat-me signal on cancer cells, is activated in macrophages for secretion and cell-surface exposure by TLR and Btk to target cancer cells for phagocytosis, even if the cancer cells themselves do not express calreticulin.
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Nisha, Sosale, and Dennis E. Discher. "How Does CD47-SIRPα ‘Don’t Eat Me Signal’ Physically Signal Self." Blood 122, no. 21 (November 15, 2013): 953. http://dx.doi.org/10.1182/blood.v122.21.953.953.

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Abstract Resident macrophages in spleen and liver are particularly adept at recognizing foreign pathogens through recognition of ‘non-self’ proteins on the pathogen surface but also through the absence of ‘self’ proteins that are highly displayed on circulating blood cells. Red blood cells display a ‘marker of self’ protein CD47 which increases the in vivo half-life and decreases red-pulp splenic macrophage uptake of mouse RBC (Oldenborg et al, Science 2000) and also of particles displaying human-CD47 in recent studies by our group (Rodriguez et al, Science 2013). CD47 signals self through its counter receptor SIRPa, which is highly expressed on the surfaces of myeloid cells but also highly polymorphic. The CD47 protein functions in vitro as a marker of self toward human SIRPa on human macrophages and monocytes, inhibiting accumulation of myosin II motor protein to the phagocytic synapse (Tsai 2008). The work here aims to clarify when and how CD47-SIRPa inhibition physically signals ‘self’ during macrophage phagocytosis uptake. While it is clear that CD47 reduces the number of uptake events, here we use time-lapse and confocal microscopy to examine the forces of distortion imparted by phagocytes on opsonized red blood cell targets during uptake. Glutaraldehyde-fixed RBC are also used as a model to assess the affects of cell rigidity in this self-recognition process, since rigidity is relevant to processes as diverse as RBC aging and sickle RBC to malaria but also because adhesion (by macrophages) is expected to activate the myosin-II contractility system and oppose CD47 signaling. Through blocking and pharmacological approaches, we parse the pathways between foreign, self, and rigidity sensing. Disclosures: No relevant conflicts of interest to declare.
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Pinho, Sandra, Wei Qiaozhi, Maria Maryanovich, Halley Pierce, Fumio Nakahara, and Paul S. Frenette. "Vcam1 Is a "Don't-Eat-Me" Signal on Healthy Hematopoietic and Leukemic Stem Cells." Blood 128, no. 22 (December 2, 2016): 565. http://dx.doi.org/10.1182/blood.v128.22.565.565.

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Abstract Hematopoietic stem cells (HSCs) possess the ability to maintain the entire population of blood cells throughout life and to replenish the hematopoietic system after transplantation into marrow-ablated recipients. In mammalian adults, HSCs predominantly reside in the bone marrow to generate and maintain all blood cell types. HSCs, however, retain their ability to migrate to ectopic niches via the bloodstream, and traffic back to the bone marrow microenvironment via in part the interactions of alpha4 integrins with Vascular Cell Adhesion Molecule-1 (Vcam1, also known as CD106), constitutively expressed by endothelial and stromal cells. In the course of studies to investigate the role of Vcam1 in the macrophage erythroblastic niche, we have found using Vcam1-floxed mice crossed with a Csf1r-iCre (hereafter Vcam1Δ/Δ) that Vcam1 and Cre, using this transgenic line, were expressed on Lineage− (Lin−) c-Kit+ Sca1+ CD48− CD150+ HSCs. Although Vcam1Δ/Δ mice show no significant steady-state hematopoietic defect, transplantation of Vcam1Δ/Δ bone marrow, both in competitive and non-competitive settings, failed to engraft irradiated wild-type recipients. Indeed, ~80% of animals transplanted with Vcam1Δ/Δcells died, and the few that survived failed to successfully engraft secondary recipient mice. Vcam1Δ/Δ HSC/progenitors homed to bone marrow as well as wild-type counterparts and showed no detectable change in apoptosis in the bone marrow. However, syngeneic Vcam1Δ/Δ HSC/progenitors were selectively cleared in vivo by bone marrow macrophages over 4 days. The in vivo Vcam1Δ/Δ HSC/progenitor clearance did not require irradiation-induced damage since in steady-state parabiosis (Vcam1Δ/Δ and wild-type co-joined pairs), Vcam1Δ/Δ HSCs did not engraft the partner after G-CSF-induced mobilization whereas wild-type HSCs engrafted the parabiont partner. In addition, in vitro incubation of bone marrow-derived macrophages with Lin− cells revealed rapid phagocytosis by macrophages of Vcam1Δ/Δ, but not wild-type, cells and phagocytosis was also induced when the integrin alpha4 beta1 (also known as VLA-4) was blocked in wild-type Lin− cells. Thus, these results suggest that Vcam1 expressed on HSCs serves as a novel don't-eat-me signal, controlling the migration in the bone marrow by a macrophage-enabled checkpoint. Since we found that Vcam1 is expressed at higher levels on acute myelogenous leukemia (AML) cells than on healthy HSCs, and high VCAM1 expression correlates with poor prognosis in human AML patients (Ley et. al. NEJM 2013), we examined whether Vcam1 expression by AML cell could affect leukemogenesis in vivo. To test this idea, we generated AML-Vcam1Δ/Δand AML-Control cells by transduction of bone marrow Lin− c-Kit+ Sca1+ cells with the pMSCV-MLL-AF9-GFP oncogene. Strikingly, FACS analysis of primary AML recipient bone marrow revealed a marked reduction (>99%) in the number and percentage of phenotypic Lin− IL7Rα− Sca1− MLL-AF9 GFP+ c-Kithigh CD34low FcγRII/IIIhigh leukemic stem cells in AML-Vcam1Δ/Δmice compared to control. These results were confirmed by imaging analyses, which showed a marked reduction in leukemic infiltration in AML-Vcam1Δ/Δmice compared to control. Kaplan-Meier survival analysis of secondary recipient mice receiving 20,000 GFP+ leukemic cells revealed a significantly greater survival of mice harboring AML-Vcam1Δ/Δ cells relative to AML-Control (P<0.0001). To assess in a pre-clinical experimental setting whether Vcam1 inhibition can alter the course of AML, we established AML in immunocompetent C57BL/6 recipients and started therapy of moribund leukemic mice (>50% circulating AML-GFP+ cells) with a daily injection of saline, IgG control, anti-Vcam1 blocking antibody (100 μg/day), cytarabine (100 mg/kg), or a combination of anti-Vcam1/cytarabine for 5 days. Remarkably, this short treatment with anti-Vcam1 blocking antibody was able to preferentially and significantly reduce the frequency and absolute number of phenotypic bone marrow leukemic stem cells in vivo. In addition, our results suggest that using a blocking anti-Vcam1 antibody synergizes with cytarabine treatment to decrease leukemic burden in vivo. These studies lay the groundwork for the development of a new therapeutic strategy for eliminating leukemia stem cells by modulating the innate immune response. Disclosures Frenette: GSK: Research Funding; Pfizer: Consultancy; PHD Biosciences: Research Funding.
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Rivest, Serge. "A ‘don’t eat me’ immune signal protects neuronal connections." Nature 563, no. 7729 (October 29, 2018): 42–43. http://dx.doi.org/10.1038/d41586-018-07165-8.

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Russ, Atlantis, Anh B. Hua, William R. Montfort, Bushra Rahman, Irbaz Bin Riaz, Muhammad Umar Khalid, Jennifer S. Carew, Steffan T. Nawrocki, Daniel Persky, and Faiz Anwer. "Blocking “don't eat me” signal of CD47-SIRPα in hematological malignancies, an in-depth review." Blood Reviews 32, no. 6 (November 2018): 480–89. http://dx.doi.org/10.1016/j.blre.2018.04.005.

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Dissertations / Theses on the topic "“don't eat me” signal"

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Cai, Ting ting. "Study of septin 9 in the cell polarity and development of cholangiocarcinoma." Electronic Thesis or Diss., université Paris-Saclay, 2022. http://www.theses.fr/2022UPASL086.

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Le cholangiocarcinome (CCA) est un cancer du foie très agressif dont l'incidence augmente dans le monde entier. C'est le deuxième cancer primitif du foie le plus fréquent après le carcinome hépatocellulaire (CHC). Le pronostic est sombre et la mortalité élevée. La chirurgie reste le seul traitement efficace et seuls quelques patients sont éligibles à cause du diagnostic bien souvent tardif. Il devient urgent de trouver des biomarqueurs pour un diagnostic précoce et un traitement adapté. Cependant de nombreuses questions demeurent quant au mode d'initiation et de progression du CCA. La septine 9 est un membre de la famille des septines qui sont des GTPases considérées comme des éléments du cytosquelette. Ces protéines possèdent deux domaines polybasiques (PB1) et (PB2) qui permettent leur oligomerisation pour former des structures filamenteuses et favoriser leur liaison aux membranes cellulaires permettant ainsi aux septines d'assurer leurs différentes fonctions biologiques. Les travaux du laboratoire sont à la base de la découverte du domaine PB2 qui forme avec le domaine PB1 un point d'ancrage aux membranes grâce à une liaison avec les phosphoinositides. Dans la première partie de ma thèse, à l'aide de différents mutants dépourvus d'un ou des deux domaines PB que nous avons construits, nos travaux ont démontré que la septine 9 est un régulateur clé de la polarité apico-basale et que ses deux domaines PB sont nécessaires à l'homéostasie tissulaire. En culture tridimensionnelle (3D), nous avons constaté que la septine 9 est localisée à la membrane basale et que la déplétion des deux domaines PB1 et PB2 empêche la localisation membranaire de la septine 9 et conduit à un phénotype de polarité inversée dans les organoides formés en culture 3D. Ces organoides possédant un phénotype de polarité inversée, présente également un caractère invasif avec une accumulation de la cortactine et de la kinase Src à la membrane périphérique. Nous avons également démontré que l'inhibition de RhoA et principalement celles des récepteurs du TGF beta (Transforming Growth Factor) pouvaient restaurer la polarité cellulaire dans les organoides. Dans une deuxième partie, nous avons analysé l'expression et le rôle de la septine 9 dans le CCA et en particulier dans le CCA intrahépatique ou CCAi. Nous avons réalisé des analyses bio-informatique sur des données de séquencage sur cellules uniques issues de CCAi. Les résultats de ces analyses ont montré que l'expression de la septine 9 était plus élevée dans les CCAi que dans les CHC. Nous avons également montré une expression différentielle de la septine 9 et de la vimentine (marqueur des cellules mésenchymateuses) dans les cellules de CCAi. Ceci nous a permis d'identifier des trajectoires cellulaires spécifiques des cellules tumorales du CCAi. Nous avons caractérisé deux sous-populations cellulaires, l'une enrichie en vimentine et en molécules impliquées dans le remodelage de la matrice extracellulaire (MEC) et l'autre enrichie en septine 9 et en molécules du système immunitaire. En effet dans ces cellules, nous avons trouvé une corrélation positive et significative entre l'expression de la septine 9 et les gènes impliqués dans la signalisation immunitaire et nommés "don't eat me’genes" qui bloquent la dégradation par le système immunitaire des cellules tumorales qui les expriment. De plus nous avons montré que l'expression de la septine 9 régule celle des protéines des signaux "don't eat me". Par ailleurs nous montrons que la septine 9 régule la transition épithélio-mésenchymateuse (EMT) et contrôle négativement l'expression de la vimentine. Par conséquent, ces travaux nous permettent de conclure que la septine 9 est une protéine régulatrice de la polarité cellulaire et serait impliquée dans l'échappement des cellules tumorales au système immunitaire. Elle pourrait servir de biomarqueur pronostique et de cible thérapeutique potentiel du CCAi
Cholangiocarcinoma (CCA) is a very aggressive liver cancer whose incidence is increasing worldwide. It is the second most common primary liver cancer after hepatocellular carcinoma (HCC). The prognosis is grim and the mortality high. Surgery remains the only effective treatment and only a few patients are eligible because of the often-late diagnosis. It is becoming urgent to find biomarkers for early diagnosis and appropriate treatment. However, many questions remain about the mode of initiation and progression of CCA. Septin 9 is a member of the septin family which are GTPases considered as elements of the cytoskeleton. These proteins have two polybasic domains (PB1) and (PB2) which allow their oligomerization to form filamentous structures and promote their binding to cell membranes, thus allowing the septins to carry out their various biological functions. The work of the laboratory is the basis of the discovery of the PB2 domain which forms with the PB1 domain an anchor to the membranes through their binding with phosphoinositides. In the first part of my thesis, using different mutants that we constructed and lacking one or both PB domains, we demonstrated that septin 9 is a key regulator of apico-basal polarity and that its two PB domains are required for tissue homeostasis. Using three-dimensional (3D) culture, we found that septin 9 is localized to the basolateral membrane of polarized organoids and that the depletion of both PB1 and PB2 domains prevents the membrane localization of septin 9 and leads to a reverse polarity phenotype in the organoids formed. These organoids possessing an inverted polarity phenotype, also present an invasive character with an accumulation of cortactin and Src kinase at the peripheral membrane. We have also demonstrated that the inhibition of RhoA and mainly that of TGF beta (Transforming Growth Factor) receptors could restore cell polarity in organoids. In a second part, we analyzed the expression and the role of septin 9 in the CCA and in particular in the intrahepatic CCA (CCAi). We performed bioinformatics analyzes on single cell sequencing data from CCAi. The results of these analyzes showed that the expression of septin 9 was higher in CCAi than in HCC. We also showed a differential expression of septin 9 and vimentin (marker of mesenchymal cells) in CCAi cells. This allowed us to identify specific cellular trajectories of CCAi tumor cells. We characterized two cell subpopulations, one enriched in vimentin and molecules involved in extracellular matrix (ECM) remodeling and the other enriched in septin 9 and immune system molecules. Indeed, in these cells, we found a positive and significant correlation between the expression of septin 9 and those of the genes involved in immune signaling and named "don't eat me" genes which block the degradation by the immune system of tumor cells that express them. In addition, we have shown that the expression of septin 9 regulates that of the "don't eat me" signal proteins. Furthermore, we show that septin 9 regulates the epithelial-mesenchymal transition (EMT) and negatively controls the expression of vimentin. Consequently, this work allows us to conclude that septin 9 is a protein that regulates cell polarity and would be involved in the escape of tumor cells from the immune system. It could serve as a prognostic biomarker and potential therapeutic target of CCAi
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Lehrman, Emily Kate. "Innate Immune Molecules Direct Microglia-Mediated Developmental Synaptic Refinement." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11650.

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Microglia, the brain's resident immune cells and phagocytes, are emerging as critical regulators of developing synaptic circuits in the healthy brain after having long been thought to function primarily during central nervous system (CNS) injury or disease. Recent work indicates that microglia engulf synapses in the developing brain; however, how microglia know which synapses to target for removal remains a major open question. For my dissertation research, I studied microglia-mediated pruning in the retinogeniculate system and sought to identify the molecules regulating microglial engulfment of synaptic inputs. I discovered that "eat me" and "don't eat me" signals, immune molecules known for either promoting or inhibiting macrophage phagocytosis of cells or debris, localize to the dorsal lateral geniculate nucleus of the thalamus (dLGN) and direct retinogeniculate refinement. We found that "eat me" signal C3 and its microglial receptor, CR3, are required for normal engulfment, and that loss of either of these molecules leads to a reduction in phagocytosis and sustained deficits in refinement. These data suggest that microglia-mediated pruning may be analogous to the removal of non-self material by phagocytes in the immune system. To test this hypothesis, I examined whether protective signals are required to prevent excess microglial engulfment, as they prevent phagocytosis of self cells in the immune system. I found that protective "don't eat me" signal CD47 is required to prevent excess microglial engulfment and retinogeniculate pruning during development. Moreover, another "don't eat me signal", CD200, also prevents overpruning. Together, these findings indicate that immune molecules instruct microglia as to which synapses to engulf and present a model in which a balance of stimulatory and inhibitory cues is necessary to guide remodeling of immature synaptic circuits. These data shed new light on mechanisms regulating synaptic refinement and microglial function in the healthy, developing CNS, and may have implications for disorders characterized by immune dysregulation and circuit disconnectivity, such as autism spectrum disorder (ASD) and schizophrenia.
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Moritz, Nadine [Verfasser], and Karl-Peter [Akademischer Betreuer] Hopfner. "Blocking the "Don't eat me" checkpoint in acute myeloid leukemia : development of a novel antibody format / Nadine Moritz ; Betreuer: Karl-Peter Hopfner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1156173124/34.

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Books on the topic "“don't eat me” signal"

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Please don't eat me. Maplewood, NJ: Blue Apple Books, 2008.

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Don't Eat Me. Soho Press, Incorporated, 2019.

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Hughes, Beryl, and Bethan Sennett. Don't Eat Me! Independently Published, 2022.

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Rodan, P. Don't Eat Me. Independently Published, 2018.

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Don't eat me. 2018.

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STOP! Don't Eat Me. PeaceDiviners International Inc., 2004.

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Norac, Carl. Monster, Don't Eat Me! Groundwood Books, 2007.

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Climo, Liz. Please Don't Eat Me. Little, Brown Books for Young Readers, 2019.

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Please Don't Eat Me. Little, Brown Books for Young Readers, 2019.

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Climo, Liz. Please Don't Eat Me. Little, Brown Books for Young Readers, 2019.

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Book chapters on the topic "“don't eat me” signal"

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Jayaram Pratima, Bichandarkoil, and Namasivayam Nalini. "Efferocytosis: An Interface between Apoptosis and Pathophysiology." In Regulation and Dysfunction of Apoptosis. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.97819.

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Several cell death modes, each with a unique feature and mode of inducing cell death have been established. Cell death occurring under physiological conditions is primarily caused by apoptosis, which is a non-inflammatory or silent process, whereas necroptosis or pyroptosis is triggered by pathogen invasion, which stimulates the immune system and induces inflammation. In physiology, clearing dead cells and associated cellular debris is necessary since billions of cells die during mammalian embryogenesis and every day in adult organisms. For degradation, dead cells produced by apoptosis are quickly engulfed by macrophages. This chapter will present a description of the phagocytosis of dead and dying cells, by a process known as efferocytosis. Macrophages and, to a lesser degree, other ‘professional’ phagocytes (such as monocytes and dendritic cells) and ‘non-professional’ phagocytes, such as epithelial cells, conduct efferocytosis. Recent discoveries have shed light on this mechanism and how it works to preserve homeostasis of tissue, repair of tissue and health of the organism. Caspases are a large family of proteases of cysteine acting in cascades. A cascade leading to activation of caspase 3 mediates apoptosis and is responsible for killing cells, hiring macrophages, and presenting a “eat me” signal(s). If macrophages do not effectively engulf apoptotic cells, they undergo secondary necrosis and release intracellular materials that reflect a molecular pattern associated with injury, which can lead to autoimmune diseases. Here, the processes of efferocytosis are illustrated and the pathophysiological effects that which occur when this phase is abrogated are highlighted.
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"They just walk out a door. It’s circular, begins again. It’s a very complicated handling of narrative. Going back to that fight in Motion Sickness, it has an ending in the sense that the two men separate, but who is the winner? You know that they’re in a relationship with each other, but the question of who won or lost will depend on the version of the story you’re going to hear from each of the participants. What does it mean to come to a conclusion? Jouissance, I suppose. Coming to a conclusion. PN: In ‘Madame Realism’, we’re told that ‘stories do not occur outside thought. Stories, in fact, are contained within thought. It’s only a story really should read, it’s a way to think’ (MR, 108). The point seems to be that narratives shouldn’t be locked up in a distinction between true and false, but are actually ways of articulating ourselves. LT: Yes, I was trying to take narrative out of the realm of untrue, irrelevant, not profound…. Some people say ‘I never read a novel, I read theory’, and so on. The same people might argue against a high/low split but say they don’t read novels. You could say the novel’s an old form; with the computer why should people read stories and novels? I wanted to argue that any form you use represents a way of thinking, ideas. Do you read things only because you identify with them or can you disidentify with them too? PN: One of the interesting things about these stories is the connection you seem to pursue between narrative and the familial, the Oedipal. ‘All ideas are married’, says Madame Realism (A, 105), and in the story called ‘Absence Makes the Heart’, the death of the father seems somehow connected with the idea of the Woman as solitary and mystified—‘Her reluctance must be read as a mystery, a deception from one whose own creation was exampled in the stories he loved’ (A, 69). It’s not immediately clear to me whether the loss of the father signals the failure of narrative or freedom from it. LT: What if the loss of the father, her recognition of him as now symbolic, in fact enables her to see herself in the story, a story that men have of her? PN: She becomes the narrator instead of being just the Woman? LT: That’s right. It’s like saying: you’re placing me in the story in certain ways but I have needs, I have desires. I’m the subject of my own story, I’m not just the object in your story. PN: There’s a passage in Motion Sickness where the narrator remembers her father’s voice: ‘It’s my father’s voice at the Leaning Tower, distracting me just the way he does when I eat veal." In Textual Practice, 59. Routledge, 2005. http://dx.doi.org/10.4324/9780203986219-25.

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Conference papers on the topic "“don't eat me” signal"

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Anderson, Katie L., Debra Lins, Jens-Peter Volkmer, Yoji Shimizu, Irving L. Weissman, Matthew Mescher, and Jaime Modiano. "Abstract A143: Melanoma cell resistance to phagocytosis is unrelated to expression of conventional “eat-me/don't eat-me” signals." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-a143.

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Tsuji, Takahiro, Hiroaki Wake, Mariko Shindo, Koichiro Haruwaka, Hitomi Ajimizu, Masatoshi Yamazoe, Tomoko Funazo, et al. "Abstract 2728: Novelin vivoimaging method to evaluate “Don't eat me” signal of tumor against microglia." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2728.

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Tsuji, Takahiro, Hiroaki Wake, Mariko Shindo, Daisuke Kato, Hiroaki Ozasa, and Toyohiro Hirai. "Abstract PO039: Novel in vivo imaging method to evaluate "Don't eat me" signal of tumor against microglia." In Abstracts: AACR Virtual Special Conference: The Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; January 11-12, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.tme21-po039.

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Weissman, Irving L. "Abstract PL02-02: Investigating inhibition of the CD47 “don't eat me” signal to enable tumor phagocytic removal and augmented cross presentation to T cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-pl02-02.

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Sue, Mayumi, Takuya Tsubaki, Yoko Ishimoto, Shinko Hayashi, Saori Ishida, Yoshitaka Isumi, Jun Ishiguro, et al. "808 Blocking “don’t-eat-me” signal of CD47-SIRPα by anti-SIRPα antibody enhances anti-tumor efficacy of trastuzumab deruxtecan." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0808.

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Chen, Peng, Min Deng, Yun Liu, Jiamei Luo, Rong Guo, Jay Mei, Bo Shan, and Bing Hou. "482 ATG-031, a first-in-class anti-CD24 antibody, showed potent preclinical anti-tumor efficacy by blocking “don’t-eat-me” signal." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0482.

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Moserova, Irena Kusova, Iva Truxova, Abhishek G, Garg, Patrizia Agostinis, Piere Francois Cartron, Sarka Vosahlikova, Radek Spisek, and Jitka Fucikova. "Abstract A039: Caspase-2 and oxidative-ER stress crosstalk regulates the exposure of “eat me” signal calreticulin by high hydrostatic pressure treated cancer cells." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-a039.

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Luo, Wen, Mitchell Cairo, Janet Ayello, Timothy Cripe, Kevin Cassady, and Hai Hoang. "802 Eliciting calreticulin-mediated “eat me” phagocytic signal is additive/synergistic with CD47 blockade in enhancing tumor associated macrophage phagocytosis of tumor cells and deceasing xenograft tumor growth in ewing sarcoma." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0802.

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