Journal of cell death最新文献

筛选
英文 中文
The ARTS of Cell Death. 细胞死亡的艺术
Journal of cell death Pub Date : 2019-04-03 eCollection Date: 2019-01-01 DOI: 10.1177/1179066019836967
Elle Koren, Yaron Fuchs
{"title":"The ARTS of Cell Death.","authors":"Elle Koren,&nbsp;Yaron Fuchs","doi":"10.1177/1179066019836967","DOIUrl":"https://doi.org/10.1177/1179066019836967","url":null,"abstract":"<p><p>Although much is known regarding intestinal stem cell (ISC) self-renewal and differentiation, the specific mechanisms used for their elimination is unclear. We recently discovered that the pro-apoptotic protein ARTS, a <i>Septin4</i> isoform, interacts with X-linked inhibitor of apoptosis (XIAP) in the ISC niche to regulate stem cell survival during intestinal homeostasis and regeneration. These findings point to an intriguing avenue of translational research, examining how manipulation of stem cell apoptosis through the ARTS/XIAP module can affect stem-cell-dependent processes.</p>","PeriodicalId":89169,"journal":{"name":"Journal of cell death","volume":"12 ","pages":"1179066019836967"},"PeriodicalIF":0.0,"publicationDate":"2019-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179066019836967","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37151544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
The Effect of Transfusion-Dependent Thalassemia Patient's Serum on Peripheral Blood Mononuclear Cell Viability. 输血依赖型地中海贫血患者血清对外周血单个核细胞活力的影响。
Journal of cell death Pub Date : 2019-01-07 eCollection Date: 2019-01-01 DOI: 10.1177/1179066018823534
Nawapong Patpan, Ratana Banjerdpongchai, Adisak Tantiworawit, Juthathip Poofery, Phimphan Komonrit, Kanda Fanhchaksai, Thanawat Rattanathammethee, Chatree Chai-Adisaksopha, Ekarat Rattarittamrong, Lalita Norasetthada, Pimlak Charoenkwan
{"title":"The Effect of Transfusion-Dependent Thalassemia Patient's Serum on Peripheral Blood Mononuclear Cell Viability.","authors":"Nawapong Patpan,&nbsp;Ratana Banjerdpongchai,&nbsp;Adisak Tantiworawit,&nbsp;Juthathip Poofery,&nbsp;Phimphan Komonrit,&nbsp;Kanda Fanhchaksai,&nbsp;Thanawat Rattanathammethee,&nbsp;Chatree Chai-Adisaksopha,&nbsp;Ekarat Rattarittamrong,&nbsp;Lalita Norasetthada,&nbsp;Pimlak Charoenkwan","doi":"10.1177/1179066018823534","DOIUrl":"https://doi.org/10.1177/1179066018823534","url":null,"abstract":"<p><p>Iron overload is a major complication in transfusion-dependent thalassemia (TDT) patients. Chronic oxidative stress from iron overload may lead to cellular damage and viability. This is a cross-sectional study. Transfusion-dependent thalassemia patients aged ⩾18 years old were enrolled. Transfusion-dependent thalassemia patient's serum and normal volunteer's serum were separately incubated with healthy peripheral blood mononuclear cells (PBMCs). The cell viability was measured by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay at 24, 48, and 72 hours. Sixty-nine TDT patients and 22 healthy controls were enrolled. The mean of PBMCs viability after incubation with serum from TDT patients was lower than that with the controls (88.65% vs 103.56% at 24 hours, 78.77% vs 112.04%% at 48 hours, and 71.18% vs 132.16%% at 72 hours, respectively). High serum ferritin level (correlation -0.29, <i>P</i> < .05) and white blood cell (WBC) count negatively affected cell viability (correlation -2.86, <i>P</i> = .05). From multivariate analysis, serum ferritin level is the only significant risk factor that is independently associated with cell viability (correlation -11.42, <i>P</i> < .001). Our findings showed that TDT patient's serum causes decreased cell viability. Serum ferritin level was a significant independent factor influencing cell viability.</p>","PeriodicalId":89169,"journal":{"name":"Journal of cell death","volume":"12 ","pages":"1179066018823534"},"PeriodicalIF":0.0,"publicationDate":"2019-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179066018823534","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36877456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Cerebellar Upregulation of Cell Surface Death Receptor-Mediated Apoptotic Factors in Harmaline-Induced Tremor: An Immunohistochemistry Study. 小脑细胞表面死亡受体介导的凋亡因子在harmaline诱导的震颤中的上调:免疫组织化学研究。
Journal of cell death Pub Date : 2018-11-05 eCollection Date: 2018-01-01 DOI: 10.1177/1179066018809091
Nour S Erekat
{"title":"Cerebellar Upregulation of Cell Surface Death Receptor-Mediated Apoptotic Factors in Harmaline-Induced Tremor: An Immunohistochemistry Study.","authors":"Nour S Erekat","doi":"10.1177/1179066018809091","DOIUrl":"https://doi.org/10.1177/1179066018809091","url":null,"abstract":"<p><p>Active caspase-3-mediated apoptosis has been implicated in the pathogenesis of harmaline-induced tremor. The aim of this study is to illustrate the impact of tremor induction on the expression of factors mediating the cell surface death receptor-dependent apoptosis. A total of 20 normal Wistar rats were randomly selected and equally divided into control and experimental groups. Tremor was induced in the experimental group by injecting the rats with a single dose of harmaline (50 mg/kg). After that, cerebellar tissues were evaluated by immunohistochemistry to examine the expression of tumor necrosis factor α (TNF-α) and active caspase-8 in the 2 groups of animals. TNF-α and active caspase-8 expression was significantly higher in cerebella from experimental rats compared with that in those from the control rats (<i>P</i> value < .01). Thus, our present data suggest the association of tremor induction with the cerebellar overexpression of TNF-α and active caspase-8, correlative with Purkinje cell (PC) loss indicated by loss of calbindin immunoreactivity, indicating the induction of the cell surface death receptor-mediated apoptosis.</p>","PeriodicalId":89169,"journal":{"name":"Journal of cell death","volume":"11 ","pages":"1179066018809091"},"PeriodicalIF":0.0,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179066018809091","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36743066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
"Programmed Cell Death: A Process of Death for Survival" - How Far Terminology Pertinent for Cell Death in Unicellular Organisms. “程序性细胞死亡:一个为生存而死亡的过程”-与单细胞生物细胞死亡相关的术语有多远?
Journal of cell death Pub Date : 2018-08-02 eCollection Date: 2018-01-01 DOI: 10.1177/1179066018790259
Shiv Shanker Pandey, Samer Singh, Chandramani Pathak, Budhi Sagar Tiwari
{"title":"\"Programmed Cell Death: A Process of Death for Survival\" - How Far Terminology Pertinent for Cell Death in Unicellular Organisms.","authors":"Shiv Shanker Pandey,&nbsp;Samer Singh,&nbsp;Chandramani Pathak,&nbsp;Budhi Sagar Tiwari","doi":"10.1177/1179066018790259","DOIUrl":"https://doi.org/10.1177/1179066018790259","url":null,"abstract":"<p><p>Programmed cell death (PCD) is genetically regulated phenomenon of selective elimination of target cells that are either under pathological conditions or unwanted for organism's normal growth and development due to other reasons. The process although being genetically controlled is physiological in nature that renders some hallmarks like blebs in the cell membrane, lobe formation in nuclear membrane, DNA nicks resulting to DNA ladder of 200 bp, and downstream activation of caspases. Moreover, as the process refers to the death of \"targeted cell\", the term is exclusively suitable for multicellular organisms. Number of reports advocate similar type of cell death process in unicellular organisms. As cell death in unicellular organisms is also reflected by the signature of PCD obtained in metazoans, such cell death has been grouped under the broad category of PCD. It is pertinent to mention that by definition a unicellular organism is made of a single cell wherein it carries out all of its life processes. Using the term \"Programmed Cell Death\" with a preset \"survival strategy of the organism\" for unicellular organisms looks misnomer. Therefore, this correspondence argues and requests recommendation committee on cell death to revisit for the nomenclature of the cell death process in the unicellular organisms.</p>","PeriodicalId":89169,"journal":{"name":"Journal of cell death","volume":"11 ","pages":"1179066018790259"},"PeriodicalIF":0.0,"publicationDate":"2018-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179066018790259","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36403014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 15
Oncoprotein Stathmin Modulates Sensitivity to Apoptosis in Hepatocellular Carcinoma Cells During Hepatitis C Viral Replication. 丙型肝炎病毒复制过程中肝癌细胞凋亡敏感性的调控
Journal of cell death Pub Date : 2018-07-04 eCollection Date: 2018-01-01 DOI: 10.1177/1179066018785141
Nu T Lu, Natalie M Liu, Darshil Patel, James Q Vu, Lisa Liu, Chae Yeon Kim, Peter Cho, Ronik Khachatoorian, Nikita Patel, Clara E Magyar, Ekambaram Ganapathy, Vaithilingaraja Arumugaswami, Asim Dasgupta, Samuel Wheeler French
{"title":"Oncoprotein Stathmin Modulates Sensitivity to Apoptosis in Hepatocellular Carcinoma Cells During Hepatitis C Viral Replication.","authors":"Nu T Lu,&nbsp;Natalie M Liu,&nbsp;Darshil Patel,&nbsp;James Q Vu,&nbsp;Lisa Liu,&nbsp;Chae Yeon Kim,&nbsp;Peter Cho,&nbsp;Ronik Khachatoorian,&nbsp;Nikita Patel,&nbsp;Clara E Magyar,&nbsp;Ekambaram Ganapathy,&nbsp;Vaithilingaraja Arumugaswami,&nbsp;Asim Dasgupta,&nbsp;Samuel Wheeler French","doi":"10.1177/1179066018785141","DOIUrl":"https://doi.org/10.1177/1179066018785141","url":null,"abstract":"<p><p>Patients with chronic hepatitis C virus (HCV) infection risk complications of cirrhosis, liver failure, and hepatocellular carcinoma (HCC). Previously, our proteomic examination of hepatocytes carrying a HCV-replicon revealed that deregulation of cytoskeletal dynamics may be a potential mechanism of viral-induced HCC growth. Here, we demonstrate the effect of HCV replication on the microtubule regulator stathmin (STMN1) in HCC cells. We further explore how the altered activity or synthesis of stathmin affects cellular proliferation and sensitivity to apoptosis in control HCC cells (Huh7.5) and experimental HCV-replicon harboring HCC cells (R-Huh7.5). The HCV-replicon harboring HCC cells (R-Huh 7.5) lack viral structural genes/proteins for acute infectivity and thus is the standard model for in vitro chronic infection study. Knockdown of endogenous stathmin reduced sensitivity to apoptosis in replicon cells. Meanwhile, constitutively active stathmin increased sensitivity to apoptosis in replicon cells. In addition, overexpression of constitutively active stathmin reduced cell proliferation in both control and replicon cells. These findings implicate, for the first time, a novel role for stathmin in viral replication-related apoptosis. Stathmin's potential role in HCV replication and HCC make it a candidate for the future study of viral-induced malignancies.</p>","PeriodicalId":89169,"journal":{"name":"Journal of cell death","volume":"11 ","pages":"1179066018785141"},"PeriodicalIF":0.0,"publicationDate":"2018-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179066018785141","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36333626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Neisseria gonorrhoeae-Induced Inflammatory Pyroptosis in Human Macrophages is Dependent on Intracellular Gonococci and Lipooligosaccharide. 淋病奈瑟菌诱导的人巨噬细胞炎症性热亡依赖于细胞内淋球菌和低脂糖。
Journal of cell death Pub Date : 2018-01-03 eCollection Date: 2018-01-01 DOI: 10.1177/1179066017750902
Jessica Leigh Ritter, Caroline Attardo Genco
{"title":"<i>Neisseria gonorrhoeae</i>-Induced Inflammatory Pyroptosis in Human Macrophages is Dependent on Intracellular Gonococci and Lipooligosaccharide.","authors":"Jessica Leigh Ritter,&nbsp;Caroline Attardo Genco","doi":"10.1177/1179066017750902","DOIUrl":"https://doi.org/10.1177/1179066017750902","url":null,"abstract":"<p><p><i>Neisseria gonorrhoeae</i>, the human obligate pathogen responsible for the sexually transmitted disease gonorrhea, has evolved several mechanisms to evade the host immune response. One such mechanism is the modulation of host cell death pathways. In this study, we defined cell death pathways induced by <i>N gonorrhoeae</i> in human monocyte-derived macrophages (MDMs). In a dose-dependent manner, <i>N gonorrhoeae</i> stimulation of MDMs resulted in caspase 1 and 4-dependent cell deaths, indicative of canonical and noncanonical pyroptosis, respectively. Internalization of bacteria or stimulation with lipooligosaccharide (LOS) specifically induced pyroptosis in MDMs and increased secretion of IL-1β. Collectively, our results demonstrate that <i>N gonorrhoeae</i> induces inflammatory pyroptosis in human macrophages due in part to intracellular LOS. We propose that this in turn may exacerbate inflammatory outcomes observed during mucosal infection.</p>","PeriodicalId":89169,"journal":{"name":"Journal of cell death","volume":"11 ","pages":"1179066017750902"},"PeriodicalIF":0.0,"publicationDate":"2018-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179066017750902","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35823187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 12
Spleen Tyrosine Kinase Inhibition Modulates p53 Activity. 脾脏酪氨酸激酶抑制调节p53活性。
Journal of cell death Pub Date : 2017-09-20 eCollection Date: 2017-01-01 DOI: 10.1177/1179066017731564
Mohammad Althubiti
{"title":"Spleen Tyrosine Kinase Inhibition Modulates p53 Activity.","authors":"Mohammad Althubiti","doi":"10.1177/1179066017731564","DOIUrl":"https://doi.org/10.1177/1179066017731564","url":null,"abstract":"<p><p>Spleen tyrosine kinase (SYK) is a cytoplasmic enzyme that promotes survival and proliferation of B cells. SYK inhibition has shown promising results in the treatment of arthritis and chronic lymphocytic leukemia (CLL). However, in other context, it has been shown that SYK overexpression in epithelial cancer cells induced senescence in p53-dependent mechanism, which underscored its antineoplastic activity in vitro. Here, we show that SYK was induced in response of DNA damage in parallel with p53 levels. In addition, using chemical inhibitors of SYK reduced p53 levels in HCT116 and HT1080 cell lines, which underlines the role of SYK inhibition on p53 activity. Furthermore, SYK inhibition modulated the cell growth, which resulted in a decreasing in cell death. Interestingly, SYK expression showed a positive prognosis in patients with solid tumors in correlations with their survival rates, as expected negative correlation was seen between SYK expression and survival rate of patients with CLL. In conclusion, these findings demonstrate that SYK inhibition modulates p53 expression and activity in HCT116 and HT1080 cells. Reconsidering using of SYK inhibitors in clinical setting in the future should be evaluated carefully in accordance with these findings to prevent the formation of secondary malignancies.</p>","PeriodicalId":89169,"journal":{"name":"Journal of cell death","volume":"10 ","pages":"1179066017731564"},"PeriodicalIF":0.0,"publicationDate":"2017-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179066017731564","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35663861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
In Vitro Neurotoxicity Resulting from Exposure of Cultured Neural Cells to Several Types of Nanoparticles. 培养的神经细胞暴露于几种纳米颗粒导致的体外神经毒性。
Journal of cell death Pub Date : 2017-03-23 eCollection Date: 2017-01-01 DOI: 10.1177/1179670717694523
Stephen F Larner, Jonathan Wang, Jared Goodman, Megan B O'Donoghue Altman, Meiguo Xin, Kevin K W Wang
{"title":"In Vitro Neurotoxicity Resulting from Exposure of Cultured Neural Cells to Several Types of Nanoparticles.","authors":"Stephen F Larner,&nbsp;Jonathan Wang,&nbsp;Jared Goodman,&nbsp;Megan B O'Donoghue Altman,&nbsp;Meiguo Xin,&nbsp;Kevin K W Wang","doi":"10.1177/1179670717694523","DOIUrl":"https://doi.org/10.1177/1179670717694523","url":null,"abstract":"<p><p>Laboratory and industrial production of various nanoparticles, single-walled nanotubes (SWNTs), fullerene (C60), cadmium selenide (CdSe) quantum dots, carbon black (CB), and dye-doped silica nanospheres (NSs), has greatly increased in the past 15 years. However, little research has been done to analyze the toxicity of these materials. With recent studies showing that nano-substances can cross the blood-brain barrier, we examined the neurotoxicity of these manufactured nanoparticles. By employing the rat PC-12 neuronal-like cell line as the basis for our studies, we were able to evaluate the toxicity caused by these five nanoparticles. The level of toxicity was measured by testing for cell viability using the lactate dehydrogenase (LDH) cell viability assay, morphological analysis of changes in cellular structures, and Western blot analyses of αII-spectrin breakdown products (SBDP) as cell death indicators. Our results showed cytotoxicity in nondifferentiated PC-12 cells exposed to CB (10-100 μg/mL), SWNTs (10-100 μg/mL), C60 (100 μg/mL), CdSe (10 μg/mL), CB (500 μg/mL), and dye-doped silicon NSs (10 μg/mL). Exposure to higher concentrations (100 μg/mL) of SWNTs, CB, and C60 increased the formation of SBDP150/145, as well as cell membrane contraction and the formation of cytosolic vacuoles. The incorporations of the nanoparticles into cell cytoplasm were observed using the fluorescent dye-doped NSs in both nondifferentiated and nerve growth factor (NGF)-differentiated PC-12 cells. When PC-12 cells are differentiated, they appeared to be even more sensitive to cytotoxicity of nanoparticles such as CB 10 nm (10-100 μg/mL), CB 100 nm (10-100 μg/mL), and CdSe (1-10 μg/mL).</p>","PeriodicalId":89169,"journal":{"name":"Journal of cell death","volume":"10 ","pages":"1179670717694523"},"PeriodicalIF":0.0,"publicationDate":"2017-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179670717694523","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34966709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 30
In Vitro Cell Death Determination for Drug Discovery: A Landscape Review of Real Issues. 药物发现的体外细胞死亡测定:真实问题的景观回顾。
Journal of cell death Pub Date : 2017-02-24 eCollection Date: 2017-01-01 DOI: 10.1177/1179670717691251
Benoite Méry, Jean-Baptiste Guy, Alexis Vallard, Sophie Espenel, Dominique Ardail, Claire Rodriguez-Lafrasse, Chloé Rancoule, Nicolas Magné
{"title":"In Vitro Cell Death Determination for Drug Discovery: A Landscape Review of Real Issues.","authors":"Benoite Méry,&nbsp;Jean-Baptiste Guy,&nbsp;Alexis Vallard,&nbsp;Sophie Espenel,&nbsp;Dominique Ardail,&nbsp;Claire Rodriguez-Lafrasse,&nbsp;Chloé Rancoule,&nbsp;Nicolas Magné","doi":"10.1177/1179670717691251","DOIUrl":"https://doi.org/10.1177/1179670717691251","url":null,"abstract":"Cell death plays a crucial role for a myriad of physiological processes, and several human diseases such as cancer are characterized by its deregulation. There are many methods available for both quantifying and qualifying the accurate process of cell death which occurs. Choosing the right assay tool is essential to generate meaningful data, provide sufficient information for clinical applications, and understand cell death processes. In vitro cell death assays are important steps in the search for new therapies against cancer as the ultimate goal remains the elaboration of drugs that interfere with specific cell death mechanisms. However, choosing a cell viability or cytotoxicity assay among the many available options is a daunting task. Indeed, cell death can be approached by several viewpoints and require a more holistic approach. This review provides an overview of cell death assays usually used in vitro for assessing cell death so as to elaborate new potential chemotherapeutics and discusses considerations for using each assay.","PeriodicalId":89169,"journal":{"name":"Journal of cell death","volume":"10 ","pages":"1179670717691251"},"PeriodicalIF":0.0,"publicationDate":"2017-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179670717691251","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34966708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 63
Crosstalk Between Apoptosis and Autophagy: Environmental Genotoxins, Infection, and Innate Immunity. 细胞凋亡与自噬之间的相互关系:环境基因毒性、感染和先天免疫。
Journal of cell death Pub Date : 2017-02-20 eCollection Date: 2017-01-01 DOI: 10.1177/1179670716685085
Michael G Kemp
{"title":"Crosstalk Between Apoptosis and Autophagy: Environmental Genotoxins, Infection, and Innate Immunity.","authors":"Michael G Kemp","doi":"10.1177/1179670716685085","DOIUrl":"10.1177/1179670716685085","url":null,"abstract":"<p><p>Autoimmune disorders constitute a major and growing health concern. However, the genetic and environmental factors that contribute to or exacerbate disease symptoms remain unclear. Type I interferons (IFNs) are known to break immune tolerance and be elevated in the serum of patients with autoimmune diseases such as lupus. Extensive work over the past decade has characterized the role of a protein termed stimulator of interferon genes, or STING, in mediating IFN expression and activation in response to cytosolic DNA and cyclic dinucleotides. Interestingly, this STING-dependent innate immune pathway both utilizes and is targeted by the cell's autophagic machinery. Given that aberrant interplay between the apoptotic and autophagic machineries contributes to deregulation of the STING-dependent pathway, IFN-regulated autoimmune phenotypes may be influenced by the combined exposure to environmental carcinogens and pathogenic microorganisms and viruses. This review therefore summarizes recent data regarding these important issues in the field of autoimmunity.</p>","PeriodicalId":89169,"journal":{"name":"Journal of cell death","volume":"9 ","pages":"1179670716685085"},"PeriodicalIF":0.0,"publicationDate":"2017-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/de/79/10.1177_1179670716685085.PMC5392045.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34964664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书