CD95

出典: meddic

Fas antigen, APO-1. Tumor necrosis factor receptor family, member 6
FasFas抗原


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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2013/08/07 15:23:54」(JST)

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英文文献

  • Regulation of T lymphocyte apoptotic markers is associated to cell activation during the acute phase of dengue.
  • Torrentes-Carvalho A1, Marinho CF2, de Oliveira-Pinto LM2, de Oliveira DB2, Damasco PV3, Cunha RV4, de Souza LJ5, de Azeredo EL2, Kubelka CF6.Author information 1Laboratório de Imunologia Viral, Instituto Oswaldo Cruz/FIOCRUZ, RJ, Brazil. Electronic address: torrentes@ioc.fiocruz.br.2Laboratório de Imunologia Viral, Instituto Oswaldo Cruz/FIOCRUZ, RJ, Brazil.3Hospital Universitário Pedro Ernesto, UERJ and Hospital Universitário Gafreé-Guinle, UNIRIO, RJ, Brazil.4Departamento de Clínica Médica, FM, Universidade Federal do Mato Grosso do Sul, Campo Grande, MS, Brazil.5Centro de Referência em Dengue e Faculdade de Medicina, Campos de Goytacazes, RJ, Brazil.6Laboratório de Imunologia Viral, Instituto Oswaldo Cruz/FIOCRUZ, RJ, Brazil. Electronic address: claire@ioc.fiocruz.br.AbstractDengue fever, a public health problem in Brazil, may present severe clinical manifestations as result of an increased vascular permeability and coagulation disorders. T cell activation is a critical event for an effective immune response against infection, including the production of cytokines. We aim to reveal mechanisms that modulate the virus-cell interaction, with an emphasis on cell death. Apoptosis is involved in lymphocyte homeostasis, contributes to the clearance of virus-infected cells but also may play a role in the pathogenesis. Phosphatidylserine exposure on CD8T lymphocytes from dengue patients support early apoptotic processes and loss of genomic integrity, observed by DNA fragmentation in T lymphocytes and indicating late apoptosis. These T cells express activation and cytotoxic phenotypes as revealed by CD29 and CD107a upregulation. Higher frequencies of CD95 were detected in T lymphocytes mainly in those with the cytotoxic profile (CD107a(+)) and lower levels of anti-apoptotic molecule Bcl-2, suggesting that both CD4(+) and CD8(+) T cell subsets are more susceptible to apoptosis during acute dengue. The analysis of apoptosis-related protein expression profile showed that not only molecules with pro- but also those with anti-apoptotic functions are overexpressed, indicating that survival mechanisms could be possibly protecting cells against apoptosis caused by viral, immune, oxidative and/or genotoxic stresses. These observations led us to propose that in dengue patients there is an association between T cell susceptibility to apoptosis and the activation state. The mechanisms for understanding the immunopathogenesis during dengue infection are discussed.
  • Immunobiology.Immunobiology.2014 May;219(5):329-40. doi: 10.1016/j.imbio.2013.11.002. Epub 2014 Jan 9.
  • Dengue fever, a public health problem in Brazil, may present severe clinical manifestations as result of an increased vascular permeability and coagulation disorders. T cell activation is a critical event for an effective immune response against infection, including the production of cytokines. We a
  • PMID 24508270
  • Constitutive expression of murine c-FLIPR causes autoimmunity in aged mice.
  • Ewald F1, Annemann M1, Pils MC2, Plaza-Sirvent C1, Neff F3, Erck C4, Reinhold D5, Schmitz I1.Author information 11] Institute of Molecular and Clinical Immunology, Otto-von-Guericke-University Magdeburg, Leipziger Str. 44, Magdeburg, Germany [2] Research Group of Systems-Oriented Immunology and Inflammation Research, Department of Immune Control, Helmholtz Centre for Infection Research, Inhoffenstr. 7, Braunschweig, Germany.2Mouse Pathology, Animal Experimental Unit, Helmholtz Centre for Infection Research, Inhoffenstr. 7, Braunschweig, Germany.3Institute of Pathology, Helmholtz Centre Munich, Ingolstaedter Landstr. 1, Neuherberg, Germany.4Cellular Proteome Research, Department of Structure and Function of Proteins, Helmholtz Centre for Infection Research, Inhoffenstr. 7, Braunschweig, Germany.5Institute of Molecular and Clinical Immunology, Otto-von-Guericke-University Magdeburg, Leipziger Str. 44, Magdeburg, Germany.AbstractDeath receptor-mediated apoptosis is a key mechanism for the control of immune responses and dysregulation of this pathway may lead to autoimmunity. Cellular FLICE-inhibitory proteins (c-FLIPs) are known as inhibitors of death receptor-mediated apoptosis. The only short murine c-FLIP splice variant is c-FLIPRaji (c-FLIPR). To investigate the functional role of c-FLIPR in the immune system, we used the vavFLIPR mouse model constitutively expressing murine c-FLIPR in all hematopoietic compartments. Lymphocytes from these mice are protected against CD95-mediated apoptosis and activation-induced cell death. Young vavFLIPR mice display normal lymphocyte compartments, but the lymphocyte populations alter with age. We identified reduced levels of T cells and slightly higher levels of B cells in 1-year-old vavFLIPR mice compared with wild-type (WT) littermates. Moreover, both B and T cells from aged vavFLIPR animals show activated phenotypes. Sera from 1-year-old WT and transgenic animals were analysed for anti-nuclear antibodies. Notably, elevated titres of these autoantibodies were detected in vavFLIPR sera. Furthermore, tissue damage in kidneys and lungs from aged vavFLIPR animals was observed, indicating that vavFLIPR mice develop a systemic lupus erythematosus-like phenotype with age. Taken together, these data suggest that c-FLIPR is an important modulator of apoptosis and enforced expression leads to autoimmunity.
  • Cell death & disease.Cell Death Dis.2014 Apr 10;5:e1168. doi: 10.1038/cddis.2014.138.
  • Death receptor-mediated apoptosis is a key mechanism for the control of immune responses and dysregulation of this pathway may lead to autoimmunity. Cellular FLICE-inhibitory proteins (c-FLIPs) are known as inhibitors of death receptor-mediated apoptosis. The only short murine c-FLIP splice variant
  • PMID 24722293
  • Death Induced by CD95 or CD95 Ligand Elimination.
  • Hadji A1, Ceppi P1, Murmann AE1, Brockway S1, Pattanayak A1, Bhinder B2, Hau A1, De Chant S1, Parimi V3, Kolesza P3, Richards J4, Chandel N5, Djaballah H2, Peter ME6.Author information 1Division of Hematology/Oncology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA.2HTS Core Facility, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.3Department of Pathology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA.4Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.5Division of Pulmonary and Cell and Molecular Biology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA.6Division of Hematology/Oncology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. Electronic address: m-peter@northwestern.edu.AbstractCD95 (Fas/APO-1), when bound by its cognate ligand CD95L, induces cells to die by apoptosis. We now show that elimination of CD95 or CD95L results in a form of cell death that is independent of caspase-8, RIPK1/MLKL, and p53, is not inhibited by Bcl-xL expression, and preferentially affects cancer cells. All tumors that formed in mouse models of low-grade serous ovarian cancer or chemically induced liver cancer with tissue-specific deletion of CD95 still expressed CD95, suggesting that cancer cannot form in the absence of CD95. Death induced by CD95R/L elimination (DICE) is characterized by an increase in cell size, production of mitochondrial ROS, and DNA damage. It resembles a necrotic form of mitotic catastrophe. No single drug was found to completely block this form of cell death, and it could also not be blocked by the knockdown of a single gene, making it a promising way to kill cancer cells.
  • Cell reports.Cell Rep.2014 Apr 10;7(1):208-22. doi: 10.1016/j.celrep.2014.02.035. Epub 2014 Mar 20.
  • CD95 (Fas/APO-1), when bound by its cognate ligand CD95L, induces cells to die by apoptosis. We now show that elimination of CD95 or CD95L results in a form of cell death that is independent of caspase-8, RIPK1/MLKL, and p53, is not inhibited by Bcl-xL expression, and preferentially affects cancer c
  • PMID 24656822

和文文献

  • B細胞の成熟過程でのアポトーシス抑制と腫瘍化 (特集 細胞死と造血器腫瘍)
  • CD95による腫瘍の増殖促進
  • Peripheral regulatory T cells from silicosis patients are susceptible to CD95-mediated apoptosis

関連リンク

CD95(FasまたはAPO-1)抗原は、分子量40-50kDaの膜貫通型糖タンパクです。腫瘍壊死因子(TNF)スーパーファミリーに属し、システィンに富む繰り返し配列を3箇所含みます。この細胞表面分子は、アポトーシス(プログラム細胞死)を ...
Protein, molecular pathway, molecule, protein kinase ... The activity of CD95 is controlled in a variety of ways. Recent studies suggest the intracellular outcome of CD95 ligation is dependent upon the nature and - most likely ...

関連画像

Figure 3.You need to enable Javascript. to cd95 the disc assembles fadd procaspaseTransduction PathwayMarantz CD95 DR compact disc driveFigure 2.


★リンクテーブル★
リンク元表面抗原分類」「FAS」「Fas抗原
拡張検索CD95 ligand」「CD95リガンド」「CD95 antigen
関連記事CD

表面抗原分類」

  [★]

cluster of differentiation, CD
  • 細胞の表面抗原を認識する抗体を整理した分類
Bリンパ球 CD10,CD19,CD20
Tリンパ球 CD2,CD3,CD5,CD7
幹細胞 CD34
顆粒球 CD13,CD33
単球 CD14:LPSをリガンドとし、Toll-like receptorと共役して細胞内シグナルを伝達する分子。
巨核球 CD41(GpIIb),CD42(GpIb)
NK細胞CD16(IgGのFc部に対する受容体)、CD56(NCAM-I)


CD1 CD21 CD41 CD61 CD81
CD2 CD22 CD42 CD62 CD82
CD3 CD23 CD43 CD63 CD83
CD4 CD24 CD44 CD64 CD84
CD5 CD25 CD45 CD65 CD85
CD6 CD26 CD46 CD66 CD86
CD7 CD27 CD47 CD67 CD87
CD8 CD28 CD48 CD68 CD88
CD9 CD29 CD49 CD69 CD89
CD10 CD30 CD50 CD70 CD90
CD11 CD31 CD51 CD71 CD91
CD12 CD32 CD52 CD72 CD92
CD13 CD33 CD53 CD73 CD93
CD14 CD34 CD54 CD74 CD94
CD15 CD35 CD55 CD75 CD95
CD16 CD36 CD56 CD76 CD96
CD17 CD37 CD57 CD77 CD97
CD18 CD38 CD58 CD78 CD98
CD19 CD39 CD59 CD79 CD99
CD20 CD40 CD60 CD80 CD100


FAS」

  [★]


Fas抗原」

  [★]

Fas antigen
Apo-1抗原 Apo-1 antigenCD95
Fas受容体CD95抗原APO-1抗原


CD95 ligand」

  [★]

CD95リガンド

CD95LFas ligandFas ligand proteinFasL protein


CD95リガンド」

  [★]

CD95 ligandCD95L
FasリガンドFasリガンドタンパク質


CD95 antigen」

  [★]

CD95抗原

APO-1 antigenFas antigenFas receptor


CD」

  [★]

PrepTutorEJDIC   license prepejdic

「certificate of deposit / (また『C.D.』)Civil Defense民間防衛」


"http://meddic.jp/CD95" より作成


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