The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations
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Apoptosis induced by the nuclear death domain protein p84N5 is inhibited by association with Rb proteinThe Fas-FADD death domain complex structure reveals the basis of DISC assembly and disease mutationsAdvances in the management and understanding of autoimmune lymphoproliferative syndrome (ALPS)I-PLA(2) activation during apoptosis promotes the exposure of membrane lysophosphatidylcholine leading to binding by natural immunoglobulin M antibodies and complement activationC-Reactive protein binds to apoptotic cells, protects the cells from assembly of the terminal complement components, and sustains an antiinflammatory innate immune response: implications for systemic autoimmunityFAS haploinsufficiency is a common disease mechanism in the human autoimmune lymphoproliferative syndromeFAS (CD95) mutations are rare in gastric MALT lymphoma but occur more frequently in primary gastric diffuse large B-cell lymphomaPrecise mapping of the CD95 pre-ligand assembly domain.Dominant inhibition of Fas ligand-mediated apoptosis due to a heterozygous mutation associated with autoimmune lymphoproliferative syndrome (ALPS) Type IbAnti-platelet antibodies associated with the Canale-Smith syndrome bind to the same platelet glycoprotein complexes as those of idiopathic thrombocytopenic purpura patients.Exonic deletion of CASP10 in a patient presenting with systemic juvenile idiopathic arthritis, but not with autoimmune lymphoproliferative syndrome type IIa.Many checkpoints on the road to cell death: regulation of Fas-FasL interactions and Fas signaling in peripheral immune responses.The spectrum of apoptotic defects and clinical manifestations, including systemic lupus erythematosus, in humans with CD95 (Fas/APO-1) mutations.Somatic FAS mutations are common in patients with genetically undefined autoimmune lymphoproliferative syndrome.Genetic basis of the complex pathological manifestations of collagen disease: lessons from MRL/lpr and related mouse models.Autoimmune lymphoproliferative syndrome type III: an indefinite disorder.Autoimmune lymphoproliferative syndrome type III, an indefinite disorder.Onset of autoimmune lymphoproliferative syndrome (ALPS) in humans as a consequence of genetic defect accumulationSoluble fas and the -670 polymorphism of fas in lupus nephritisFrequent deletion of Fas gene sequences encoding death and transmembrane domains in nasal natural killer/T-cell lymphoma.Contribution of apoptosis and apoptosis-related proteins to the malformation of the primitive intrahepatic biliary system in Meckel syndrome.SPOTS: signaling protein oligomeric transduction structures are early mediators of death receptor-induced apoptosis at the plasma membrane.Genetic defects of apoptosis and primary immunodeficiency.FAS system deregulation in T-cell lymphoblastic lymphomaCD95-mediated cell signaling in cancer: mutations and post-translational modulations.Camptothecin induces the transit of FasL trimers to the cell surface in apoptotic HEp-2 cells.Detection, epitope-mapping and function of anti-Fas autoantibody in patients with silicosis.A membrane-bound Fas decoy receptor expressed by human thymocytes.Structure of the Fas/FADD complex: a conditional death domain complex mediating signaling by receptor clustering.A missense mutation in the extracellular domain of Fas: the most common change in Argentinean patients with autoimmune lymphoproliferative syndrome represents a founder effect.Use of GC clamps in DHPLC mutation scanningAutoimmune lymphoproliferative syndrome: response to mycophenolate mofetil and pyrimethamine/sulfadoxine in a 5-year-old child.Caspases. Multifunctional proteases.Deletion of PTEN and BMPR1A on chromosome 10q23 is not always associated with juvenile polyposis of infancy.A constitutive cytoprotective pathway protects endothelial cells from lipopolysaccharide-induced apoptosis.Necessary role of phosphatidylinositol 3-kinase in transforming growth factor beta-mediated activation of Akt in normal and rheumatoid arthritis synovial fibroblasts.A variant of death-receptor 3 associated with rheumatoid arthritis interferes with apoptosis-induction of T cell.Inactivation of the Fas gene by Alu insertion: retrotransposition in an intron causing splicing variation and autoimmune lymphoproliferative syndrome.FAS Haploinsufficiency Caused by Extracellular Missense Mutations Underlying Autoimmune Lymphoproliferative Syndrome.Fas promoter region gene polymorphism is associated with an increased risk for myocardial infarction.
P2860
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P2860
The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations
description
1999 nî lūn-bûn
@nan
1999 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations
@ast
The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations
@en
type
label
The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations
@ast
The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations
@en
prefLabel
The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations
@ast
The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations
@en
P2093
P2860
P356
P1476
The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations
@en
P2093
A K Vaishnaw
J R Orlinick
P H Krammer
P2860
P304
P356
10.1172/JCI5121
P407
P577
1999-02-01T00:00:00Z