Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiency - Test2 - elhamkhani - TriplyDB

Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiency

Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiency

http://www.wikidata.org/entity/Q28204372

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Whole-exome-sequencing-based discovery of human FADD deficiency Calcium binding of ARC mediates regulation of caspase 8 and cell death No death without life: vital functions of apoptotic effectors Control of autophagic cell death by caspase-10 in multiple myeloma Second messenger role for Mg2+ revealed by human T-cell immunodeficiency The Fas-associated death domain protein is required in apoptosis and TLR-induced proliferative responses in B cells Advances in the management and understanding of autoimmune lymphoproliferative syndrome (ALPS)Revised diagnostic criteria and classification for the autoimmune lymphoproliferative syndrome (ALPS): report from the 2009 NIH International Workshop How I treat autoimmune lymphoproliferative syndrome Use of rituximab for refractory cytopenias associated with autoimmune lymphoproliferative syndrome (ALPS)Towards in vivo application of RNA interference - new toys, old problems Converging roles of caspases in inflammasome activation, cell death and innate immunity Viral infection and the evolution of caspase 8-regulated apoptotic and necrotic death pathways New roles for old enzymes: killer caspases as the engine of cell behavior changes RIPK-dependent necrosis and its regulation by caspases: a mystery in five acts c-FLIP-Short reduces type I interferon production and increases viremia with coxsackievirus B3 Caspase 3-Dependent Cell Death of Neurons Contributes to the Pathogenesis of West Nile Virus Encephalitis Old, new and emerging functions of caspases.FAS haploinsufficiency is a common disease mechanism in the human autoimmune lymphoproliferative syndrome Development of lymphoma in Autoimmune Lymphoproliferative Syndrome (ALPS) and its relationship to Fas gene mutations FLIP and the death effector domain family Causes and consequences of the autoimmune lymphoproliferative syndrome TIPE2, a negative regulator of innate and adaptive immunity that maintains immune homeostasis N-terminal fragment of c-FLIP(L) processed by caspase 8 specifically interacts with TRAF2 and induces activation of the NF-kappaB signaling pathway Partial cleavage of RasGAP by caspases is required for cell survival in mild stress conditions.Apoptotic regulation of epithelial cellular extrusion Dominant inhibition of Fas ligand-mediated apoptosis due to a heterozygous mutation associated with autoimmune lymphoproliferative syndrome (ALPS) Type Ib Spatial differences in active caspase-8 defines its role in T-cell activation versus cell death Management of Evans syndrome.Extreme lymphoproliferative disease and fatal autoimmune thrombocytopenia in FasL and TRAIL double-deficient mice Exonic deletion of CASP10 in a patient presenting with systemic juvenile idiopathic arthritis, but not with autoimmune lymphoproliferative syndrome type IIa.Updated Understanding of Autoimmune Lymphoproliferative Syndrome (ALPS).CCL2 and interleukin-6 promote survival of human CD11b+ peripheral blood mononuclear cells and induce M2-type macrophage polarization IL-15 maintains T-cell survival via S-nitrosylation-mediated inhibition of caspase-3 Caspases and nitric oxide broadly regulate dendritic cell maturation and surface expression of class II MHC proteins.When apoptosis meets autophagy: deciding cell fate after trauma and sepsis.Activation of gamma delta T cells by Borrelia burgdorferi is indirect via a TLR- and caspase-dependent pathway The Jekyll and Hyde functions of caspases.Caspase-3 is transiently activated without cell death during early antigen driven expansion of CD8(+) T cells in vivo.ALPS-ten lessons from an international workshop on a genetic disease of apoptosis

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Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiency

http://www.wikidata.org/entity/Q28204372

description

2002 nî lūn-bûn

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2002 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2002 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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name

Pleiotropic defects in lymphoc ...... lead to human immunodeficiency

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Pleiotropic defects in lymphoc ...... lead to human immunodeficiency

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Pleiotropic defects in lymphoc ...... lead to human immunodeficiency

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type

label

Pleiotropic defects in lymphoc ...... lead to human immunodeficiency

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Pleiotropic defects in lymphoc ...... lead to human immunodeficiency

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Pleiotropic defects in lymphoc ...... lead to human immunodeficiency

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prefLabel

Pleiotropic defects in lymphoc ...... lead to human immunodeficiency

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Pleiotropic defects in lymphoc ...... lead to human immunodeficiency

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Pleiotropic defects in lymphoc ...... lead to human immunodeficiency

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Pleiotropic defects in lymphoc ...... lead to human immunodeficiency

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Christina K Speirs

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Craig G Hall

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Hyung J Chun

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Janet K Dale

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Jennifer Puck

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Jin Wang

http://www.w3.org/2001/XMLSchema#string

Joie Davis

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Lixin Zheng

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Manzoor Ahmad

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Michael J Lenardo

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P2860

Inherited human Caspase 10 mutations underlie defective lymphocyte and dendritic cell apoptosis in autoimmune lymphoproliferative syndrome type II

Caspase-10 is an initiator caspase in death receptor signaling

Duplexes of 21-nucleotide RNAs mediate RNA interference in cultured mammalian cells

Fas ligand mutation in a patient with systemic lupus erythematosus and lymphoproliferative disease

Death receptor recruitment of endogenous caspase-10 and apoptosis initiation in the absence of caspase-8

Essential requirement for caspase-8/FLICE in the initiation of the Fas-induced apoptotic cascade

Mutations in Fas associated with human lymphoproliferative syndrome and autoimmunity.

Fas gene mutations in the Canale-Smith syndrome, an inherited lymphoproliferative disorder associated with autoimmunity.

Mature T lymphocyte apoptosis--immune regulation in a dynamic and unpredictable antigenic environment.

Defective CD95/APO-1/Fas signal complex formation in the human autoimmune lymphoproliferative syndrome, type Ia.

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395-9

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3000584

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10.1038/NATURE01063

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6905

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419

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1011505339

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12353035

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