About: Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand

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scientific journal article

Attributes	Values
rdf:type	Item
description	artículu científicu espublizáu en 1994 (ast) vědecký článek publikovaný v roce 1994 (cs) 1994 թուականի Մարտին հրատարակուած գիտական յօդուած (hyw) наукова стаття, опублікована в березні 1994 (uk) 1994 թվականի մարտին հրատարակված գիտական հոդված (hy) vedecký článok (publikovaný 1994/03/25) (sk) wetenschappelijk artikel (gepubliceerd op 1994/03/25) (nl) مقالة علمية (نشرت في 25-3-1994) (ar) article scientifique publié en 1994 (fr) scientific journal article (en) im März 1994 veröffentlichter wissenschaftlicher Artikel (de)
publication date	wds:Q28513283-FAAB1FC4-6EE9-41EC-9238-DC242C44F9EC
publication date	1994-03-25 00:00:00Z (xsd:dateTime)
language of work or name	wds:Q28513283-AAF1527C-D748-4184-B912-A7A9336A34C9
language of work or name	English
cites work	wds:Q28513283-FA80CFDE-6BF4-4C72-82AF-A4CCE86762AA
cites work	Lethal effect of the anti-Fas antibody in mice
author name string	wds:Q28513283-186906B9-D982-4032-8019-B795FF0D47C5 wds:Q28513283-56AABB0D-1A6C-4470-9EB2-634C276939F3 wds:Q28513283-5B3C79F1-86F4-41CE-B2A1-CFA34DB020CC wds:Q28513283-65093456-4610-4F7C-A520-589A0BCEB668 wds:Q28513283-986842ED-16D5-4936-89CC-027D144FAD16 wds:Q28513283-AE7EE8D2-9A53-4CCF-AE9D-244423C64ACA wds:Q28513283-B8FDA4FA-9254-4015-AEF0-8BBC783D2DB1
OpenCitations bibliographic resource ID	wds:Q28513283-26B8D145-30D4-44A3-8B67-C75A5043AF8F
OpenCitations bibliographic resource ID	https://w3id.org/oc/corpus/br/649891
author name string	S. Nagata M. Tanaka T. Takahashi N. A. Jenkins N. G. Copeland T. Suda C. I. Brannan
OpenCitations bibliographic resource ID	649891
rdfs:label	Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand (en) Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand (nl) Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand (ast)
skos:prefLabel	Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand (en) Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand (nl) Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand (ast)
name	Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand (en) Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand (nl) Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand (ast)
title	wds:Q28513283-422D5C5B-5A2B-4BEA-98A6-6AA69819FC20
title	Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand (en)
page(s)	wds:Q28513283-FBB3D452-1A72-4766-842C-A44004EB1393
page(s)	969–976
instance of	wds:Q28513283-73F6F349-8AAF-4AFD-A7E7-EB62640DAC0E
instance of	scholarly article
main subject	wds:Q28513283-4C7B47FB-A407-473A-B004-2AD519528222 wds:Q28513283-69CBBEF6-8E71-4626-B945-5C758040C182
main subject	wd:Q21494938 Fas ligand (TNF superfamily, member 6)
PubMed ID	wds:Q28513283-068A870B-863E-4B8C-8F49-4A7E561BFD6D
PubMed ID	http://rdf.ncbi.nlm.nih.gov/pubchem/reference/7511063
PubMed ID	7511063
published in	wds:Q28513283-6257C783-7C5E-4C5E-A227-75EBB5A76931
published in	Cell
issue	wds:Q28513283-2329B149-0C70-44F2-A6C1-1857778AE43D
volume	wds:Q28513283-1AF3BB5A-1FE4-4A6F-83E9-999628945853
issue	6
volume	76
DOI	wds:Q28513283-82844838-A903-4668-B548-3FEF6EB1A0D2
DOI	http://dx.doi.org/10.1016/0092-8674(94)90375-1
DOI	10.1016/0092-8674(94)90375-1
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q28513283
is cites work of	Fas ligand mutation in a patient with systemic lupus erythematosus and lymphoproliferative disease Molecular characterization of murine and human OX40/OX40 ligand systems: identification of a human OX40 ligand as the HTLV-1-regulated protein gp34 Fas receptor expression in germinal-center B cells is essential for T and B lymphocyte homeostasis T cell-specific ablation of Fas leads to Fas ligand-mediated lymphocyte depletion and inflammatory pulmonary fibrosis Systemic lupus erythematosus: multiple immunological phenotypes in a complex genetic disease. Elimination of antigen-presenting cells and autoreactive T cells by Fas contributes to prevention of autoimmunity Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease. CD95 (Fas)-dependent elimination of self-reactive B cells upon interaction with CD4+ T cells. Lack of both Fas ligand and perforin protects from flavivirus-mediated encephalitis in mice Pathogenesis of systemic lupus erythematosus Over-expression of the decoy receptor 3 (DcR3) gene in peripheral blood mononuclear cells (PBMC) derived from silicosis patients Defective apoptosis due to a point mutation in the death domain of CD95 associated with autoimmune lymphoproliferative syndrome, T-cell lymphoma, and Hodgkin's disease Regulation of Fas(Apo-1/CD95)- and perforin-mediated lytic pathways of primary cytotoxic T lymphocytes by the protooncogene bcl-2 T follicular helper cells during immunity and tolerance. Defective expression of the apoptosis-inducing CD95 (Fas/APO-1) molecule on T and B cells in IDDM Cif (Cytochrome c efflux-inducing factor) activity is regulated by Bcl-2 and caspases and correlates with the activation of Bid. Hyperproliferation and dysregulation of IL-4 expression in NF-ATp-deficient mice Nitric oxide negatively regulates Fas CD95-induced apoptosis through inhibition of ubiquitin-proteasome-mediated degradation of FLICE inhibitory protein Opposing effects of transmembrane and soluble Fas ligand expression on inflammation and tumor cell survival Fas ligand triggers pulmonary silicosis Essential roles of the Fas-Fas ligand pathway in the development of pulmonary fibrosis Serum levels of soluble Fas ligand in patients with silicosis Detection of alternatively spliced variant messages of Fas gene and mutational screening of Fas and Fas ligand coding regions in peripheral blood mononuclear cells derived from silicosis patients Elevated soluble Fas/APO-1 (CD95) levels in silicosis patients without clinical symptoms of autoimmune diseases or malignant tumours Soluble Fas mRNA is dominantly expressed in cases with silicosis RNA interference targeting Fas protects mice from fulminant hepatitis Historical perspectives on tumor necrosis factor and its superfamily: 25 years later, a golden journey The many roles of FAS receptor signaling in the immune system Cloaked in ubiquitin, a killer hides in plain sight: the molecular regulation of RIPK1. Bcl–2 protects from lethal hepatic apoptosis induced by an ant–Fas antibody in mice Molecular cloning reveals that the p160 Myb-binding protein is a novel, predominantly nucleolar protein which may play a role in transactivation by Myb A critical role for complement in maintenance of self-tolerance High Fas ligand expression on lymphocytes in lesions of ulcerative colitis

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