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Times Cited: 72
Times Cited
Times Co-cited
Similarity
Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome.
G H Fisher, F J Rosenberg, S E Straus, J K Dale, L A Middleton, A Y Lin, W Strober, M J Lenardo, J M Puck. Cell 1995
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Mutations in Fas associated with human lymphoproliferative syndrome and autoimmunity.
F Rieux-Laucat, F Le Deist, C Hivroz, I A Roberts, K M Debatin, A Fischer, J P de Villartay. Science 1995
F Rieux-Laucat, F Le Deist, C Hivroz, I A Roberts, K M Debatin, A Fischer, J P de Villartay. Science 1995
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Missense mutations in the Fas gene resulting in autoimmune lymphoproliferative syndrome: a molecular and immunological analysis.
A Bettinardi, D Brugnoni, E Quiròs-Roldan, A Malagoli, S La Grutta, A Correra, L D Notarangelo. Blood 1997
A Bettinardi, D Brugnoni, E Quiròs-Roldan, A Malagoli, S La Grutta, A Correra, L D Notarangelo. Blood 1997
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Fas ligand mutation in a patient with systemic lupus erythematosus and lymphoproliferative disease.
J Wu, J Wilson, J He, L Xiang, P H Schur, J D Mountz. J Clin Invest 1996
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Clincal, immunologic, and genetic features of an autoimmune lymphoproliferative syndrome associated with abnormal lymphocyte apoptosis.
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Fas gene mutations in the Canale-Smith syndrome, an inherited lymphoproliferative disorder associated with autoimmunity.
J Drappa, A K Vaishnaw, K E Sullivan, J L Chu, K B Elkon. N Engl J Med 1996
J Drappa, A K Vaishnaw, K E Sullivan, J L Chu, K B Elkon. N Engl J Med 1996
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Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis.
R Watanabe-Fukunaga, C I Brannan, N G Copeland, N A Jenkins, S Nagata. Nature 1992
R Watanabe-Fukunaga, C I Brannan, N G Copeland, N A Jenkins, S Nagata. Nature 1992
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Inherited human Caspase 10 mutations underlie defective lymphocyte and dendritic cell apoptosis in autoimmune lymphoproliferative syndrome type II.
J Wang, L Zheng, A Lobito, F K Chan, J Dale, M Sneller, X Yao, J M Puck, S E Straus, M J Lenardo. Cell 1999
J Wang, L Zheng, A Lobito, F K Chan, J Dale, M Sneller, X Yao, J M Puck, S E Straus, M J Lenardo. Cell 1999
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Autoimmune lymphoproliferative syndrome with defective Fas: genotype influences penetrance.
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Clinical, immunological, and pathological consequences of Fas-deficient conditions.
F Le Deist, J F Emile, F Rieux-Laucat, M Benkerrou, I Roberts, N Brousse, A Fischer. Lancet 1996
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The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations.
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Autoimmune lymphoproliferative syndrome (ALPS) in a child from consanguineous parents: a dominant or recessive disease?
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The clinical spectrum in a large kindred with autoimmune lymphoproliferative syndrome caused by a Fas mutation that impairs lymphocyte apoptosis.
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The development of lymphomas in families with autoimmune lymphoproliferative syndrome with germline Fas mutations and defective lymphocyte apoptosis.
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Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand.
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A novel lymphoproliferative/autoimmune syndrome resembling murine lpr/gld disease.
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Pathological findings in human autoimmune lymphoproliferative syndrome.
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Deficiency of the Fas apoptosis pathway without Fas gene mutations in pediatric patients with autoimmunity/lymphoproliferation.
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Fas/Apo1 mutations and autoimmune lymphoproliferative syndrome in a patient with type 2 autoimmune hepatitis.
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FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex.
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Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiency.
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Autoimmune lymphoproliferative syndrome with somatic Fas mutations.
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An inherited disorder of lymphocyte apoptosis: the autoimmune lymphoproliferative syndrome.
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Characteristic T helper 2 T cell cytokine abnormalities in autoimmune lymphoproliferative syndrome, a syndrome marked by defective apoptosis and humoral autoimmunity.
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Defective CD95/APO-1/Fas signal complex formation in the human autoimmune lymphoproliferative syndrome, type Ia.
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FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis.
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Cytotoxicity-dependent APO-1 (Fas/CD95)-associated proteins form a death-inducing signaling complex (DISC) with the receptor.
F C Kischkel, S Hellbardt, I Behrmann, M Germer, M Pawlita, P H Krammer, M E Peter. EMBO J 1995
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Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death.
M P Boldin, T M Goncharov, Y V Goltsev, D Wallach. Cell 1996
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Autocrine T-cell suicide mediated by APO-1/(Fas/CD95)
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B Huang, M Eberstadt, E T Olejniczak, R P Meadows, S W Fesik. Nature 1996
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A novel protein domain required for apoptosis. Mutational analysis of human Fas antigen.
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Mature T lymphocyte apoptosis--immune regulation in a dynamic and unpredictable antigenic environment.
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Increases in circulating and lymphoid tissue interleukin-10 in autoimmune lymphoproliferative syndrome are associated with disease expression.
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A homozygous Fas ligand gene mutation in a patient causes a new type of autoimmune lymphoproliferative syndrome.
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Revised diagnostic criteria and classification for the autoimmune lymphoproliferative syndrome (ALPS): report from the 2009 NIH International Workshop.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.