Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiency (Q28204372)

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object named as

Joie Davis

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Suzanne Skoda-Smith

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object named as

Suzanne Skoda-Smith

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author name string

Hyung J Chun

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Lixin Zheng

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Manzoor Ahmad

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Jin Wang

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Christina K Speirs

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Richard M Siegel

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Janet K Dale

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Craig G Hall

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T Prescott Atkinson

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Stephen E Straus

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Michael J Lenardo

Caspase-10 is an initiator caspase in death receptor signaling

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publication date

26 September 2002

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language of work or name

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419

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issue

6905

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page(s)

395-9

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Die and let live: eliminating dangerous lymphocytes

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

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Early activation of caspases during T lymphocyte stimulation results in selective substrate cleavage in nonapoptotic cells

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Caspase activation is required for T cell proliferation

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

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Membrane Oligomerization and Cleavage Activates the Caspase-8 (FLICE/MACHα1) Death Signal

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

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Caspase-3-Like Activity Is Necessary for IL-2 Release in Activated Jurkat T-cells

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Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome

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Novel Fas (CD95/APO-1) mutations in infants with a lymphoproliferative disorder

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Autoimmune lymphoproliferative syndrome: types I, II and beyond

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Triggering of human natural killer cells through CD16 induces tyrosine phosphorylation of the p72syk kinase

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