Fas preassociation required for apoptosis signaling and dominant inhibition by pathogenic mutations.
R M Siegel, J K Frederiksen, D A Zacharias, F K Chan, M Johnson, D Lynch, R Y Tsien, M J Lenardo. Science 2000
Times Cited: 499
Times Cited: 499
Times Cited
Times Co-cited
Similarity
A domain in TNF receptors that mediates ligand-independent receptor assembly and signaling.
F K Chan, H J Chun, L Zheng, R M Siegel, K L Bui, M J Lenardo. Science 2000
F K Chan, H J Chun, L Zheng, R M Siegel, K L Bui, M J Lenardo. Science 2000
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Identification and characterization of a ligand-independent oligomerization domain in the extracellular region of the CD95 death receptor.
G Papoff, P Hausler, A Eramo, M G Pagano, G Di Leve, A Signore, G Ruberti. J Biol Chem 1999
G Papoff, P Hausler, A Eramo, M G Pagano, G Di Leve, A Signore, G Ruberti. J Biol Chem 1999
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Membrane-bound Fas ligand only is essential for Fas-induced 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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Preligand assembly domain-mediated ligand-independent association between TRAIL receptor 4 (TR4) and TR2 regulates TRAIL-induced apoptosis.
Lauren Clancy, Karen Mruk, Kristina Archer, Melissa Woelfel, Juthathip Mongkolsapaya, Gavin Screaton, Michael J Lenardo, Francis Ka-Ming Chan. Proc Natl Acad Sci U S A 2005
Lauren Clancy, Karen Mruk, Kristina Archer, Melissa Woelfel, Juthathip Mongkolsapaya, Gavin Screaton, Michael J Lenardo, Francis Ka-Ming Chan. Proc Natl Acad Sci U S A 2005
20
The Fas-FADD death domain complex structure unravels signalling by receptor clustering.
Fiona L Scott, Boguslaw Stec, Cristina Pop, Małgorzata K Dobaczewska, JeongEun J Lee, Edward Monosov, Howard Robinson, Guy S Salvesen, Robert Schwarzenbacher, Stefan J Riedl. Nature 2009
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Conversion of membrane-bound Fas(CD95) ligand to its soluble form is associated with downregulation of its proapoptotic activity and loss of liver toxicity.
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Yes and PI3K bind CD95 to signal invasion of glioblastoma.
Susanne Kleber, Ignacio Sancho-Martinez, Benedict Wiestler, Alexandra Beisel, Christian Gieffers, Oliver Hill, Meinolf Thiemann, Wolf Mueller, Jaromir Sykora, Andreas Kuhn,[...]. Cancer Cell 2008
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The Fas-FADD death domain complex structure reveals the basis of DISC assembly and disease mutations.
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Structural Basis and Functional Role of Intramembrane Trimerization of the Fas/CD95 Death Receptor.
Qingshan Fu, Tian-Min Fu, Anthony C Cruz, Prabuddha Sengupta, Stacy K Thomas, Shuqing Wang, Richard M Siegel, Hao Wu, James J Chou. Mol Cell 2016
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The TNF and TNF receptor superfamilies: integrating mammalian biology.
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Mutations in Fas associated with human lymphoproliferative syndrome and autoimmunity.
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Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome.
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A death effector domain chain DISC model reveals a crucial role for caspase-8 chain assembly in mediating apoptotic cell death.
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The naturally processed CD95L elicits a c-yes/calcium/PI3K-driven cell migration pathway.
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The many roles of FAS receptor signaling in the immune system.
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The transmembrane form of tumor necrosis factor is the prime activating ligand of the 80 kDa tumor necrosis factor receptor.
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The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosis.
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Crystal structure of the soluble human 55 kd TNF receptor-human TNF beta complex: implications for TNF receptor activation.
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Yohei Mukai, Teruya Nakamura, Mai Yoshikawa, Yasuo Yoshioka, Shin-ichi Tsunoda, Shinsaku Nakagawa, Yuriko Yamagata, Yasuo Tsutsumi. Sci Signal 2010
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13
Autoimmune lymphoproliferative syndrome with somatic Fas mutations.
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12
Revised diagnostic criteria and classification for the autoimmune lymphoproliferative syndrome (ALPS): report from the 2009 NIH International Workshop.
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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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CD95 promotes tumour growth.
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The molecular architecture of the TNF superfamily.
Jean-Luc Bodmer, Pascal Schneider, Jürg Tschopp. Trends Biochem Sci 2002
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12
Two adjacent trimeric Fas ligands are required for Fas signaling and formation of a death-inducing signaling complex.
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12
Palmitoylation of CD95 facilitates formation of SDS-stable receptor aggregates that initiate apoptosis signaling.
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Natural history of autoimmune lymphoproliferative syndrome associated with FAS gene mutations.
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NMR structure and mutagenesis of the Fas (APO-1/CD95) death domain.
B Huang, M Eberstadt, E T Olejniczak, R P Meadows, S W Fesik. Nature 1996
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Solution NMR investigation of the CD95/FADD homotypic death domain complex suggests lack of engagement of the CD95 C terminus.
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Membrane Fas ligand kills human peripheral blood T lymphocytes, and soluble Fas ligand blocks the killing.
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Defective CD95/APO-1/Fas signal complex formation in the human autoimmune lymphoproliferative syndrome, type Ia.
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10
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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Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis.
Andrew Oberst, Christopher P Dillon, Ricardo Weinlich, Laura L McCormick, Patrick Fitzgerald, Cristina Pop, Razq Hakem, Guy S Salvesen, Douglas R Green. Nature 2011
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10
CD95-ligand on peripheral myeloid cells activates Syk kinase to trigger their recruitment to the inflammatory site.
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10
CD95L cell surface cleavage triggers a prometastatic signaling pathway in triple-negative breast cancer.
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Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis.
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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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Dominant negative effects of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor 4 on TRAIL receptor 1 signaling by formation of heteromeric complexes.
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Co-operative and Hierarchical Binding of c-FLIP and Caspase-8: A Unified Model Defines How c-FLIP Isoforms Differentially Control Cell Fate.
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Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death.
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Fas transduces activation signals in normal human T lymphocytes.
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9
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.