A FADD-dependent innate immune mechanism in mammalian cells

[1]  Shizuo Akira,et al.  The RNA helicase RIG-I has an essential function in double-stranded RNA-induced innate antiviral responses , 2004, Nature Immunology.

[2]  Osamu Takeuchi,et al.  The Roles of Two IκB Kinase-related Kinases in Lipopolysaccharide and Double Stranded RNA Signaling and Viral Infection , 2004, The Journal of experimental medicine.

[3]  F. Martinon,et al.  RIP1 is an essential mediator of Toll-like receptor 3–induced NF-κB activation , 2004, Nature Immunology.

[4]  T. Maniatis,et al.  IFN-regulatory factor 3-dependent gene expression is defective in Tbk1-deficient mouse embryonic fibroblasts , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[5]  Richard A Flavell,et al.  Upregulation of costimulatory molecules induced by lipopolysaccharide and double-stranded RNA occurs by Trif-dependent and Trif-independent pathways , 2003, Nature Immunology.

[6]  J. Hoffmann,et al.  The immune response of Drosophila , 2003, Nature.

[7]  S. Akira,et al.  Selective contribution of IFN-α/β signaling to the maturation of dendritic cells induced by double-stranded RNA or viral infection , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[8]  S. Akira,et al.  Role of Adaptor TRIF in the MyD88-Independent Toll-Like Receptor Signaling Pathway , 2003, Science.

[9]  Persephone Borrow,et al.  Viral infection switches non-plasmacytoid dendritic cells into high interferon producers , 2003, Nature.

[10]  Guo-Ping Zhou,et al.  Triggering the Interferon Antiviral Response Through an IKK-Related Pathway , 2003, Science.

[11]  T. Maniatis,et al.  IKKε and TBK1 are essential components of the IRF3 signaling pathway , 2003, Nature Immunology.

[12]  T. Akazawa,et al.  TICAM-1, an adaptor molecule that participates in Toll-like receptor 3–mediated interferon-β induction , 2003, Nature Immunology.

[13]  D. Gubb,et al.  The Drosophila immune defense against gram-negative infection requires the death protein dFADD. , 2002, Immunity.

[14]  J. Darnell,et al.  Signalling: STATs: transcriptional control and biological impact , 2002, Nature Reviews Molecular Cell Biology.

[15]  B. Lemaître,et al.  Inducible Expression of Double-Stranded RNA Reveals a Role for dFADD in the Regulation of the Antibacterial Response in Drosophila Adults , 2002, Current Biology.

[16]  T. Taniguchi,et al.  The interferon-α/β system in antiviral responses: a multimodal machinery of gene regulation by the IRF family of transcription factors , 2002 .

[17]  R. Flavell,et al.  Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3 , 2001, Nature.

[18]  C. Janeway,et al.  The Toll receptor family and microbial recognition. , 2000, Trends in microbiology.

[19]  P. Roberts,et al.  Essential role for the dsRNA-dependent protein kinase PKR in innate immunity to viral infection. , 2000, Immunity.

[20]  P. Roberts,et al.  Alpha/Beta Interferons Potentiate Virus-Induced Apoptosis through Activation of the FADD/Caspase-8 Death Signaling Pathway , 2000, Journal of Virology.

[21]  M. Karin,et al.  JNK2 and IKKbeta are required for activating the innate response to viral infection. , 1999, Immunity.

[22]  B. Williams,et al.  PKR; a sentinel kinase for cellular stress , 1999, Oncogene.

[23]  G. Stark,et al.  How cells respond to interferons. , 1998, Annual review of biochemistry.

[24]  J. Beckmann,et al.  Targeted disruption of the mouse Caspase 8 gene ablates cell death induction by the TNF receptors, Fas/Apo1, and DR3 and is lethal prenatally. , 1998, Immunity.

[25]  D. Goeddel,et al.  FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis. , 1998, Science.

[26]  T. Maniatis,et al.  Virus infection induces the assembly of coordinately activated transcription factors on the IFN-beta enhancer in vivo. , 1998, Molecular cell.

[27]  Stefan Grimm,et al.  The Death Domain Kinase RIP Mediates the TNF-Induced NF-κB Signal , 1998 .

[28]  Matthias Mann,et al.  FLICE, A Novel FADD-Homologous ICE/CED-3–like Protease, Is Recruited to the CD95 (Fas/APO-1) Death-Inducing Signaling Complex , 1996, Cell.

[29]  Arul M. Chinnaiyan,et al.  FADD, a novel death domain-containing protein, interacts with the death domain of fas and initiates apoptosis , 1995, Cell.

[30]  E. Kopp.  IFN-regulatory factor 3-dependent gene expression is defective in Tbk1-deficient mouse embryonic fibroblasts , 2004 .

[31]  S. Akira,et al.  Toll-like receptors. , 2003, Annual review of immunology.