Akt-Dependent Manner B Activation in a Phosphatidylinositol κ NF-Antioxidant c-FLIP Inhibits Fas Ligand-Induced Data

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• Model-based dissection of CD95 signaling dynamics reveals both a pro- and antiapoptotic role of c-FLIPL

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• Localization of Fas/CD95 into the Lipid Rafts on Down-Modulation of the Phosphatidylinositol 3-Kinase Signaling Pathway

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• Integrating cell-signalling pathways with NF-kappaB and IKK function.

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• the Journal of Immunology

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• Phosphatidylinositol 3-Kinase/Akt Positively Regulates Fas (CD95)-Mediated Apoptosis in Epidermal Cl41 Cells

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• c-FLIPR, a New Regulator of Death Receptor-induced Apoptosis*

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• The caspase-8 modulator c-FLIP.

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• Nitric Oxide Negatively Regulates Fas CD95-induced Apoptosis through Inhibition of Ubiquitin-Proteasome-mediated Degradation of FLICE Inhibitory Protein*

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• Regulation of Fas (CD95)‐induced apoptotic and necrotic cell death by reactive oxygen species in macrophages

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• Wortmannin elevates tumor necrosis factor-related apoptosis-inducing ligand sensitivity in LNCaP cells through down-regulation of IAP-2 protein.

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• NFκB activation by Fas is mediated through FADD, caspase-8, and RIP and is inhibited by FLIP

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• N-Terminal Fragment of c-FLIP(L) Processed by Caspase 8 Specifically Interacts with TRAF2 and Induces Activation of the NF-κB Signaling Pathway

  2004cited by this paper
• The flip side of FLIP.

  2004cited by this paper
• KSHV vFLIP binds to IKK-gamma to activate IKK.

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• Regulation of Fas (CD95)-induced apoptosis by nuclear factor-kappaB and tumor necrosis factor-alpha in macrophages.

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• The Long Form of FLIP Is an Activator of Caspase-8 at the Fas Death-inducing Signaling Complex*

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• c‐FLIPL is a dual function regulator for caspase‐8 activation and CD95‐mediated apoptosis

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• Critical roles of TRAF2 and TRAF5 in tumor necrosis factor-induced NF-κB activation and protection from cell death

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• The Human Herpes Virus 8-encoded Viral FLICE Inhibitory Protein Physically Associates with and Persistently Activates the IκB Kinase Complex*

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• FLICE-Inhibitory Proteins: Regulators of Death Receptor-Mediated Apoptosis

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• Akt and Bcl-xL Promote Growth Factor-independent Survival through Distinct Effects on Mitochondrial Physiology*

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• Regulation of lymphocyte proliferation and death by flip

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• Phosphatidylinositol 3-Kinase/Akt Signaling Controls Endothelial Cell Sensitivity to Fas-Mediated Apoptosis via Regulation of FLICE-Inhibitory Protein (FLIP)

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• Tumor Necrosis Factor-α Generates Reactive Oxygen Species via a Cytosolic Phospholipase A2-linked Cascade*

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• Protein kinases as mediators of phosphoinositide 3-kinase signaling.

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• The caspase-8 inhibitor FLIP promotes activation of NF-κB and Erk signaling pathways

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• Role of reactive oxygen species (ROS) in apoptosis induction

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• PI3-K/AKT regulation of NF-kappaB signaling events in suppression of TNF-induced apoptosis.

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• NF-κB activation by tumour necrosis factor requires the Akt serine–threonine kinase

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• The Role of c-FLIP in Modulation of CD95-induced Apoptosis*

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• Tumor necrosis factor receptor and Fas signaling mechanisms.

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• Abnormal morphogenesis but intact IKK activation in mice lacking the IKKalpha subunit of IkappaB kinase.

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• Apoptosis, proliferation and NF‐κB activation induced by agonistic Fas antibodies in the human myeloma cell line OH‐2: amplification of Fas‐mediated apoptosis by tumor necrosis factor

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• Modulation of the NF-kappa B pathway by virally encoded death effector domains-containing proteins.

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• Hydrogen peroxide-induced apoptosis is CD95-independent, requires the release of mitochondria-derived reactive oxygen species and the activation of NF-kappaB.

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• Role of Reactive Oxygen Intermediates in Activation-induced CD95 (APO-1/Fas) Ligand Expression*

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• Cellular stimulation via CD95 involves activation of phospho-inositide-3-kinase

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• Regulation of the proinflammatory effects of Fas ligand (CD95L).

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• Oxidative stress and hypoxia/reoxygenation trigger CD95 (APO‐1/Fas) ligand expression in microglial cells

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• I-FLICE, a Novel Inhibitor of Tumor Necrosis Factor Receptor-1- and CD-95-induced Apoptosis*

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• Inhibition of death receptor signals by cellular FLIP

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• MRIT, a novel death-effector domain-containing protein, interacts with caspases and BclXL and initiates cell death.

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• Regulation of apoptosis through CD95 (APO-I/Fas) receptor-ligand interaction.

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• The CD95 (APO-1/Fas) Receptor Activates NF-B Independently of Its Cytotoxic Function (*)

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• The NF-kappa B and I kappa B proteins: new discoveries and insights.

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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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• Suppression of TNF-alpha-induced apoptosis by NF-kappaB.

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• Constitutive NF-kappa B activation, enhanced granulopoiesis, and neonatal lethality in I kappa B alpha-deficient mice.

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• Purification and characterization of the Fas-ligand that induces apoptosis

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• Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family.

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• H2O2 and antioxidants have opposite effects on activation of NF‐kappa B and AP‐1 in intact cells: AP‐1 as secondary antioxidant‐responsive factor.

  1993cited by this paper

• No citing papers are available for this paper.