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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-κB

Oncogene, 1999-01, Vol.18 (3), p.747-757

1999

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Enhancement of T Cell Receptor Signaling by a Mild Oxidative Shift in the Intracellular Thiol Pool

The Journal of immunology (1950), 2000-10, Vol.165 (8), p.4319-4328

2000

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Repression of NF-κB impairs HeLa cell proliferation by functional interference with cell cycle checkpoint regulators

Oncogene, 1999-05, Vol.18 (21), p.3213-3225

1999

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Mixed-Lineage Kinase 3 Delivers CD3/CD28-Derived Signals into the IκB Kinase Complex

Molecular and Cellular Biology, 2000-04, Vol.20 (7), p.2556-2568

2000

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Tyrosine-phosphorylated Vav1 as a Point of Integration for T-cell Receptor- and CD28-mediated Activation of JNK, p38, and Interleukin-2 Transcription

The Journal of biological chemistry, 2000-06, Vol.275 (24), p.18160-18171

2000

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Various glucocorticoids differ in their ability to induce gene expression, apoptosis and to repress NF-κB-dependent transcription

FEBS letters, 1998-12, Vol.441 (3), p.441-446

1998

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Caspase-dependent cleavage and inactivation of the Vav1 proto-oncogene product during apoptosis prevents IL-2 transcription

Oncogene, 2000-02, Vol.19 (9), p.1153-1163

2000

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CD95‐induced JNK activation signals are transmitted by the death‐inducing signaling complex (DISC), but not by Daxx

International journal of cancer, 2001-07, Vol.93 (2), p.185-191

2001

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The antiinflammatory sesquiterpene lactone parthenolide inhibits NF-kappa B by targeting the I kappa B kinase complex

The Journal of immunology (1950), 1999-11, Vol.163 (10), p.5617-5623

1999

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Sesquiterpene Lactones Specifically Inhibit Activation of NF-κB by Preventing the Degradation of IκB-α and IκB-β

The Journal of biological chemistry, 1998-01, Vol.273 (3), p.1288-1297

1998

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Inhibition of tyrosine phosphatases induces apoptosis independent from the CD95 system

Cell death and differentiation, 1999-09, Vol.6 (9), p.833-841

1999

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The Human Papillomavirus Oncoprotein E7 Attenuates NF-κB Activation by Targeting the IκB Kinase Complex

The Journal of biological chemistry, 2002-07, Vol.277 (28), p.25576-25582

2002

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The pro‐ or anti‐apoptotic function of NF‐κB is determined by the nature of the apoptotic stimulus

European journal of biochemistry, 2000-06, Vol.267 (12), p.3828-3835

2000

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Co‐stimulatory effect of nitric oxide on endothelial NF‐κB implies a physiological self‐amplifying mechanism

European journal of immunology, 1998-08, Vol.28 (8), p.2276-2282

1998

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Synergistic Activation of NF-κB by Functional Cooperation between Vav and PKCθ in T Lymphocytes

The Journal of biological chemistry, 2000-08, Vol.275 (32), p.24547-24551

2000

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Vav synergizes with protein kinase C theta to mediate IL-4 gene expression in response to CD28 costimulation in T cells

The Journal of immunology (1950), 2000-04, Vol.164 (7), p.3829-3836

2000

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Protein Kinase C θ Cooperates with Vav1 to Induce JNK Activity in T-cells

The Journal of biological chemistry, 2001-06, Vol.276 (23), p.20022-20028

2001

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Tumor Necrosis Factor-α-induced Cell Killing and Activation of Transcription Factor NF-κB Are Uncoupled in L929 Cells

The Journal of biological chemistry, 1998-07, Vol.273 (29), p.18117-18121

1998

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The human papillomavirus oncoprotein E7 attenuates NF-kappa B activation by targeting the Ikappa B kinase complex

The Journal of biological chemistry, 2002-07, Vol.277 (28), p.25576-25582

2002

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The Human Papillomavirus Oncoprotein E7 Attenuates NF-ÎºB Activation by Targeting the IÎºB Kinase Complex

The Journal of biological chemistry, 2002-07, Vol.277 (28), p.25576

2002

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Protein Kinase C Î¸ Cooperates with Vav1 to Induce JNK Activity in T-cells

The Journal of biological chemistry, 2001-06, Vol.276 (23), p.20022

2001

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Synergistic Activation of NF-ÎºB by Functional Cooperation between Vav and PKCÎ¸ in T Lymphocytes

The Journal of biological chemistry, 2000-08, Vol.275 (32), p.24547

2000

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Tyrosine-phosphorylated Vav1 as a Point of Integration for T-cell Receptor- and CD28-mediated Activation of JNK, p38, and Interleukin-2 Transcription210

The Journal of biological chemistry, 2000-06, Vol.275 (24), p.18160-18171

2000

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Tumor Necrosis Factor-Î±-induced Cell Killing and Activation of Transcription Factor NF-ÎºB Are Uncoupled in L929 Cells

The Journal of biological chemistry, 1998-07, Vol.273 (29), p.18117

1998

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Sesquiterpene Lactones Specifically Inhibit Activation of NF-ÎºB by Preventing the Degradation of IÎºB-Î± and IÎºB-Î

The Journal of biological chemistry, 1998-01, Vol.273 (3), p.1288

1998

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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-κB

Enhancement of T Cell Receptor Signaling by a Mild Oxidative Shift in the Intracellular Thiol Pool

Repression of NF-κB impairs HeLa cell proliferation by functional interference with cell cycle checkpoint regulators

Mixed-Lineage Kinase 3 Delivers CD3/CD28-Derived Signals into the IκB Kinase Complex

Tyrosine-phosphorylated Vav1 as a Point of Integration for T-cell Receptor- and CD28-mediated Activation of JNK, p38, and Interleukin-2 Transcription

Various glucocorticoids differ in their ability to induce gene expression, apoptosis and to repress NF-κB-dependent transcription

Caspase-dependent cleavage and inactivation of the Vav1 proto-oncogene product during apoptosis prevents IL-2 transcription

CD95‐induced JNK activation signals are transmitted by the death‐inducing signaling complex (DISC), but not by Daxx

The antiinflammatory sesquiterpene lactone parthenolide inhibits NF-kappa B by targeting the I kappa B kinase complex

Sesquiterpene Lactones Specifically Inhibit Activation of NF-κB by Preventing the Degradation of IκB-α and IκB-β

Inhibition of tyrosine phosphatases induces apoptosis independent from the CD95 system

The Human Papillomavirus Oncoprotein E7 Attenuates NF-κB Activation by Targeting the IκB Kinase Complex

The pro‐ or anti‐apoptotic function of NF‐κB is determined by the nature of the apoptotic stimulus

Co‐stimulatory effect of nitric oxide on endothelial NF‐κB implies a physiological self‐amplifying mechanism

Synergistic Activation of NF-κB by Functional Cooperation between Vav and PKCθ in T Lymphocytes

Vav synergizes with protein kinase C theta to mediate IL-4 gene expression in response to CD28 costimulation in T cells

Protein Kinase C θ Cooperates with Vav1 to Induce JNK Activity in T-cells

Tumor Necrosis Factor-α-induced Cell Killing and Activation of Transcription Factor NF-κB Are Uncoupled in L929 Cells

The human papillomavirus oncoprotein E7 attenuates NF-kappa B activation by targeting the Ikappa B kinase complex

The Human Papillomavirus Oncoprotein E7 Attenuates NF-ÎºB Activation by Targeting the IÎºB Kinase Complex

Protein Kinase C Î¸ Cooperates with Vav1 to Induce JNK Activity in T-cells

Synergistic Activation of NF-ÎºB by Functional Cooperation between Vav and PKCÎ¸ in T Lymphocytes

Tyrosine-phosphorylated Vav1 as a Point of Integration for T-cell Receptor- and CD28-mediated Activation of JNK, p38, and Interleukin-2 Transcription210

Tumor Necrosis Factor-Î±-induced Cell Killing and Activation of Transcription Factor NF-ÎºB Are Uncoupled in L929 Cells

Sesquiterpene Lactones Specifically Inhibit Activation of NF-ÎºB by Preventing the Degradation of IÎºB-Î± and IÎºB-Î

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