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Tumor Necrosis Factor-alpha
Miz1 is a signal- and pathway-specific modulator or regulator (SMOR) that suppresses TNF-alpha-induced JNK1 activation.
Site-specific ubiquitination is required for relieving the transcription factor Miz1-mediated suppression on TNF-a-induced JNK activation and inflammation.
The absence of NF-kappaB-mediated inhibition of c-Jun N-terminal kinase activation contributes to tumor necrosis factor alpha-induced apoptosis.
Androgen via p21 inhibits tumor necrosis factor alpha-induced JNK activation and apoptosis.
Temporal control of TNFa signaling by Miz1.
KEAP1 E3 ligase-mediated downregulation of NF-kappaB signaling by targeting IKKbeta.
Inactivation of BAD by IKK inhibits TNFa-induced apoptosis independently of NF-?B activation.
Signaling intermediates required for NF-kappa B activation and IL-8 expression in CF bronchial epithelial cells.
TNF-alpha-induced apoptosis of macrophages following inhibition of NF-kappa B: a central role for disruption of mitochondria.
Cyclic AMP inhibits p38 activation via CREB-induced dynein light chain.
c-Jun N-terminal protein kinase 1 (JNK1), but not JNK2, is essential for tumor necrosis factor alpha-induced c-Jun kinase activation and apoptosis.
The true face of JNK activation in apoptosis.
A five-year itch in TNF-alpha cytotoxicity: the time factor determines JNK action.