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NF-κB-inducing kinase (NIK) is activated in pancreatic β-cells but does not contribute to the development of diabetes
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NIK promotes tissue destruction independently of the alternative NF-κB pathway through TNFR1/RIP1-induced apoptosis
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RIPK3 contributes to TNFR1-mediated RIPK1 kinase-dependent apoptosis in conditions of cIAP1/2 depletion or TAK1 kinase inhibition
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GSK3-Mediated BCL-3 phosphorylation modulates its degradation and its oncogenicity