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PKD1 — RELA

Text-mined interactions from Literome

Storz et al., EMBO J 2003 : PKD activates NF-kappaB through the IKK complex and more specifically, IKKbeta, leading to I(kappa)B(alpha) degradation
Storz et al., Mol Cell Biol 2004 : We also show that other PKCs, including PKCepsilon and PKCzeta, do not participate in PKD activation or NF-kappaB induction
Storz et al., Mol Pharmacol 2004 : Resveratrol, a potent antioxidant, blocks both PKD activation and NF-kappaB induction
Arnold et al., Mol Cell Biol 2005 : Upon T-cell receptor stimulation, PKD robustly augments HPK1 kinase activity in Jurkat T cells and enhances HPK1-driven SAPK/JNK and NF-kappaB activation ; conversely, antisense down-regulation of PKD results in reduced HPK1 activity
Banzi et al., Biochem Biophys Res Commun 2006 : Polycystin-1 promotes PKCalpha mediated NF-kappaB activation in kidney cells
Park et al., J Immunol 2008 : Knockdown of PKD1 revealed that PKD1 is required for activation of NF-kappaB and MAPKs, and subsequent expression of cytokines in response to CpG-B DNA
Yuan et al., Am J Physiol Gastrointest Liver Physiol 2008 (Pancreatitis) : Here, we demonstrate that protein kinase D1 (PKD1) is a key downstream target of PKCdelta and PKCepsilon in pancreatic acinar cells stimulated by two major secretagogues, CCK-8 and the cholinergic agonist carbachol ( CCh ), and that PKD1 is necessary for NF-kappaB activation induced by CCK-8 and CCh ... Either inhibition of PKCdelta or epsilon by isoform-specific inhibitory peptides, genetic deletion of PKCdelta and epsilon in pancreatic acinar cells, or knockdown of PKD1 by using small interfering RNAs in AR42J cells resulted in a marked decrease in PKD1 and NF-kappaB activation stimulated by CCK-8 or CCh. Conversely, overexpression of PKD1 resulted in augmentation of CCK-8- and CCh stimulated NF-kappaB activation
Harikumar et al., Mol Cancer Ther 2010 (Carcinoma, Pancreatic Ductal...) : Using Panc-1 as a model system, we showed that CRT0066101 reduced bromodeoxyuridine incorporation ; increased apoptosis ; blocked neurotensin induced PKD1/2 activation ; reduced neurotensin induced, PKD mediated Hsp27 phosphorylation ; attenuated PKD1 mediated NF-kappaB activation ; and abrogated the expression of NF-kappaB dependent proliferative and prosurvival proteins