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Helicobacter pylori VacA activates the p38/activating transcription factor 2-mediated signal pathway in AZ-521 cells 总被引:3,自引:0,他引:3
Nakayama M Kimura M Wada A Yahiro K Ogushi K Niidome T Fujikawa A Shirasaka D Aoyama N Kurazono H Noda M Moss J Hirayama T 《The Journal of biological chemistry》2004,279(8):7024-7028
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In this study, we examined the signal transduction of dibutyryl cyclic adenosine monophosphate (dBcAMP) to stimulate the release of nitric oxide (NO) and interleukin-6 (IL-6) from J774 macrophages. These actions of dBcAMP were diminished by the presence of the inhibitors of protein kinase A (PKA), protein kinase C (PKC), p38 MAPK and nuclear factor-kappa B (NF-kappaB). In contrast, Go 6976 and PD98059 had no significant effects. Consistently, dBcAMP caused membrane translocation of PKCbetaII, delta, mu, lambda and zeta isoforms, and increased atypical protein kinase C (aPKC) and p38 MAPK activities. The nuclear translocation and DNA-binding study revealed that dBcAMP stimulated NF-kappaB, activator protein-1 (AP-1), and CAAT/enhancer-binding protein (c/EBPbeta). Via PKA, PKC and p38 MAPK-dependent signals, dBcAMP also induced inhibitory subunit of NF-kappaB (IkappaB) degradation, IkappaB kinase (IKK) activation, nuclear translocation of NF-kappaB subunit p65 and its association with the CREB-binding protein (CBP). These results illustrate that PKA activation in macrophages is able to stimulate PKC and p38 MAPK, which lead to IKK-dependent NF-kappaB activation and contribute to the induction of inducible nitric oxide synthase (iNOS) and IL-6 genes. 相似文献
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Pathak SK Basu S Bhattacharyya A Pathak S Banerjee A Basu J Kundu M 《Journal of immunology (Baltimore, Md. : 1950)》2006,177(11):7950-7958
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Meraro D Gleit-Kielmanowicz M Hauser H Levi BZ 《Journal of immunology (Baltimore, Md. : 1950)》2002,168(12):6224-6231
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van der Stoep N Quinten E van den Elsen PJ 《Journal of immunology (Baltimore, Md. : 1950)》2002,169(9):5061-5071