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- 저자 : HyeonJoo Cheon (검색결과 3 건)
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HyeonJoo Cheon,Young-Seok Woo,Ji Young Lee,Hee Sook Kim,Hyun Jin Kim,Sungwon Cho,Nam Hee Won,Jeongwon Sohn 생화학분자생물학회 2007 Experimental and molecular medicine Vol.39 No.4
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a proto-typic halogenated aromatic hydrocarbon (HAH), is part of its toxic effects appears to be derived from its ability to induce TNF-α production. However, the sig-naling pathway of TCDD that leads to TNF-α ex-pression has not been elucidated. In this study, we in-vestigated the signaling mechanism of TCD-induced TNF-α expression in PMA-differentiated THP-1 macrophages. TCDD induced both mRNA and protein expression of TNF-α in a dose- and time-dependent manner. αreceptor (AhR) inhibitor, prevented the TCDD-induced expression of TNF-α at both mRNA and protein levels. Genistein, a protein tyrosine kinase (PTK) inhibitor, and PD153035, an EGFR inhibitor, also blocked the in-crease of TNF-α expression by TCDD, indicating the role of EGFR in TCDD-induced TNF-α expression. On the other hand, P2, a c-Src specific inhibitor, did not affect TCDD-induced TNF-α expression. EGFR phos-treatment. TCDD-induced EGFR activation was AhR-dependent since co-treatment with α-NF pre-vented it. ERK was found to be a downstream efector of EGFR activation in the signaling pathway leading to TNF-α production after TCDD stimulation. Activation of ERK was observed from 30 min after TCDD treatment. PD98059, an inhibitor of the MEK-ERK path-way, completely prevented the TNF-α mRNA and pro-tein expression induced by TCDD, whereas inhibitors EGFR inhibitor, as well as α-NF significantly reduced ERK phosphorylation, suggesting that ERK activation by TCDD was mediated by both EGFR and AhR. These results indicate that TNF-α production by TCDD in dif-ferentiated THP-1 macrophages is AhR-dependent and involves activation of EGFR and ERK, but not c-Src, JNK, nor p38 MAPK. A signaling pathway is pro-posed where TCDD induces sequential activation of AhR, EGFR and ERK, leading to the increased ex-pression of TNF-α.
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Prostaglandin E2 augments IL-10 signaling and function.
Cheon, Hyeonjoo,Rho, Young Hee,Choi, Seong Jae,Lee, Young Ho,Song, Gwan Gyu,Sohn, Jeongwon,Won, Nam Hee,Ji, Jong Dae Williams Wilkins 2006 JOURNAL OF IMMUNOLOGY Vol.177 No.2
<P>In inflamed joints of rheumatoid arthritis, PGE(2) is highly expressed, and IL-10 and IL-6 are also abundant. PGE(2) is a well-known activator of the cAMP signaling pathway, and there is functional cross-talk between cAMP signaling and the Jak-STAT signaling pathway. In this study, we evaluated the modulating effect of PGE(2) on STAT signaling and its biological function induced by IL-10 and IL-6, and elucidated its mechanism in THP-1 cells. STAT phosphorylation was determined by Western blot, and gene expression was analyzed using real-time PCR. Pretreatment with PGE(2) significantly augmented IL-10-induced STAT3 and STAT1 phosphorylation, as well as suppressors of cytokine signaling 3 (SOCS3) and IL-1R antagonist gene expression. In contrast, PGE(2) suppressed IL-6-induced phosphorylation of STAT3 and STAT1. These PGE(2)-induced modulating effects were largely reversed by actinomycin D. Pretreatment with dibutyryl cAMP augmented IL-10-induced, but did not change IL-6-induced STAT3 phosphorylation. Misoprostol, an EP2/3/4 agonist, and butaprost, an EP2 agonist, augmented IL-10-induced STAT3 phosphorylation and SOCS3 gene expression, but sulprostone, an EP1/3 agonist, had no effect. H89, a protein kinase A inhibitor, and LY294002, a PI3K inhibitor, diminished PGE(2)-mediated augmentation of IL-10-induced STAT3 phosphorylation. In this study, we found that PGE(2) selectively regulates cytokine signaling via increased intracellular cAMP levels and de novo gene expression, and these modulating effects may be mediated through EP2 or EP4 receptors. PGE(2) may modulate immune responses by alteration of cytokine signaling in THP-1 cells.</P>
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Roles of unphosphorylated ISGF3 in HCV infection and interferon responsiveness
Sung, Pil Soo,Cheon, HyeonJoo,Cho, Chung Hwan,Hong, Seon-Hui,Park, Do Youn,Seo, Hyung-Il,Park, Su-Hyung,Yoon, Seung Kew,Stark, George R.,Shin, Eui-Cheol Proceedings of the National Academy of Sciences 2015 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.112 No.33
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