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| 1 | Different contributions of STAT3, ERK1/2, and PI3-K signaling to cardiomyocyte hypertrophy by cardiotrophin-1显示文摘AIM: To assess the contribution of signal transducer and activator of transcription 3(JAK-STAT3) pathway, extracellular signal-regulated kinases1/2 (ERK1/2) pathway, and phosphatidylinositol 3-kinase (PI3-K) pathway to cardiomyocytes hypertrophy induced by cardiotrophin-1 (CT-1), a new member of interleukin-6 (IL-6) family of cytokines. METHODS: STAT3, ERK1/2, and PI3-K were assessed by Western blot analysis. Activity of ERK1/2 was also confirmed by in-gel kinase assay. Hypertrophy of cardiomyocyte was evaluated by [^3H]leucine incorporation and cellular protein-to-DNA ratio. RESULTS: CT-1 simultaneously activated phosphorylation of STAT3, ERK1/2, and PI3-K in rat cardiomyocytes. Parthenolide, an inhibitor of STAT, suppressed CT-1-induced [^3H]leucine incorporation by 88.3% and protein-to-DNA ratio by 75.0%. U0126, an MEK1/2 inhibitor, increased CT-1-induced the phosphorylation of STAT3 in a dose-dependent manner and, consistently, augmented CT-1-induced increase in [^3H]leucine incorporation and cellular protein-to-DNA ratio by 17.6% and 16.3%, respectively. Wortmannin, a PI3-K inhibitor, did not influence CT-1-induced [^3H]leucine incorporation and cellular protein-to-DNA ratio. CONCLUSION: The hypertrophic effect of CT-1 was essentially mediated by STAT3, independent of PI3-K, and negatively regulated by ERK1/2 via inhibiting the phosphorylation of STAT3. The interaction between STAT3 and ERK1/2 in CT-1-induced signaling contributes to development of cardiac hypertrophy. | Ze-junTIAN WeiCUI Yong-junLI Yu-mingHAO JunDU FanLIU HuiZHANG Xiu-guangZU Su-yunLIU LiCHEN WeiAN | 2004 | Acta Pharmacologica Sinica2004，25，9： | 16 |
| 2 | Loss of C-terminal α-helix decreased SDF-1α-mediated signaling and chemotaxis without influencing CXCR4 internalization显示文摘AIM: To investigate the possibility that a novel α-helix-defective mutant of stromal cell-derived factor-1α (SDF- 1α) (SDF-1/54R) acts as an antagonist of CXC chemokine receptor 4 (CXCR4). METHODS: According to the genetic sequence of natural SDF-1α, a recombinant α-helix-defective mutant of SDF-1α was designed and some biologic characteristics of this mutant were demonstrated. The migration of Jurkat cells was assessed with chemo- tactic assay. ERK phosphorylation was analyzed by Western blot with a specific anti-phospho-ERK1/2 antibody. Intracellular calcium influx was examined by flow cytometer with a calcium indicator dye Fluo-3AM. The CXCR4 on the cell surface was detected by flow cytometer with a PE conjoined anti-human CXCR4 antibody. RESULTS: Compared with native SDF-1α, SDF-1/54R displayed apparent decrease in chemotactic ability, ERK1/2 activation, and intracellular calcium influx in Jurkat cells. However, the binding to CXCR4 and inducing CXCR4 internalization of SDF-1/54R did not change outstandingly. Moreover, a competitive inhibitory effect of SDF-1/54R on the migration of Jurkat cells induced by native SDF-1α was confirmed. CONCLUSION: α-helix-defective mutant of SDF-1α, SDF-1/54R that remained both the N-terminus and the central β-sheet region, decreased SDF-1α-medi- ated signaling and chemotaxis but did not influence CXCR4 internalization, which suggested that SDF-1/54R might be developed as an anti-CHIV inhibitor with high biological potency and low side-effect. | Shao-huiCAI YiTAN Xian-daREN Xiao-hongLI Shao-xiCAI JunDU | 2004 | Acta Pharmacologica Sinica2004，25，2： | 12 |
| 3 | Binding activity of H-Ras is necessary for in vivo inhibition of ASK1 activity显示文摘H-Ras is well known as one of the essential components of Ras/Raf/MEK/ERK cascade, which is a critical prosurvival signaling mechanism in most eukaryotic cells. Ras targets Raf/MEK/ERK cascade by integrating and transmitting extracellular signals from growth factor receptors to Raf, leading to the propagation of signals to modulate a serious of cellular survival events. Apoptosis signal-regulating kinasel (ASK1) serves as a general mediator of cell death because it is responsive to a variety of death signals. In this study, we found that H-Ras interacted with ASK1 to cause the inhibition of both ASK1 activity and ASK1-induced apoptosis in vivo, which was reversed only partially by addition of RafS621A, an antagonist of Raf, whereas MEK inhibitor, PD98059, and PI3K inhibitor, LY294002, did not disturb the inhibitory effect of H-Ras on ASK-1-induced apoptosis. Furthermore, by means of immunoprecipitate and kinase assays, we demonstrated that the interaction between H-Ras and ASK1 as well as the inhibition of ASK1 activity were dependent on the binding activity of H-Ras. These results suggest that a novel mechanism may be involved in H-Rasmediated cell survival in addition to the well established MEK/ERK and PI3K/Akt kinase-dependent enhancement of cell survival. | JunDU ShaoHuiCAI ZheSHI FumihikoNAGASE | 2004 | Cell Research2004，14，2： | 3 |
| 4 | STUDY ON THE SURFACE MODIFICATION OF NANO-TiO_2 BY GRAFTING PMMA/PBMA AND ITS THERMAL STABILITY显示文摘The surface of nano-TiO2 was encapsulated with hydroxyl-propyl-methyl cellulose (HPMC), and then cografted with acrylates. Conditions of absorbing and grafting have been studied. Modified nano-TiO2 particles were characterized by FT-IR spectra, TEM and TG analysis. It was convinced from FT-IR studies that both methyl methacrylate (MMA) and butylmethacrylate (BMA) were co-grafted onto the surface of nano-TiO2 particles. TEM images show that the surface of nanoTiO2 particles was successfully modified by a thick layer of film-like polymer. TG results demonstrate that the decomposition temperature of HPMC-g-PMMA/PBMA, which has been grafted onto the surface of nano-TiO2, is 56.9 K higher than that of HPMC-g-PMMA/PBMA. | 宇海银 Jia-shanGu JunDu Ming-yunGuan | 2005 | Chinese Journal of Polymer Science2005，23，3： | 3 |
| 5 | Zebrafish tiggy-winkle hedgehog promoter directs notochord and floor plate green fluorescence protein expression in transgenic zebrafish embryos显示文摘 | Mary Dienhart | 2001 | Developmental Dynamics2001，222，： | 1 |
| 6 | Actin phosphorylation correlates with actin sequestration in ATP-depleted rabbit renal proximal tubules显示文摘Objective: To demonstrate the relation sh ip between actin phosphorylation and actin sequestration in ATP-depleted rabbi t renal proximal tubules. Methods: Using two-dimensional electr ophoreses and Western blotting to analyze the phosphorylation state of the seque stered actin in rabbit renal proximal tubules. Results: The anal ytical result of the sequestered actin indicated that nearly half of the actin w as phosphorylated on serine residue(s). Conclusion: Result sugge sted a close correlation between actin sequestration and actin phosphorylation i n ATP-depleted rabbit renal proximal tubules. | YingchunLi~ YingbinGe JunDu RongZhou JinChen LuoGu | 2005 | Journal of Nanjing Medical University2005，19，2： | 1 |
| 7 | Red Capitalists: Political Connections and Firm Performance in China显示文摘 | JunDu SourafelGirma | 2010 | Kyklos2010，，4： | 1 |
| 8 | Invulnerabilityofscale-freenetworkagainstcriticalnodefailuresbasedonarenewedcascadingfailuremodel显示文摘 | XingzhaoPeng HongYao JunDu etal | 2015 | Statistical MechanicsandIts Applications2015，421，3： | 1 |
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