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您的检索式：作者名="Sidong Cai"
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| 1 | Differential impairment of regulatory T cells rather than effector T cells by paclitaxel-based chemotherapy显示文摘 | Lei Zhang Kamtai Dermawan Meilin Jin Rongjun Liu Huiru Zheng Lin Xu Yi Zhang Yuchan Cai Yiwei Chu Sidong Xiong | 2008 | Clinical Immunology2008，，： | 1 |
| 2 | The poly(ADP-ribosyl)ation of BRD4 mediated by PARP1 promoted pathological cardiac hypertrophy显示文摘The bromodomain and extraterminal(BET)family member BRD4 is pivotal in the pathogenesis of cardiac hypertrophy.BRD4 induces hypertrophic gene expression by binding to the acetylated chromatin,facilitating the phosphorylation of RNA polymerases II(Pol II)and leading to transcription elongation.The present study identified a novel post-translational modification of BRD4:poly(ADPribosyl)ation(PARylation),that was mediated by poly(ADP-ribose)polymerase-1(PARP1)in cardiac hypertrophy.BRD4 silencing or BET inhibitors JQ1 and MS417 prevented cardiac hypertrophic responses induced by isoproterenol(ISO),whereas overexpression of BRD4 promoted cardiac hypertrophy,confirming the critical role of BRD4 in pathological cardiac hypertrophy.PARP1 was activated in ISOinduced cardiac hypertrophy and facilitated the development of cardiac hypertrophy.BRD4 was involved in the prohypertrophic effect of PARP1,as implied by the observations that BRD4 inhibition or silencing reversed PARP1-induced hypertrophic responses,and that BRD4 overexpression suppressed the antihypertrophic effect of PARP1 inhibitors.Interactions of BRD4 and PARP1 were observed by coimmunoprecipitation and immunofluorescence.PARylation of BRD4 induced by PARP1 was investigated by PARylation assays.In response to hypertrophic stimuli like ISO,PARylation level of BRD4 was elevated,along with enhanced interactions between BRD4 and PARP1.By investigating the PARylation of truncation mutants of BRD4,the C-terminal domain(CTD)was identified as the PARylation modification sites of BRD4.PARylation of BRD4 facilitated its binding to the transcription start sites(TSS)of hypertrophic genes,resulting in enhanced phosphorylation of RNA Pol II and transcription activation of hypertrophic genes.The present findings suggest that strategies targeting inhibition of PARP1-BRD4 might have therapeutic potential for pathological cardiac hypertrophy. | Zhenzhen Li Zhen Guo Rui Lan Sidong Cai Zhirong Lin Jingyan Li Junjian Wang Zhuoming Li Peiqing Liu | 2021 | Acta Pharmaceutica Sinica B2021，11，5： | 0 |
| 3 | C-reactive protein functions as a negative regulator of macrophage activation induced by apoptotic DNA显示文摘C-reactive protein(CRP),an acute-phase protein with an ability to bind to nuclear antigen,has been reported to regulate cytokine secretion and modulate immune responses.We previously reported that activated syngeneic lymphocyte-derived apoptotic DNA(apopDNA)could induce macrophage activation and contribute to the initiation and progression of lupus nephritis.It is reasonable to hypothesize that CRP might regulate apopDNA-induced macrophage activation.Herein,CRP was shown to promote macrophage-mediated apopDNA uptake by binding to apopDNA(CRP/apopDNA complex).Notably,CRP/apopDNA treatment inhibited the production of inflammatory cytokines and chemokines by macrophages which could be induced by apopDNA alone.Further coculture and transwell studies revealed that CRP/apopDNA-induced macrophages prohibited apopDNA-induced macrophage activation in an IL-10 dependent manner.These results provide insight into the potential mechanism of CRP regulatory activity in macrophage activation induced by apopDNA in the context of lupus nephritis and other autoimmune diseases. | Weijuan Zhang Yanxing Cai Wei Xu Sidong Xiong | 2011 | Protein & Cell2011，2，8： | 0 |
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