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81.
Changchun Cao Xiaoyan Dong Xiaobing Wu Boyun Wen Gang Ji Lingpeng Cheng Hongrong Liu 《Journal of virology》2012,86(22):12322-12329
Adenovirus (Ad) cell attachment is initiated by the attachment of the fiber protein to a primary receptor (usually CAR or CD46). This event is followed by the engagement of the penton base protein with a secondary receptor (integrin) via its loop region, which contains an Arg-Gly-Asp (RGD) motif, to trigger virus internalization. To understand the well-orchestrated adenovirus cell attachment process that involves the fiber and the penton base, we reconstructed the structure of an Ad5F35 capsid, comprising an adenovirus type 5 (Ad5) capsid pseudotyped with an Ad35 fiber, at a resolution of approximately 4.2 Å. The fiber-penton base interaction in the cryo-electron microscopic (cryo-EM) structure of Ad5F35 is similar to that in the cryo-EM structure of Ad5, indicating that the fiber-penton base interaction of adenovirus is conserved. Our structure also confirms that the C-terminal segment of the fiber tail domain constitutes the bottom trunk of the fiber shaft. Based on the conserved fiber-penton base interaction, we have proposed a model for the interaction of Ad5F35 with its primary and secondary receptors. This model could provide insight for designing adenovirus gene delivery vectors. 相似文献
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83.
小麦TaMlo基因的原核表达、抗体制备及细胞化学分析(简报) 总被引:1,自引:0,他引:1
白粉病菌(Blumeria graminis)是一类高度专化性的寄生真菌,可侵染650多种单子叶植物和 9000多种双子叶植物,能够引起多种麦类作物的白粉病,给农业生产带来巨大的损失。由于白粉病菌生理小种多、变异快,所以利用专化性抗病基因难以解决植物的持久抗病性问题。人们在研究大麦白粉病时.发现大麦Mlo基因的隐性突变可导致大麦对绝大多数白粉病菌生理小种的高效持久的广谱抗病性。Schulze-Lefert等多家实验室合作于1997年成功克隆了野生的 Mlo基因。进一步研究表明.该基因编码一种植物特有的具有7个跨膜区和羧基端长尾的膜蛋白(Mlo),它可能对植物细胞的坏死起负调控作用。但Mlo基因如何表达及其在白粉病菌发育中的作用机制尚不清楚。 相似文献
84.
Zhu XM Yao FH Yao YM Dong N Yu Y Sheng ZY 《The international journal of biochemistry & cell biology》2012,44(7):1097-1105
High mobility group box-1 protein (HMGB1) had been proved to induce maturation and activation of dendritic cell (DC), however, the endogenous changes and mechanisms underlying are unknown. Since endoplasmic reticulum stress (ERS) activates an adaptive unfolded protein response (UPR) that facilitates cellular survival and repair, we hypothesized that HMGB1 may regulate the function of DC by modulating ERS. In our study, HMGB1 stimulation induced significant ERS responses in DCs in a time- and dose-dependent manner, demonstrated by the up-regulation of a number of ERS markers. Gene silence of XBP-1 in splenic DCs decreased the levels of CD80, CD86 as well as major histocompatibility complex (MHC)-II expression and cytokine secretion after HMGB1 treatment, when compared with untransfected or nontargeting-transfected DCs (all P<0.05). Moreover, XBP-1 silenced DCs after treatment with HMGB1 failed to stimulate notable proliferation and differentiation of T cells, unlike normal DCs or nontargeting-transfected DCs (all P<0.05). Gene silence of XBP-1 resulted in down-regulation of the receptor for advanced glycation end products (RAGE) expression on the surface of splenic DCs induced by HMGB1 stimulation (P<0.05). These findings demonstrate an important role for ERS and its regulator XBP-1 in HMGB1-induced maturation and activation of DCs. 相似文献
85.
Huo Y Guo X Li H Xu H Halim V Zhang W Wang H Fan YY Ong KT Woo SL Chapkin RS Mashek DG Chen Y Dong H Lu F Wei L Wu C 《The Journal of biological chemistry》2012,287(25):21492-21500
Increasing evidence demonstrates the dissociation of fat deposition, the inflammatory response, and insulin resistance in the development of obesity-related metabolic diseases. As a regulatory enzyme of glycolysis, inducible 6-phosphofructo-2-kinase (iPFK2, encoded by PFKFB3) protects against diet-induced adipose tissue inflammatory response and systemic insulin resistance independently of adiposity. Using aP2-PFKFB3 transgenic (Tg) mice, we explored the ability of targeted adipocyte PFKFB3/iPFK2 overexpression to modulate diet-induced inflammatory responses and insulin resistance arising from fat deposition in both adipose and liver tissues. Compared with wild-type littermates (controls) on a high fat diet (HFD), Tg mice exhibited increased adiposity, decreased adipose inflammatory response, and improved insulin sensitivity. In a parallel pattern, HFD-fed Tg mice showed increased hepatic steatosis, decreased liver inflammatory response, and improved liver insulin sensitivity compared with controls. In both adipose and liver tissues, increased fat deposition was associated with lipid profile alterations characterized by an increase in palmitoleate. Additionally, plasma lipid profiles also displayed an increase in palmitoleate in HFD-Tg mice compared with controls. In cultured 3T3-L1 adipocytes, overexpression of PFKFB3/iPFK2 recapitulated metabolic and inflammatory changes observed in adipose tissue of Tg mice. Upon treatment with conditioned medium from iPFK2-overexpressing adipocytes, mouse primary hepatocytes displayed metabolic and inflammatory responses that were similar to those observed in livers of Tg mice. Together, these data demonstrate a unique role for PFKFB3/iPFK2 in adipocytes with regard to diet-induced inflammatory responses in both adipose and liver tissues. 相似文献
86.
Min Ki Jee Ji Hoon Kim Yong Man Han Sung Jun Jung Kyung Sun Kang Dong Wook Kim Soo Kyung Kang 《PloS one》2010,5(2)
Background and Methods
In this study, we utilized a combination of low oxygen tension and a novel anti-oxidant, 4-(3,4-dihydroxy-phenyl)-derivative (DHP-d) to directly induce adipose tissue stromal cells (ATSC) to de-differentiate into more primitive stem cells. De-differentiated ATSCs was overexpress stemness genes, Rex-1, Oct-4, Sox-2, and Nanog. Additionally, demethylation of the regulatory regions of Rex-1, stemnesses, and HIF1α and scavenging of reactive oxygen species were finally resulted in an improved stem cell behavior of de-differentiate ATSC (de-ATSC). Proliferation activity of ATSCs after dedifferentiation was induced by REX1, Oct4, and JAK/STAT3 directly or indirectly. De-ATSCs showed increased migration activity that mediated by P38/JUNK and ERK phosphorylation. Moreover, regenerative efficacy of de-ATSC engrafted spinal cord-injured rats and chemical-induced diabetes animals were significantly restored their functions.Conclusions/Significance
Our stem cell remodeling system may provide a good model which would provide insight into the molecular mechanisms underlying ATSC proliferation and transdifferentiation. Also, these multipotent stem cells can be harvested may provide us with a valuable reservoir of primitive and autologous stem cells for use in a broad spectrum of regenerative cell-based disease therapy. 相似文献87.
88.
89.
90.
Despite the importance of stem cells in plant and animal development, the common mechanisms of stem cell maintenance in both systems have remained elusive. Recently, the importance of hydrogen peroxide (H2O2) signaling in priming stem cell differentiation has been extensively studied in animals. Here, we show that different forms of reactive oxygen species (ROS) have antagonistic roles in plant stem cell regulation, which were established by distinct spatiotemporal patterns of ROS‐metabolizing enzymes. The superoxide anion () is markedly enriched in stem cells to activate WUSCHEL and maintain stemness, whereas H2O2 is more abundant in the differentiating peripheral zone to promote stem cell differentiation. Moreover, H2O2 negatively regulates biosynthesis in stem cells, and increasing H2O2 levels or scavenging leads to the termination of stem cells. Our results provide a mechanistic framework for ROS‐mediated control of plant stem cell fate and demonstrate that the balance between and H2O2 is key to stem cell maintenance and differentiation. 相似文献