TWO NEW SPECIES OF THE GENUS PHYTOCORIS FALLEN (HE-TEROPTERA: MIRIDAE) FROM CHINA

Abstract In this paper, two new species of the genus Phytocoris Fallen ( Ph. nitrariae sp. nov., Ph. macer sp. nov.) are described from China. Both of these two species belong to the subgenus Sooso-capsus Wagner when Wagner's system (1970) is used.     

In vitro selected peptides bind with thymidylate synthase mRNA and inhibit its translation

Thymidylate synthase (TS), an essential enzyme for catalyzing the biosynthesis of thymidylate, is a critical therapeutic target in cancer therapy. Recent studies have shown that TS functions as an RNA-binding protein by interacting with two different sequences on its own mRNA, thus, repressing translational efficiency. In this study, peptides binding TS RNA with high affinity were isolated using mRNA display from a large peptide library (＞1013 different sequences). The randomized library was subjected up to twelve rounds of in vitro selection and amplification. Comparing the amino acid composition of the selected peptides (12th round, R12) with those from the initial random library (round zero, R0), the basic and aromatic residues in the selected peptides were enriched significantly, suggesting that these peptide regions might be important in the peptide-TS mRNA interaction. Categorizing the amino acids at each random position based on their physicochemical properties and comparing the distributions with those of the initial random pool, an obvious basic charge characteristic was found at positions 1, 12, 17 and 18, suggesting that basic side chains participate in RNA binding. Secondary structure prediction showed that the selected peptides of R12 pool represented a helical propensity compared with R0 pool, and the regions were rich in basic residues. The electrophoretic gel mobility shift and in vitro translation assays showed that the peptides selected using mRNA display could bind TS RNA specifically and inhibit the translation of TS mRNA. Our results suggested that the identified peptides could be used as new TS inhibitors and developed to a novel class of anticancer agents.     

Inhibition of IFN-gamma receptor signaling by hepatitis C virus non-structural protein NS4B]

The function of NS4B is incompletely understood. The aim of the study is to understand the influence of NS4B on anti-viral response. After cell line stably expressing NS4B established, the influence of IFN-alpha of different concentration on VSV was studied using plaque assay; cell expression profiling caused by NS4B was studied using DNA microarray, and the IFNGR1 fluorescence intensity was analyzed. Our data showed that HCV-NS4B could suppress immuno-associated gene expression, in particular, IFN-gamma receptor signal transduction-related genes. Taken together, NS4B could play some roles in HCV resistance to IFN therapy.     

肝癌细胞系差异性表达的糖结合蛋白研究

糖结合蛋白(glycan-binding protein,GBP)在细胞生命周期中扮演着重要角色,如细胞识别、运输、免疫、代谢、增殖分化及细胞间的相互作用等.目前,对GBP的改变对细胞生物过程产生影响的研究甚少.本研究用糖芯片技术对肝癌细胞系Hep G2和正常肝细胞系L02表达的GBP进行研究;糖细胞化学验证确定差异表达GBP在肝癌细胞系中的变化和分布.结果显示,8种糖探针(如SL、LNT和Gal NAc等)和5种糖探针(如Man、Man-9-Glycan,Xyl等)分别对应的GBP在Hep G2细胞中表达上调或下调.糖细胞化学结果显示:Gal NAc识别的GBPs主要表达在Hep G2的胞膜、中央胞质、核周胞质区域,而在L02的相同区域表达减弱;Neu Ac识别的GBPs主要表达在L02的胞膜区及核周胞质区,而在Hep G2细胞的相同区域表达减弱.这些数据为寻找新的肝癌发病机制和抗肿瘤策略提供了有用信息.     

Comparative Effects of Hispidulin,Genistein, and Icariin with Estrogen on Bone Tissue in Ovariectomized Rats

Icariin, Genistein, and Hispidulin have been proven to have estrogen-like and antiosteoporotic activity and can be potentially used for the treatment of osteoporosis. The present study found that Icariin, Genistein, and Hispidulin treatments, emulating estrogen, significantly contributed to bone density. Comparative effects of Icariin, Genistein, and Hispidulin with estrogen on in ovariectomized rats were investigated. Our results showed that genistein was found to have superior bone protective effects against osteoporosis among genistein, Icariin, and Hispidulin.     

水分胁迫对甘薯叶肉细胞光合电子传递的影响

水分胁迫降低了甘薯叶肉细胞的光合能力。在有解偶联剂存在时,水分胁迫对叶肉细胞的光合电子传递没有影响,但在无解偶联剂存在下,水分胁迫促进了甘薯叶肉细胞的光合电子传递,表现出明显的解偶联效应。水分胁迫伤害了甘薯叶绿体偶联因子结构,使ATP合成受阻,叶肉细胞的光合滞后期加长。     

NEDD4 promotes cell growth and motility in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related death worldwide. In China, the situation is even worse as cancer incidence and mortality continue to increase rapidly. Although tremendous progress has been made toward HCC treatments, the benefits for liver cancer patients are still limited. Therefore, it is necessary to identify and develop novel therapeutic methods. Neuronally expressed developmentally downregulated 4 (NEDD4), an E3 ubiquitin ligase, plays a critical role in the development and progression of various types of human cancers. In our study, NEDD4 acts as an oncoprotein in both QGY7703 and SMMC7721 liver cancer cell lines. We found that depletion of NEDD4 by siRNA transfection led to inhibition of cell growth, invasion and migration, and promotion of apoptosis. In contrast, overexpression of NEDD4 via plasmid transfection resulted in facilitated cell proliferation, invasion and migration, and decreased apoptosis. Importantly, we observed that tumor suppressor LATS1, also a core component of Hippo pathway, was negatively regulated by NEDD4 in liver cancer cells. Our findings suggested that NEDD4 may be involved in the HCC progression via regulating LATS1 associated signaling pathway. Therefore, targeting NEDD4-LATS1 signaling could be a potential therapeutic option for HCC treatment.     

The molecular basis of spinocerebellar ataxia type 48 caused by a de novo mutation in the ubiquitin ligase CHIP

The spinocerebellar ataxias (SCAs) are a class of incurable diseases characterized by degeneration of the cerebellum that results in movement disorder. Recently, a new heritable form of SCA, spinocerebellar ataxia type 48 (SCA48), was attributed to dominant mutations in STIP1 homology and U box-containing 1 (STUB1); however, little is known about how these mutations cause SCA48. STUB1 encodes for the protein C terminus of Hsc70 interacting protein (CHIP), an E3 ubiquitin ligase. CHIP is known to regulate proteostasis by recruiting chaperones via a N-terminal tetratricopeptide repeat domain and recruiting E2 ubiquitin-conjugating enzymes via a C-terminal U-box domain. These interactions allow CHIP to mediate the ubiquitination of chaperone-bound, misfolded proteins to promote their degradation via the proteasome. Here we have identified a novel, de novo mutation in STUB1 in a patient with SCA48 encoding for an A52G point mutation in the tetratricopeptide repeat domain of CHIP. Utilizing an array of biophysical, biochemical, and cellular assays, we demonstrate that the CHIP^A52G point mutant retains E3-ligase activity but has decreased affinity for chaperones. We further show that this mutant decreases cellular fitness in response to certain cellular stressors and induces neurodegeneration in a transgenic Caenorhabditis elegans model of SCA48. Together, our data identify the A52G mutant as a cause of SCA48 and provide molecular insight into how mutations in STUB1 cause SCA48.     

Effect of silicon-doped calcium phosphate cement on angiogenesis based on controlled macrophage polarization

Vascularization is an important early indicator of osteogenesis involving biomaterials.Bone repair and new bone formation are associated with extensive neovascu...