The Role of Protein Kinase D1 in HIV-1 Replication

PKD家族由PKD1，PKD2h和PKD3组成，通常主要分布在胞浆，但在刺激条件下，可转位到各亚细胞结构。这些激酶在生理和病理过程中，具有广泛而重要的作用。包括线粒体氧化应激，T细胞受体信号，心肌基因表达和心肌收缩，细胞凋亡和肿瘤发生等。它们的功能还涉及许多细胞生物学过程，例如高尔基体组织，蛋白运输，高尔基体囊泡分泌以及其他各种细胞信号途径等。 本研究中，我们发现，Hela细胞虽然不表达内源性PKD1，但却能异位表达外源导入的PKD1，并且可以刺激HIV-LTR荧光虫酶报告基因的蛋白表达。然而对HIV-LTR启动子进行各种删除突变，并不能抑制PKD1所刺激的HIV-LTR荧光虫酶报告基因的蛋...The Protein kinase D (PKD) enzymes, which comprise of three isoforms (PKD1/PKDμ, PKD2 and PKD3/PKDυ), are generally localized to the cytosol, but in stimulated cells, they are translocated to various subcellular compartments. These enzymes play numerous roles in a variety of normal and pathological processes including transcriptional response to mitochondrial oxidative stress, T-cell receptor sign...学位：工学硕士院系专业：生命科学学院生物学系_生物化学与分子生物学学号：2172007115410

CHARACTERIZATION OF FACTORS INVOLVED IN HOST-VIRAL INTERACTIONS AND HOW THEY CONTRIBUTE TO HEPATITIS C VIRUS-INDUCED CELL DEATH

Ph.DDOCTOR OF PHILOSOPH

Modulation of programmed cell death pathways by the hepatitis C virus

10.2741/3709Frontiers in Bioscience162608-1

The p7 protein of the hepatitis C virus induces cell death differently from the influenza A virus viroporin M2

10.1016/j.virusres.2012.12.005Virus Research 1721-224-3

The mechanisms and factors that induce trained immunity in arthropods and mollusks

Besides dividing the organism’s immune system into adaptive and innate immunity, it has long been thought that only adaptive immunity can establish immune memory. However, many studies have shown that innate immunity can also build immunological memory through epigenetic reprogramming and modifications to resist pathogens’ reinfection, known as trained immunity. This paper reviews the role of mitochondrial metabolism and epigenetic modifications and describes the molecular foundation in the trained immunity of arthropods and mollusks. Mitochondrial metabolism and epigenetic modifications complement each other and play a key role in trained immunity

Antibacterial Activity and Mechanism of Peptide PV-Q5 against <i>Vibrio parahaemolyticus</i> and <i>Escherichia coli</i>, Derived from Salt-Fermented <i>Penaeus vannamei</i>

The increasing threat posed by antibiotic-resistant pathogens has prompted a shift to the use of naturally-derived antimicrobial peptides (AMPs) in place of chemical preservatives in controlling foodborne pathogens. In this study, ten peptides were identified from salt-fermented shrimps (Penaeus vannamei) using ultra-performance liquid chromatography-mass spectrometry. One of the peptides, designated PV-Q5 (QVRNFPRGSAASPSALASPR), with most features of an AMP, was further explored and found to possess strong antibacterial activity against Vibrio parahaemolyticus and Escherichia coli, with a minimum inhibitory concentration of 31.25 μg/mL. Moreover, PV-Q5 increased bacterial cell membrane permeability and ruptured bacteria cell membranes, as revealed by transmission electron microscopy. Circular dichroism analysis showed that the conformation of PV-Q5 was a random coil in phosphate-buffered saline and α-helical in sodium dodecyl sulfate, which is conducive for interaction with bacteria cell membranes. These findings indicated that PV-Q5 could find potential use in food preservation to control foodborne pathogenic bacteria

Litopenaeus vannamei hemocyanin exhibits antitumor activity in S180 mouse model in vivo.

Hemocyanin is a multifunctional glycoprotein, which also plays multiple roles in immune defense. While it has been demonstrated that hemocyanin from some mollusks can induce potent immune response and is therefore undergoing clinical trials to be used in anti-tumor immunotherapy, little is currently known about how hemocyanin from arthropods affect tumors. In this study we investigated the anti-tumor activity of hemocyanin from Litopenaeus vannamei on Sarcoma-180 (S180) tumor-bearing mice model. Eight days treatment with 4mg/kg bodyweight of hemocyanin significantly inhibited the growth of S180 up to 49% as compared to untreated. Similarly, histopathology analysis showed a significant decrease in tumor cell number and density in the tissues of treated mice. Moreover, there was a significant increase in immune organs index, lymphocyte proliferation, NK cell cytotoxic activity and serum TNF-α level, suggesting that hemocyanin could improve the immunity of the S180 tumor-bearing mice. Additionally, there was a significant increase in superoxide dismutase (SOD) activity and a decrease in the level of malondialdehyde (MDA) in serum and liver, which further suggest that hemocyanin improved the anti-oxidant ability of the S180 tumor-bearing mice. Collectively, our data demonstrated that L. vannamei hemocyanin had a significant antitumor activity in mice

Acute Hepatopancreatic Necrosis Disease (AHPND) related microRNAs in Litopenaeus vannamei infected with AHPND-causing strain of Vibrio parahemolyticus

Abstract Background Acute hepatopancreatic necrosis disease (AHPND) has emerged as a major debilitating disease that causes massive shrimp death resulting in substantial economic losses in shrimp aquaculture. Given that several diseases and infections have been associated with microRNAs (miRNAs), we conducted a comparative transcriptomic analysis using the AHPND (VA) and non-AHPND (VN) strains of Vibrio parahemolyticus to identify miRNAs potentially involved in AHPND pathogenesis in Litopenaeus vannamei. Results A total of 83 miRNAs (47 upregulated and 36 downregulated) were significantly differentially expressed between the VA and VN challenged groups, while 222 target genes of these miRNAs were predicted. Functional enrichment analysis revealed that the miRNAs target genes were involved in multiple biological processes including metabolic pathways, amoebiasis, Vibrio cholerae infection etc. Finally, interaction network and qPCR (Real-time Quantitative PCR) analysis of 12 potential key AHPND-related miRNAs and their predicted target genes, revealed their possible involvement in modulating several immune-related processes in the pathogenesis of AHPND. Conclusions We have shown using comparative transcriptomic analysis, miRNAs and their target genes that are responsive to AHPND V. parahemolyticus infection in shrimp, therefore suggesting their possible role in defense response to AHPND V. parahemolyticus infection

A <i>Litopenaeus vannamei</i> Hemocyanin-Derived Antimicrobial Peptide (Peptide B11) Attenuates Cancer Cells’ Proliferation

Antimicrobial peptides play important roles in the immune response to pathogens and tumor cells; for this reason, they are being exploited for therapeutic use. In this study, we describe a Litopenaeus vannamei hemocyanin-derived peptide, denoted B11, which shares similar features with other anticancer peptides and attenuates the proliferation of cancer cells. Cell viability assay revealed that B11 significantly inhibited the proliferation of human cervical (HeLa), human hepatocellular carcinoma (HepG2), and human esophageal cancer (EC109) cancer cell lines, but not normal liver cell lines (T-antigen-immortalized human liver epithelial (THLE) cells or THLE-3), by inducing morphological changes, nuclear condensation, and margination, features which are indicative of apoptosis. Besides, peptide B11-induced apoptosis was confirmed by isothiocyanate-labeled Annexin V/propidium iodide (Annexin V-FITC/PI) double staining of HeLa cells. Moreover, cell uptake studies, confocal microscopy, and Western blot analysis revealed that rhodamine-labeled B11 permeated HeLa cells and localized to the mitochondria, causing mitochondria dysfunction through lost mitochondrial membrane potential, which consequently triggered the induction of apoptosis. Increased expression levels of caspase-9, caspase-3, and Bax (Bcl-2-associated X) proteins, coupled with a decrease in Bcl-2 (B-cell lymphoma 2) protein, confirmed that peptide B11 induced apoptosis via the mitochondrial pathway. Thus, the hemocyanin-derived peptide, B11, inhibits the proliferation of cancer cells by causing mitochondrial dysfunction and inducing apoptotic cell death, for which reason it could be explored as an anticancer peptide

NS5B induces up-regulation of the BH3-only protein, BIK, essential for the Hepatitis C virus RNA replication and viral release

10.1016/j.virol.2014.10.027Virology47441-5