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51.
(Phi)L7 is a lytic phage infecting the gram-negative Xanthomonas campestis pv. campestris, a plant pathogen. To study phage-host interaction, a (phi)L7-resistant mutant was isolated from strain Xc17 by mini-Tn5 transposition and designated CH7LR. CH7LR could not plate (phi)L7 in double-layered assay and formed turbid clearing zones when the cell lawn was dropped with a high titer of (phi)L7. Sequence analysis showed that the mutated gene is xanA coding for phosphoglucomutase/phosphomannomutase, required for the synthesis of lipopolysaccharide and exopolysaccharide (xanthan). The involvement of xanA was confirmed by isolating another mutant with interrupted xanA and complementing with the cloned wild-type gene. Nonmucoid mutants are still sensitive to (phi)L7, indicating that xanthan is not involved in (phi)L7 adsorption. Since the mutants still exhibited low efficiencies of phage adsorption, we predict, by analogy with the cases in other bacteriophages of gram-negative bacteria, that other outer membrane components such as a protein are required for the formation of a complex receptor. 相似文献
52.
Threadfin breams and relatives of the family Nemipteridae comprise 69 currently recognized species in five genera. They are found in the tropical and subtropical Indo‐West Pacific and most are commercially important. Using recently developed molecule‐based approaches exploiting DNA sequence variation among species/specimens, this study reconstructed a comprehensive phylogeny of the Nemipteridae, examined the validity of species and explored the cryptic diversity of the family, and tested previous phylogenetic hypotheses. A combined data set (105 taxa from 41 morphospecies) with newly determined sequences from two nuclear genes (RAG1 and RH) and one mitochondrial gene (COI), and a data set with only COI gene sequences (329 newly obtained plus 328 from public databases from a total of 53 morphospecies) were used in the phylogenetic analysis. The latter was further used for species delimitation analyses with two different tools to explore species diversity. Our phylogenetic results showed that all the currently recognized genera were monophyletic. The monotypic genus Scaevius is the sister group of Pentapodus and they together are sister to Nemipterus. These three genera combined to form the sister group of the clade comprising Parascolopsis and Scolopsis. The validity of most of the examined species was confirmed except in some cases. The combined evidence from the results of different analyses revealed a gap in our existing knowledge of species diversity in the Nemipteridae. We found several currently recognized species contain multiple separately evolving metapopulation lineages within species; some lineages should be considered as new species for further assignment. Finally, some problematic sequences deposited in public databases (probably due to misidentification) were also revised in this study to improve the accuracy for prospective DNA barcoding work on nemipterid fishes. 相似文献
53.
Jing‐Yuan Chuang Wei‐Hung Yang Hsien‐Te Chen Chun‐Yin Huang Tzu‐Wei Tan Yuh‐Tzy Lin Chin‐Jung Hsu Yi‐Chin Fong Chih‐Hsin Tang 《Journal of cellular physiology》2009,220(2):418-426
CCL5 (previously called RANTES) is in the CC‐chemokine family and plays a crucial role in the migration and metastasis of human cancer cells. On the other hand, the effect of CCL5 is mediated via CCR receptor. RT‐PCR and flow cytometry studies demonstrated CCR5 but not CCR1 and CCR3 mRNA in oral cancer cell lines, especially higher in those with high invasiveness (SCC4) as compared with lower levels in HSC3 cells and SCC9 cells. Stimulation of oral cancer cells with CCL5 directly increased the migration and metalloproteinase‐9 (MMP‐9) production. MMP‐9 small interfering RNA inhibited the CCL5‐induced MMP‐9 expression and thereby significantly inhibited the CCL5‐induced cell migration. Activations of phospholipase C (PLC), protein kinase Cδ (PKCδ), and NF‐κB pathways after CCL5 treatment was demonstrated, and CCL5‐induced expression of MMP‐9 and migration activity was inhibited by the specific inhibitor of PLC, PKCδ, and NF‐κB cascades. In addition, migration‐prone sublines demonstrate that cells with increasing migration ability had more expression of MMP‐9, CCL5, and CCR5. Taken together, these results indicate that CCL5/CCR5 axis enhanced migration of oral cancer cells through the increase of MMP‐9 production. J. Cell. Physiol. 220: 418–426, 2009. © 2009 Wiley‐Liss, Inc. 相似文献
54.
Michele I. Van Dyke Hung Lee Ph.D. Jack T. Trevors Ph.D. 《Journal of industrial microbiology & biotechnology》1989,4(4):299-306
Summary The toxicity of germanium dioxide (GeO2) to 21 bacterial and 13 yeast strains was investigated in liquid broth medium to obtain information on strains tolerant to high (1 to 2 mg/ml) GeO2 concentrations.Arthrobacter sp. NRC 32005,enterobacter aerogenes NRC 2926,Klebsiella aerogenes NCTC 418 andPseudomonas putida NRC 5019 were tolerant to 1 mg/ml GeO2.Bacillus sp. RC607 was able to grow in the presence of 2 mg/ml GeO2 at pH 10 in broth culture. The yeastsCandida guilliermondii, Candida shehatae andPachysolen tannophilus were the most sensitive to GeO2 as evidenced by their diminished growth rates at a GeO2 concentration as low as 0.1 mg/ml. None of the yeast strains tested exhibited growth in the presence of 1 mg/ml GeO2. The high pH of the medium containing germanium may be partially responsible for the growth inhibition of the yeast cultures. Select bacterial cultures previously exposed to 1 mg/ml GeO2 could tolerate and grow better at 2 mg/ml GeO2, suggesting the existence of very efficient adaptive mechanisms. The pH of the medium could modulate GeO2 tolerance and this effect was found to be strain-dependent. 相似文献
55.
Tsai JJ Liu SH Yin SC Yang CN Hsu HS Chen WB Liao EC Lee WJ Pan HC Sheu ML 《PloS one》2011,6(9):e23249
Background
Allergic disease can be characterized as manifestations of an exaggerated inflammatory response to environmental allergens triggers. Mite allergen Der-p2 is one of the major allergens of the house dust mite, which contributes to TLR4 expression and function in B cells in allergic patients. However, the precise mechanisms of Der-p2 on B cells remain obscure.Methodology/Principal Findings
We investigated the effects of Der-p2 on proinflammatory cytokines responses and Toll-like receptor-4 (TLR4)-related signaling in human B cells activation. We demonstrated that Der-p2 activates pro-inflammatory cytokines, TLR4 and its co-receptor MD2. ERK inhibitor PD98059 significantly enhanced TLR4/MD2 expression in Der-p2-treated B cells. Der-p2 markedly activated mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) and decreased p38 phosphorylation in B cells. MKP-1-siRNA downregulated TLR4/MD2 expression in Der-p2-treated B cells. In addition, Der-p2 significantly up-regulated expression of co-stimulatory molecules and increased B cell proliferation. Neutralizing Der-p2 antibody could effectively abrogate the Der-p2-induced B cell proliferation. Der-p2 could also markedly induce NF-κB activation in B cells, which could be counteracted by dexamethasone.Conclusions/Significance
These results strongly suggest that Der-p2 is capable of triggering B cell activation and MKP-1-activated p38/MAPK dephosphorylation-regulated TLR4 induction, which subsequently enhances host immune, defense responses and development of effective allergic disease therapeutics in B cells. 相似文献56.
Basalo IM Mauck RL Kelly TA Nicoll SB Chen FH Hung CT Ateshian GA 《Journal of biomechanical engineering》2004,126(6):779-786
Interstitial fluid pressurization plays an important role in cartilage biomechanics and is believed to be a primary mechanism of load support in synovial joints. The objective of this study was to investigate the effects of enzymatic degradation on the interstitial fluid load support mechanism of articular cartilage in unconfined compression. Thirty-seven immature bovine cartilage plugs were tested in unconfined compression before and after enzymatic digestion. The peak fluid load support decreased significantly (p < 0.0001) from 84 +/- 10% to 53 +/- 19% and from 80 +/- 10% to 46 +/- 21% after 18-hours digestion with 1.0 u/mg-wet-weight and 0.7 u/mg-wet-weight of collagenase, respectively. Treatment with 0.1 u/ml of chondroitinase ABC for 24 hours also significantly reduced the peak fluid load support from 83 +/- 12% to 48 +/- 16% (p < 0.0001). The drop in interstitial fluid load support following enzymatic treatment is believed to result from a decrease in the ratio of tensile to compressive moduli of the solid matrix. 相似文献
57.
Hsu EC Lin YC Hung CS Huang CJ Lee MY Yang SC Ting LP 《Journal of biomedical science》2007,14(6):731-744
Summary Protein-tyrosine phosphatase PTPN3 is a membrane-associated non-receptor protein-tyrosine phosphatase. PTPN3 contains a N-terminal
FERM domain, a middle PDZ domain, and a C-terminal phosphatase domain. Upon co-expression of PTPN3, the level of human hepatitis
B viral (HBV) RNAs, 3.5 kb, 2.4/2.1 kb, and 0.7 kb transcribed from a replicating HBV expression plasmid is significantly
reduced in human hepatoma HuH-7 cells. When the expression of endogenous PTPN3 protein is diminished by specific small interfering
RNA, the expression of HBV genes is enhanced, indicating that the endogenous PTPN3 indeed plays a suppressive role on HBV
gene expression. PTPN3 can interact with HBV core protein. The interaction is mediated via the PDZ domain of PTPN3 and the
carboxyl-terminal last four amino acids of core. Either deletion of PDZ domain of PTPN3 or substitution of PDZ ligand in core
has no effect on PTPN3-mediated suppression. These results clearly show that the interaction of PTPN3 with core is not required
for PTPN3 suppressive effect. Mutation of 359serine and 835serine of 14-3-3β binding sites to alanine, which slightly reduces the interaction with 14-3-3β, does not influence the PTPN3
effect. In contrast, mutation of the invariant 842cysteine residue in phosphatase domain to serine, which makes the phosphatase activity inactive, does not change its subcellular
localization and interaction with core or 14-3-3β, but completely abolishes PTPN3-mediated suppression. Furthermore, deletion
of FERM domain does not affect the phosphatase activity or interaction with 14-3-3β, but changes the subcellular localization
from cytoskeleton-membrane interface to cytoplasm and nucleus, abolishes binding to core, and diminishes the PTPN3 effect
on HBV gene expression. Taken together, these results demonstrate that the phosphatase activity and FERM domain of PTPN3 are
essential for its suppression of HBV gene expression.
En-Chi Hsu, Yen-Cheng Lin have equal contributions to this work. 相似文献
58.
59.
Bretones G Acosta JC Caraballo JM Ferrándiz N Gómez-Casares MT Albajar M Blanco R Ruiz P Hung WC Albero MP Perez-Roger I León J 《The Journal of biological chemistry》2011,286(11):9815-9825
SKP2 is the ubiquitin ligase subunit that targets p27(KIP1) (p27) for degradation. SKP2 is induced in the G(1)-S transit of the cell cycle, is frequently overexpressed in human cancer, and displays transformation activity in experimental models. Here we show that MYC induces SKP2 expression at the mRNA and protein levels in human myeloid leukemia K562 cells with conditional MYC expression. Importantly, in these systems, induction of MYC did not activate cell proliferation, ruling out SKP2 up-regulation as a consequence of cell cycle entry. MYC-dependent SKP2 expression was also detected in other cell types such as lymphoid, fibroblastic, and epithelial cell lines. MYC induced SKP2 mRNA expression in the absence of protein synthesis and activated the SKP2 promoter in luciferase reporter assays. With chromatin immunoprecipitation assays, MYC was detected bound to a region of human SKP2 gene promoter that includes E-boxes. The K562 cell line derives from human chronic myeloid leukemia. In a cohort of chronic myeloid leukemia bone marrow samples, we found a correlation between MYC and SKP2 mRNA levels. Analysis of cancer expression databases also indicated a correlation between MYC and SKP2 expression in lymphoma. Finally, MYC-induced SKP2 expression resulted in a decrease in p27 protein in K562 cells. Moreover, silencing of SKP2 abrogated the MYC-mediated down-regulation of p27. Our data show that SKP2 is a direct MYC target gene and that MYC-mediated SKP2 induction leads to reduced p27 levels. The results suggest the induction of SKP2 oncogene as a new mechanism for MYC-dependent transformation. 相似文献
60.
Chen YJ Huang WC Wei YL Hsu SC Yuan P Lin HY Wistuba II Lee JJ Yen CJ Su WC Chang KY Chang WC Chou TC Chou CK Tsai CH Hung MC 《PloS one》2011,6(6):e21428