Academic literature on the topic 'Proteine pre-s'
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Journal articles on the topic "Proteine pre-s"
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Zhao, Lina, Yiwen Sun, Dongbiao Yang, et al. "Effects of Sporidiobolus pararoseus Y16 on Postharvest Blue Mold Decay and the Defense Response of Apples." Journal of Food Quality 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/6731762.
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The efficacy of Sporidiobolus pararoseus Y16 in controlling postharvest blue mold caused by Penicillium expansum on apples and the defense response involved were evaluated. The results suggested that the decay incidence of blue mold of apples treated by S. pararoseus Y16 was significantly reduced compared with the control. In vitro testing indicated that germination of spores and germ tube length of P. expansum were markedly inhibited by S. pararoseus Y16. Meanwhile, polyphenol oxidase (PPO), peroxidase (POD), phenylalanine ammonia lyase (PAL), and catalase (CAT) activities and several pathogenesis-related (PR) gene expression levels (including PR3, PR4, PR5, and PR9) were determined. In apples, the activities of PPO, POD, CAT, and PAL were significantly induced by S. pararoseus Y16 treatment compared with the control fruits. The relative expression levels of PR3 and PR4 were significantly induced at 4 and 6 d, while PR5 was significantly induced at 4 and 6 d and PR9 was significantly induced at 4 d. Therefore, the reduction in apple fruit decay by S. pararoseus Y16 treatment could be related to the increased activities of related enzymes and proteins involved in the defense against pathogens, which suggest that S. pararoseus Y16 is a potential antagonistic yeast.
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Kuijpers, Leo, Marjolijn Koens, Iain Murray-Lyon, et al. "Pre-S proteins in hepatitis b." Journal of Medical Virology 28, no. 1 (1989): 47–51. http://dx.doi.org/10.1002/jmv.1890280111.
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Halimeh, Susan, Hannelore Rott, Ihsan Osseiran, Guenther Kappert, and Manuela Siebert. "Reference Ranges of Coagulation Parameters in Pregnancies of Healthy Women and Women with Mild Bleeding Disorders." Blood 124, no. 21 (2014): 5068. http://dx.doi.org/10.1182/blood.v124.21.5068.5068.
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Abstract Introduction: It is well know that most of the coagulation factor increase during pregnancy in healthy women. Nevertheless the uninterrupted course of coagulation parameters from the beginning until the end of a pregnancy in healthy women has not been described yet. Only reference ranges for the third month and the sixth month of pregnancy are evaluated. There aren't any data available for the course of coagulation parameters during pregnancy in women with known coagulation disorders. In 2012 we started a study to investigate reference ranges during pregnancy for all coagulation factors, anticoagulants and activation markers of coagulation in 100 healthy pregnant women and 100 pregnant women with a previously known mild bleeding disorders. The study has been approved by the Ethics Committee Nordrhein. Samples and Methods: We analysed samples of pregnant women by conducting the following tests: Blood count, VWF:RCo, VWF:Ag, VWF:CB, Fibrinogen (Clauss), activities of FII, FV, FVII, FVIII (clotting and chromogenic), FIX, FX, FXI, FXII, FXIII. d-dimer, prothrombin fragment 1.2, Quick, partial thromboplastin time, plasma thrombin time , CRP, proteine S, proteine C, antithrombin, Lupus antigoaculant, ACA, ß2-GP in week 10, 16, 22, 28, 34, 40 and 6 weeks post partum (max. +/- 1) Interim Results: Currently 21 pregnant women were included in our study. 16 obviously healthy women were used to calculate the reference ranges for pregnancy. Because of strict inclusion and exclusion criteria (no previous spontaneous abortion, no previous placenta haematoma, no previous pre-eclampsia and only natural pregnancies) most of the women are in the group of the no known coagulation disorder so far. Discussion/Conclusion: There are signs that defects in the coagulation system can be associated to complications during pregnancy like child loss, intrauterine haematoma and genital bleeding. The evaluation of reference ranges helps to detect and to value coagulation disorders during pregnancy. It might be possible to explain the higher abortion rate in women with mild bleeding disorders by determination of reference values of all pro- and anticoagulants during pregnancy. If a treatment with coagulation factor concentrates can help to prevent miscarriage is still subject of ongoing studies. Determination of reference ranges for coagulation factors in the third trimenon might help to determine the peripartum bleeding risk of women with mild coagulation disorders and to help to decide whether a women needs coagulation factor concentrate during labour. Limitation: Based on the strict inclusion and exclusion criteria the number of patients is small. Disclosures Halimeh: Biotest: The authors declare that they receive research grant from Biotest AG Other. Rott:Biotest: The authors declare that they receive research grant from Biotest AG Other. Osseiran:Biotest: The authors declare that they receive research grant from Biotest AG Other. Kappert:Biotest: The authors declare that they receive research grant from Biotest AG Other. Siebert:Biotest: The authors declare that they receive research grant from Biotest AG Other.
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Cho, E. W., J. H. Park, O. J. Yoo, and K. L. Kim. "Translocation and accumulation of exogeneous hepatitis B virus preS surface proteins in the cell nucleus." Journal of Cell Science 114, no. 6 (2001): 1115–23. http://dx.doi.org/10.1242/jcs.114.6.1115.
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Recurrent reports about protease-sensitive sites in the junction of the preS and S region of the hepatitis B virus large surface protein have raised the question about a possible biological role of S protein-depleted, independent preS protein fragments in the virus life cycle. In the present study, this question was addressed by exogenous introduction of fluorescence-labeled recombinant preS proteins into permeabilized HepG2 cells. While maltose-binding proteins (MBP) were evenly distributed throughout the cytoplasm, MBP-preS fusion proteins selectively accumulated in the nucleus. Using truncated preS proteins, the effective domain for this nuclear accumulation was localized around the preS2 region. The mode of this action differs from conventional nuclear translocation mechanism in its energy- and mediator-independency and in that it is not saturated regardless of the increase of preS protein concentration. The biological meaning of this phenomenon has to be further studied. However, in regard to hepatitis B virus infection, this observation might provide a clue for unveiling the still poorly characterized events after initial internalization of the virus, which might make use of the nuclear translocation effect of the preS2 region to facilitate the infection.
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Park, Soyeong, Andrew Auyeung, Denis L. Lee, Paul F. Lambert, Evie H. Carchman, and Nathan M. Sherer. "HIV-1 Protease Inhibitors Slow HPV16-Driven Cell Proliferation through Targeted Depletion of Viral E6 and E7 Oncoproteins." Cancers 13, no. 5 (2021): 949. http://dx.doi.org/10.3390/cancers13050949.
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High-risk human papillomavirus strain 16 (HPV16) causes oral and anogenital cancers through the activities of two viral oncoproteins, E6 and E7, that dysregulate the host p53 and pRb tumor suppressor pathways, respectively. The maintenance of HPV16-positive cancers requires constitutive expression of E6 and E7. Therefore, inactivating these proteins could provide the basis for an anticancer therapy. Herein we demonstrate that a subset of aspartyl protease inhibitor drugs currently used to treat HIV/AIDS cause marked reductions in HPV16 E6 and E7 protein levels using two independent cell culture models: HPV16-transformed CaSki cervical cancer cells and NIKS16 organotypic raft cultures (a 3-D HPV16-positive model of epithelial pre-cancer). Treatment of CaSki cells with some (lopinavir, ritonavir, nelfinavir, and saquinavir) but not other (indinavir and atazanavir) protease inhibitors reduced E6 and E7 protein levels, correlating with increased p53 protein levels and decreased cell viability. Long-term (>7 day) treatment of HPV16-positive NIKS16 raft cultures with saquinavir caused epithelial atrophy with no discernible effects on HPV-negative rafts, demonstrating selectivity. Saquinavir also reduced HPV16′s effects on markers of the cellular autophagy pathway in NIKS16 rafts, a hallmark of HPV-driven pre-cancers. Taken together, these data suggest HIV-1 protease inhibitors be studied further in the context of treating or preventing HPV16-positive cancers.
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Rasheva, Vanya I., David Knight, Przemyslaw Bozko, Katherine Marsh, and Maxim V. Frolov. "Specific Role of the SR Protein Splicing Factor B52 in Cell Cycle Control in Drosophila." Molecular and Cellular Biology 26, no. 9 (2006): 3468–77. http://dx.doi.org/10.1128/mcb.26.9.3468-3477.2006.
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ABSTRACT E2F and retinoblastoma tumor suppressor protein pRB are important regulators of cell proliferation; however, the regulation of these proteins in vivo is not well understood. In Drosophila there are two E2F genes, an activator, de2f1, and a repressor, de2f2. The loss of de2f1 gives rise to the G1/S block accompanied by the repression of E2F-dependent transcription. These defects can be suppressed by mutation of de2f2. In this work, we show that the de2f1 mutant phenotype is rescued by the loss of the pre-mRNA splicing factor SR protein B52. Mutations in B52 restore S phase in clones of de2f1 mutant cells and phenocopy the loss of the de2f2 function. B52 acts upstream of de2f2 and plays a specific role in regulation of de2f2 pre-mRNA splicing. In B52-deficient cells, the level of dE2F2 protein is severely reduced and the expression of dE2F2-dependent genes is deregulated. Reexpression of the intronless copy of dE2F2 in B52-deficient cells restores the dE2F2-mediated repression. These results uncover a previously unrecognized role of the splicing factor in maintaining the G1/S block in vivo by specific regulation of the dE2F2 repressor function.
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Schumacher, Julia, David Rosenkranz, and Holger Herlyn. "Mating systems and protein–protein interactions determine evolutionary rates of primate sperm proteins." Proceedings of the Royal Society B: Biological Sciences 281, no. 1775 (2014): 20132607. http://dx.doi.org/10.1098/rspb.2013.2607.
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To assess the relative impact of functional constraint and post-mating sexual selection on sequence evolution of reproductive proteins, we examined 169 primate sperm proteins. In order to recognize potential genome-wide trends, we additionally analysed a sample of altogether 318 non-reproductive (brain and postsynaptic) proteins. Based on cDNAs of eight primate species (Anthropoidea), we observed that pre-mating sperm proteins engaged in sperm composition and assembly show significantly lower incidence of site-specific positive selection and overall lower non-synonymous to synonymous substitution rates ( d N / d S ) across sites as compared with post-mating sperm proteins involved in capacitation, hyperactivation, acrosome reaction and fertilization. Moreover, database screening revealed overall more intracellular protein interaction partners in pre-mating than in post-mating sperm proteins. Finally, post-mating sperm proteins evolved at significantly higher evolutionary rates than pre-mating sperm and non-reproductive proteins on the branches to multi-male breeding species, while no such increase was observed on the branches to unimale and monogamous species. We conclude that less protein–protein interactions of post-mating sperm proteins account for lowered functional constraint, allowing for stronger impact of post-mating sexual selection, while the opposite holds true for pre-mating sperm proteins. This pattern is particularly strong in multi-male breeding species showing high female promiscuity.
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Lin, Yueh-Te, Long-Bin Jeng, Wen-Ling Chan, Ih-Jen Su, and Chiao-Fang Teng. "Hepatitis B Virus Pre-S Gene Deletions and Pre-S Deleted Proteins: Clinical and Molecular Implications in Hepatocellular Carcinoma." Viruses 13, no. 5 (2021): 862. http://dx.doi.org/10.3390/v13050862.
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Hepatocellular carcinoma (HCC) is one of the most frequent and fatal human cancers worldwide and its development and prognosis are intimately associated with chronic infection with hepatitis B virus (HBV). The identification of genetic mutations and molecular mechanisms that mediate HBV-induced tumorigenesis therefore holds promise for the development of potential biomarkers and targets for HCC prevention and therapy. The presence of HBV pre-S gene deletions in the blood and the expression of pre-S deleted proteins in the liver tissues of patients with chronic hepatitis B and HBV-related HCC have emerged as valuable biomarkers for higher incidence rates of HCC development and a higher risk of HCC recurrence after curative surgical resection, respectively. Moreover, pre-S deleted proteins are regarded as important oncoproteins that activate multiple signaling pathways to induce DNA damage and promote growth and proliferation in hepatocytes, leading to HCC development. The signaling molecules dysregulated by pre-S deleted proteins have also been validated as potential targets for the prevention of HCC development. In this review, we summarize the clinical and molecular implications of HBV pre-S gene deletions and pre-S deleted proteins in HCC development and recurrence and highlight their potential applications in HCC prevention and therapy.
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Natoli, G., C. Balsano, ML Avantaggiati, et al. "Characterization of the sequences acitivated by the truncated pre-S/S proteins." Journal of Hepatology 13 (January 1991): S55. http://dx.doi.org/10.1016/0168-8278(91)91209-y.
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Winter, Christine, Christel Schwegmann-Wessels, Ulrich Neumann, and Georg Herrler. "The Spike Protein of Infectious Bronchitis Virus Is Retained Intracellularly by a Tyrosine Motif." Journal of Virology 82, no. 6 (2007): 2765–71. http://dx.doi.org/10.1128/jvi.02064-07.
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ABSTRACT We have analyzed the intracellular transport of the spike (S) protein of infectious bronchitis virus (IBV), an avian coronavirus. Surface expression was analyzed by immunofluorescence microscopy, by surface biotinylation, and by syncytium formation by S-expressing cells. By applying these methods, the S protein was found to be retained intracellularly. Tyr1143 in the cytoplasmic tail was shown to be a crucial component of the retention signal. Deletion of a dilysine motif that has previously been suggested to function as a retrieval signal did not abolish intracellular retention. Treatment of the S proteins with endoglycosidases did not reveal any differences between the parental and the mutant proteins. Furthermore, all S proteins analyzed were posttranslationally cleaved into the subunits S1 and S2. In coexpression experiments, the S protein was found to colocalize with a Golgi marker. Taken together, these results indicate that the S protein of IBV is retained at a late Golgi compartment. Therefore, this viral surface protein differs from the S proteins of transmissible gastroenteritis virus and severe acute respiratory syndrome coronavirus, which are retained at a pre-Golgi compartment or transported to the cell surface, respectively. The implications of these differences are discussed.
Dissertations / Theses on the topic "Proteine pre-s"
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Zoulim, Fabien. "Signification de l'expression des proteines pre-s1 dans le serum et les cellules mononucleees du sang au cours des infections chroniques dues au virus de l'hepatite b." Lyon 1, 1990. http://www.theses.fr/1990LYO1M151.
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Kuroda, Shun'ichi. "STUDIES ON HEPATITIS B VIRUS ENVELOPE PROTEIN CONTAINING PRE-S PEPTIDE." Kyoto University, 1992. http://hdl.handle.net/2433/168904.
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本文データは平成22年度国立国会図書館の学位論文(博士)のデジタル化実施により作成された画像ファイルを基にpdf変換したものであるKyoto University (京都大学)
0048
新制・論文博士
博士(農学)
乙第8019号
論農博第1796号
新制||農||640(附属図書館)
学位論文||H4||N2518(農学部図書室)
UT51-92-U255
(主査)教授 左右田 健次, 教授 駒野 徹, 教授 清水 昌
学位規則第4条第2項該当
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Zoulim, Fabien. "Etude du cycle de replication des hepadnavirus. Biologie des proteines virales pre-s, p et x." Paris 7, 1993. http://www.theses.fr/1993PA077222.
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Le virus de l'hepatite b (vhb) est responsable, chez l'homme, d'infections chroniques a haut potentiel evolutif vers le carcinome hepatocellulaire. Il s'agit d'un virus a adn qui replique son genome par transcription inverse d'un arn pregenomique. Dans la premiere partie de ce travail, nous nous sommes interesses a la biologie clinique des infections virales chroniques a vhb. Chez les patients atteints d'hepatite chronique, nous avons pu montrer que la detection des proteines d'enveloppe pre-s dans le serum est correlee avec la presence d'une replication virale. Nous avons aussi etudie le lymphotropisme du vhb et montre que les lymphocytes du sang peripherique peuvent representer un reservoir viral extrahepatique. La deuxieme partie de ce travail concerne la biologie moleculaire du vhb. Nous avons caracterise l'amorce de la transcription inverse et montre qu'il s'agit du groupe hydroxyl d'une tyrosine de l'adn polymerase virale. Il s'agit du premier exemple de transcription inverse initiee par une amorce proteique. Enfin, nous avons etudie le role de la proteine x dans l'infection virale, dans le modele de l'hepatite de la marmotte. Cette etude a permis de demontrer que la proteine x, bien que non necessaire a la replication virale in vitro, est indispensable a l'etablissement d'une infection virale in vivo
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Oliveira, André Luiz Malavasi Longo de. "Trombofilias maternas hereditárias com e sem tromboembolismo venoso: resultados maternos e neonatais." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-25082010-112901/.
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O objetivo do presente estudo foi avaliar a diferença de resultados maternos e neonatais em gestações complicadas por trombofilias hereditárias em pacientes com e sem tromboembolismo venoso. Apesar do aumento de evidências, na literatura, sobre a associação de trombofilias congênitas e resultados obstétricos adversos, há ainda dúvida se pacientes trombofílicas com tromboembolismo venoso apresentam resultados maternos e neonatais piores que as pacientes trombofílicas sem tromboembolismo venoso. O estudo analisou 66 gestantes com trombofilias hereditárias, de forma retrospectiva observacional e comparativa, das quais 33 apresentavam tromboembolismo venoso e 36 o não apresentavam. Os principais desfechos relacionados a resultados maternos e neonatais adversos foram: pré-eclâmpsia grave, descolamento prematuro de placenta, restrição de crescimento fetal, natimortalidade, prematuridade e complicações hemorrágicas maternas. As trombofilias congênitas incluídas no estudo foram o fator V de Leiden (FVL), mutação da protrombina G20210A, mutação C677T do gene da 5,10-metilenotetrahidrofolato redutase (MTHFR), deficiência de proteína S, deficiência de proteína C e deficiência de antitrombina. Ambos os grupos apresentaram características populacionais similares. A ocorrência de complicações maternas e fetais/neonatais foi similar nos dois grupos: pré-eclâmpsia grave (P=0,097), descolamento prematuro de placenta (P=0,478), restrição de crescimento fetal (P=0,868), natimortalidade (P=0,359), prematuridade (P=0,441) e complicações hemorrágicas maternas (P=0,478). Este estudo concluiu que a presença de tromboembolismo venoso em gestantes com trombofilia hereditária apresenta resultados maternos e neonatais semelhantes àquelas com trombofilias hereditárias sem tromboembolismo venoso.The aim of this study was to evaluate differences in maternal and neonatal outcomes in pregnancies complicated by inherited thrombophilias between patients with and without venous thromboembolism. Despite increasing evidence in the literature indicating an association between inherited thrombophilias and adverse obstetric outcomes, doubts remain whether thrombophilic patients with venous thromboembolism present poorer maternal and neonatal outcomes than thrombophilic patients without venous thromboembolism. In this retrospective, observational and comparative study, 66 pregnant women with inherited thrombophilias, including 33 with venous thromboembolism and 36 without thromboembolism, were investigated. The main end-points analyzed were severe pre-eclampsia, placental abruption, fetal growth restriction, stillbirth, preterm delivery, and maternal hemorrhagic complications. The congenital thrombophilias included in this study were factor V Leiden (FVL), prothrombin G20210A mutation, C677T mutation in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene, protein S deficiency, protein C deficiency, and antithrombin deficiency. The two groups were similar in terms of population characteristics. The frequency of maternal and fetal/neonatal complications was similar in the two groups: severe pre-eclampsia (P=0.097), placental abruption (P=0.478), fetal growth restriction (P=0.868), stillbirth (P=0.359), preterm delivery (P=0.441), and maternal hemorrhagic complications (P=0.478). This study concluded that venous thromboembolism in thrombophilic patients does not worsen maternal or neonatal outcomes when compared to thrombophilic patients without venous thromboembolism.
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Gahura, Ondřej. "Regulace sestřihu pre-mRNA v S. cerevisiae: kooperace RNA a proteinů." Doctoral thesis, 2012. http://www.nusl.cz/ntk/nusl-312164.
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Ondřej Gahura, PhD Thesis 2011 Regulation of pre-mRNA splicing in S. cerevisiae: where RNA cooperates with proteins Abstract Removal of introns from protein coding transcripts occurs in two splicing reactions catalyzed by a large nuclear complex, spliceosome. The spliceosome is an extremely intricate and dynamic machine, wherein contributions of small RNA molecules and multiple proteins are coordinated to meet the requirements of absolute precision and high flexibility. For an intimate understanding of pre-mRNA splicing, it is necessary to unravel roles of individual components and to dissect the partial mechanisms. In the first part of this work, we describe the role of the Prp45 splicing factor in Saccharomyces cerevisiae. Mapping of genetic interactions of a conditionally lethal allele prp45(1-169) suggests a relationship of Prp45 to the NTC complex and to the second transesterification. Two-hybrid assay and purification of spliceosomal complexes reveal a contribution of the Prp45 C-terminus in the Prp22 helicase recruitment and/or regulation. Numerous experiments with reporter substrates document the need of Prp45 for the efficient splicing of a specific subset of introns. Our observations suggest that the function of Prp45 in splicing is conserved in evolution. The second part is devoted to the role of...
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chen, Chien-Fu, and 陳健福. "Morphologic and molecular observation ofhepatitis B virus pre-S mutant proteins-induced endoplasmic reticulum (ER) stress." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/48090995007512561038.
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碩士國立成功大學
分子醫學研究所
92
Hepatitis B virus (HBV), one of the hepadnavirus family, contains a partially double-stranded DNA genome of 3.2 kb. Individuals infected by HBV potentially become chronic carriers that are at a high risk for the development of hepatocellular carcinoma (HCC). HBV encodes three envelope proteins that named large, middle, and small surface protein. Many naturally occurring HBV mutants in sera or liver tissue of patients with chronic hepatitis B have been identified. Previously, two types of HBV pre-S mutant were identified; one contains a deletion in the pre-S1 region and the other contains a deletion in pre-S2 region. Both pre-S1 ad pre-S2 mutant surface proteins are localized in the endoplasmic reticulum (ER) with distinct distribution patterns. This study is designed to investigate the ER stress induction of specific hepatitis B virus pre-S mutant proteins in the cytoplasm. First, we used immunohistochemical staining and GFP fusion protein to monitor the localizations of pre-S mutant proteins in Huh7 cells, and pre-S mutant proteins showed a blot-like distribution pattern. Transmission electron microscope was used to monitor morphological change of ER induced by the accumulation of HBV mutant surface proteins. The expression of pre-S1 and pre-S2 mutant proteins in Huh7 cells resulted in ER proliferation and subsequently ER enlargement which looked like inclusion bodies. ER accumulations of these mutant proteins also activate ER stress signals in Huh7 cells by which ER stress marker GRP78 and GRP94 were significantly upregulated, while other chaperones and ER proteins such as Hsp60, Hsp70, Hsp90, Erp72 and Erp57 remained unchanged. Pre-S mutant proteins induced ER stress also lead to increase cytoplasmic Ca2+ concentration, but did not cause cell death. The ER accumulation effect seems to restrict to the pre-S mutant proteins without any effects on the protein trafficking of other cellular proteins. In fact, we have observed the enhanced expression of MHC class I on the surface of cells with pre-S mutant proteins. In combination of our results, pre-S mutant proteins indeed accumulate in ER, result in ER enlargement, and induce ER stress. These mutant proteins induce ER stress which leads to the release of Ca2+ from the ER and the subsequent production of reactive oxygen intermediates. In conclusion, the clinical observation of ER changes in mutant surface protein-containing hepatocytes in cirrhotic livers could be associated with different biologic functions of pre-S mutant proteins.
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Shen, Fang-Ching, and 沈芳晴. "Studies of the protein expression profiles in hepatoma cells expressing hepatitis B virus pre-S mutant large surface antigen by a proteomic analysis." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/67450360121647682097.
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碩士國立嘉義大學
食品科學暨生物藥學研究所(Graduate Institute of F
98
Chronic hepatitis B virus (HBV) infection is the major cause of hepatocellular carcinoma (HCC) in Taiwan. In previous studies, two types of mutant large HBV surface antigen (LHBS) were identified in HCC tissues. The pre-S1 and pre-S2 mutant LHBS were partially deleted of the pre-S1 and pre-S2 regions, respectively. These pre-S mutant LHBS accumulate in endplasmic reticulum (ER) and induce ER stress, which lead to oxidative DNA damage and genomic instability. In this study, we aimed to study the protein expression profiles affected by the pre-S1/S2 mutant LHBS in the hepatoma HuH-7 cells by proteomic analysis. The wild type, pre-S1 and pre-S2 mutant LHBS genes were transiently transfected into HuH-7 cells and whole cell lysates were applied to two-dimensional gel electrophoresis. The protein spots in gel were stained by silver dye and the intensity on each spot was quantified. The proteins differentially expressing in the pre-S2 mutant LHBS(+) cells were screened by using the statistical Student’s t-test, since the pre-S2 mutant type is highly associated with HCC. Proteins on the spots were then identified by mass spectrometry. The approaches of reverse transcription polymerase chain reaction (RT-PCR) and western blot were then performed to verify the protein expression levels. Among the proteins tested, NM23-H1 (nonmetastatic protein 23, homolog 1) was found to be down-regulated by the pre-S2 mutant LHBS. NM23-H1 is important in repairing DNA and regulating cancer cells’ proliferation and metastasis. Our finding suggested that the pre-S mutant LHBS causes NM23-H1 down regulation and through which it promotes HCC formation and progression. In summary, the findings in this study allow us to further understand the molecular mechanism of the pre-S mutant LHBS-induced HCC.
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近藤, 琢磨. "Involvement of pRB-Related p107 Protein in the Inhibition of S-Phase Progression in Response to Genotoxic Stress." Doctoral thesis, 2001. http://hdl.handle.net/2115/32664.
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Häcker, Irina. "Electron microscopic localization of tagged proteins in the yeast S. cerevisiae spliceosomal U4/U6.U5 trisnRNP." Doctoral thesis, 2008. http://hdl.handle.net/11858/00-1735-0000-0006-AD0F-E.
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Stráňava, Martin. "Mechanismus přenosu signálu hemovými senzorovými proteiny detekujícími kyslík." Doctoral thesis, 2016. http://www.nusl.cz/ntk/nusl-353395.
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EN Heme containing gas sensor proteins play important role in bacterial physiology in regulating many processes such as cell differentiation, virulence, biofilm formation or intercellular communication. For their structure, typical modular architecture is characteristic where various sensor domains (usually at the N-terminus) regulate the activity of the catalytic or functional domains (usually at the C-terminus). In this dissertation thesis, we focused on three representatives from the group of oxygen sensing proteins, namely histidine kinase AfGcHK, diguanylate cyclase YddV, phosphodiesterase EcDOS and also on protein RR, which is the interaction partner of AfGcHK. The main aim of the thesis was to study intra-protein/inter-domain signal transduction in two representatives of heme sensor proteins with a globin fold of the sensor domain (AfGcHK, YddV) and in one representative with PAS fold of the sensor domain (EcDOS). Another objective was to describe inter-protein signal transduction in the two component signaling system AfGcHK-RR and structurally characterize these two interacting partners. Emphasis was also placed on the study of the interaction between model sensor domains and different signaling molecules and also on function of individual amino acids involved in the binding of these...
Books on the topic "Proteine pre-s"
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Abhishek, Abhishek, and Michael Doherty. Pathophysiology of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0049.
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Calcium pyrophosphate (CPP) dihydrate crystals form extracellularly. Their formation requires sufficient extracellular inorganic pyrophosphate (ePPi), calcium, and pro-nucleating factors. As inorganic pyrophosphate (PPi) cannot cross cell membranes passively due to its large size, ePPi results either from hydrolysis of extracellular ATP by the enzyme ectonucleotide pyrophosphatase/phosphodiesterase 1 (also known as plasma cell membrane glycoprotein 1) or from the transcellular transport of PPi by ANKH. ePPi is hydrolyzed to phosphate (Pi) by tissue non-specific alkaline phosphatase. The level of extracellular PPi and Pi is tightly regulated by several interlinked feedback mechanisms and growth factors. The relative concentration of Pi and PPi determines whether CPP or hydroxyapatite crystal is formed, with low Pi/PPi ratio resulting in CPP crystal formation, while a high Pi/PPi ratio promotes basic calcium phosphate crystal formation. CPP crystals are deposited in the cartilage matrix (preferentially in the middle layer) or in areas of chondroid metaplasia. Hypertrophic chondrocytes and specific cartilage matrix changes (e.g. high levels of dermatan sulfate and S-100 protein) are related to CPP crystal deposition and growth. CPP crystals cause inflammation by engaging with the NALP3 inflammasome, and with other components of the innate immune system, and is marked with a prolonged neutrophilic inflitrate. The pathogenesis of resolution of CPP crystal-induced inflammation is not well understood.
Book chapters on the topic "Proteine pre-s"
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Natoli, G., C. Balsano, M. L. Avantaggiati, et al. "Truncated pre-S/S proteins transactivate multiple target sequences." In Chronically Evolving Viral Hepatitis. Springer Vienna, 1992. http://dx.doi.org/10.1007/978-3-7091-5633-9_14.
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Sasagawa, Toshiyuki. "Human Papillomavirus Capsid Protein-pREP in Schizosaccharomyces pombe: Efficient Assembly of the Viral Capsid Protein in S. pombe and S. cerevisiae." In Foreign Gene Expression in Fission Yeast: Schizosaccharomyces pombe. Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-03472-9_8.
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Katayama, T., T. Manabe, K. Imaizumi, et al. "The RNA-Binding Protein Causes Aberrant Splicing of Presenilin-2 Pre-mRNA in Sporadic Alzheimer�s Disease." In Molecular Neurobiology of Alzheimer Disease and Related Disorders. KARGER, 2004. http://dx.doi.org/10.1159/000078523.
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Neurath, A. Robert, and Stephen B. H. Kent. "The Pre-S Region of Hepadnavirus Envelope Proteins." In Advances in Virus Research. Elsevier, 1988. http://dx.doi.org/10.1016/s0065-3527(08)60516-3.
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"Adjuvanted RTS, S and Other Protein-Based Pre-Erythrocytic Stage Malaria Vaccines." In New Generation Vaccines. CRC Press, 2004. http://dx.doi.org/10.1201/9781439834404-76.
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Dave, Jayshree, and Rohma Ghani. "Bone and Joint Infections." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0039.
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Patients with bone and joint infections can present with native joint septic arthritis, osteomyelitis, or implant-associated bone and joint infections. Patients often present with an acute onset of hot, swollen, painful joint with restricted function in one or more joints over a couple of weeks. On examination the affected joint is painful with a limited range of movement, and fever is present. Risk factors for septic arthritis include an abnormal joint architecture due to pre-existing joint disease, e.g. patients with rheumatoid arthritis, or patients on haemodialysis, with diabetes mellitus, or older than 80 years of age. The differential diagnosis includes reactive arthritis, pre-patellar bursitis, gout, Lyme disease, brucellosis, and Whipples disease. Staphylococcus aureus is the most common cause of septic arthritis, followed by Group A streptococcus and other haemolytic streptococci including B, C and G. Gram-negative rods such as Escherichia coli are implicated in the elderly, immunosuppressed, or patients with comorbidities. Pseudomonas aeruginosa is implicated in intravenous (IV) drug users and patients post-surgery or intra-articular injections. Kingella kingae causes septic arthritis in children younger than four years of age. Neisseria gonorrhoeae, Neisseria meningitidis, and Salmonella species can also cause septic arthritis as part of a disseminated infection. Septic monoarthritis commonly occurs in patients with disseminated gonococcal infection. Blood cultures, white blood cell count, C reactive protein (CRP), electrolytes, and liver function tests are indicated. Serial CRP is useful in monitoring response to treatment. If there is a history of unprotected sexual intercourse, gonococcal testing is recommended. Brucella serology and Tropheryma whippei serology may be considered based on the clinical history. Joint fluid aspiration should be performed by a specialist within the hospital. Joint fluid aspirate is processed in the laboratory for microscopy, culture, and sensitivity. Gram stain can show an increase in neutrophils and presence of bacteria. The guidelines provided by the British Society for Rheumatology on the management of hot swollen joints in adults has provided advice for empirical treatment for suspected septic arthritis, but the local antibiotic policy should also be considered. Initial treatment is with intravenous flucloxacillin 2g four times daily, or 450– 600mg four times daily of intravenous clindamycin to cover S. aureus.
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Kumar, Vijay. "Learning from Bats to Escape from Potent or Severe Viral Infections." In Origin and Impact of COVID-19 Pandemic Originating From SARS-CoV-2 Infection Across the Globe [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98916.
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The COVID-19 pandemic that started in December 2019 in Wuhan city, China has created chaos all over the world with over 185 million infection cases and 4 million deaths world-wide. The pathogen behind COVID-19 has been identified as severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) that is more close to the previous SARS-CoV responsible for SARS epidemic 2002–2003. Although, SARS-CoV-2 also differs from SARS-CoV in many aspects as indicated by genetic studies. For example, SARS-CoV does not have a furin binding domain or site, whereas its presence in SARS-CoV-2 spike (S) protein increases its potential for infectivity. The horseshoe bats (Rhinolphus species) from China are considered as primary animal reservoirs for SARS-CoV and SARS-CoV-2. However, along with CoVs, bats also harbor many other viral pathogens (Ebola, Nipah, and Hendra viruses) without having serious infections. The bat physiology plays a crucial role in harboring these viruses along with adaptations to longevity and slow aging process. The immune system plays a crucial role in the clearance or establishment of the infection. Present chapter discusses different immunological aspects (innate immune response comprising the virus recognizing pattern recognition receptors (PRRs), type 1 interferon production, pro- and anti-inflammatory immune response, and adaptive immune response) that help bats to control viral infection without getting a severe infection as compared to other mammals, including humans.
Conference papers on the topic "Proteine pre-s"
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O'hara, Patrick J., Frank A. Grant, A. Betty, J. Haldmen, and Mark J. Murray. "Structure of the Human Factor VII Gene." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643786.
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Factor VII is a member of a family of vitamin K-dependent, gamma-carboxylated plasma protein which includes factor IX, factor X, protein C, protein S and prothrombin. Activated factor VII (factor Vila) is a plasma serine protease which participates in a cascade of reactions leading to the coagulation of blood. Two overlapping genomic clones containing sequences encoding human factor VII were isolated and characterized. The complete sequence of the gene was determined and found to span 12.8 kilobases. The mRNA for factor VII as demonstrated by cDNA cloning is polyadenylated at multiple sites but contains only one AAUAAA poly-A signal sequence. The mRNA can undergo alternative splicing forming one transcript containing eight segments as exons and another with an additional exon which encodes a larger pre-pro leader sequence. The portion of the pre-pro leader coded for by the additional exon has no known counterpart in the other vitamin K-dependent proteins. The positions of the introns with respect to the amino acid sequence encoded by the eight essential exons of factor VII are the same as those present in factor IX, factor X, protein C and the first three exons of prothrombin. These exons code for domains generally conserved among members of this gene family, including a pre-pro leader (the essential exon la and alternative exon lb), a gamma-carboxylated domain (exons 2 and 3) a growth factor domain (exons 4 and 5) an activation region (exon 6) and a serine protease (exon 8). The corresponding introns in these genes are dissimilar with respect to size and sequence, with the exception of the third intron in factor VII and protein C. Four introns and a portion of exon 8 in factor VII contain regions made up of tandem repeats of oligonucleotide monomer elements. More than a quarter of the intron sequences and more than a third of the 3' untranslated portion of the mRNA transcript consist of these minisatellite tandem repeats. This type of structure is responsible for polymorphisms due to allelic variation in repeat copy number in other areas of the human genome. Tandem repeats can evolve as a result of random crossover in DNA whose sequence is not maintained by selection. This suggests that much of the sequence information present in the introns and untranslated portion of the message is dispensable.
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Vigano D'Angelo, S., F. Gilardoni, M. P. Seveso, A. Marassi, G. Mari, and A. D'Angelo. "REDUCTION OF THE ANTICOAGULANT ACTIVITY OF PROTEIN C AND PROTEIN S DURING THE POSTOPERATIVE PERIOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644287.
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Protein S circulates in plasma as free protein S and in complex with C4b-binding protein, an inhibitor of complement activation. Only free protein S functions as the cofactor for the anticoagulant and profibrinolytic effects of activated protein C. Since isolated reductions of protein C and protein S result in increased thrombotic risk, only measurement of both proteins permits comprehensive evaluation of the antithrombotic potential of the protein C system. No information is available on protein C and protein S functional levels during the postoperative period, an established prothrombotic condition. The plasma changes of protein C, protein S and C4b-binding protein were followed in 40 patients with no malignancy undergoing abdominal surgery. No significant change of protein C and protein S activi ty was observed following minor operations. After major surgery, protein C anticoagulant activity dropped to 80% of preoperative levels during the first postoperative week (p<0.00l). Significant increase of both total protein S antigen (110%, p< 0.01) and C4b-binding protein (130%, p<0.001) were observed after major surgery resulting in reduction of free protein S antigen to 86% of pre operative values (p<0.001). Protein S anticoagulant activity matched the changes of free protein S antigen.Albeit transient and moderate, the observed reductions of both protein C and protein S may act synergistically to cause significant impairment of the antithrombotic potential during the postoperative period. The effect of heparin prophylaxis on protein C and protein S postoperative levels is currently under investigation.
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Lijnen, H. R., L. Nelles, G. Lemmens, D. Collen, and W. E. Holmes. "A FUSION PROTEIN OF THE A-CHAIN OF t-PA WITH LOW Mr scu-PA COMBINES THE FIBRIN-SPECIFICITY OF BOTH MOLECULES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643943.
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A hybrid human cDNA was constructed by ligation of a cDNA fragment of tissue-type plasminogen activator (t-PA), encoding 5∲-untranslated, the pre-pro region and amino acids Ser 1 through Thr 263, with a cDNA fragment of urokinase-type plasminogen activator (u-PA), encoding amino acids Leu 144 through Leu 411. The hybrid cDNA was expressed in Chinese Hamster Ovary Cells and the translation product purified from the conditioned cell culture media in the presence of aprotinin. On SDS-gel electrophoresis under reducing conditions, the protein migrated as a single band with approximate Mr 70,000 and on immunoblot-ting, it reacted with rabbit antisera raised against human t-PA and against human u-PA. The urokinase-like amidolytic activity (S-2444) of the protein’ was 320 IU/mg but increased to 43,000 IU/mg after treatment with plasmin, which resulted in conversion of the single chain molecule (t-PA/scu-PA) to a two-chain molecule (t-PA/tcu-PA).Both proteins activated plasminogen directly with Michaelis constant (Km) 1.5 μM and catalytic rate constant (km2) 0.0058 s-1 for t-PA/scu-PA and with K = 80 μM and = 5.6 s-1 for t-PA/tcu-PA. CBNr-digested fibrinogen stimulated the activation rate of plasminogen with t-PA/tcu-PA (increase of k2/Km of 88-fold).Both t-PA/scu-PA and t-PA/tcu-PA bound specifically to fibrin albeit ^np$re weakly than t-PA. In an in vitro system composed of a human I-fibrin labeled plasma clot immersed in human plasma, the t-PA/tcu-PA hybrid has a higher fibrin-selectivity of clot lysis than tcu-PA, but this difference was not evident between t-PA/scu-PA and scu-PA. The stability of the t-PA/scu-PA hybrid in plasma was much higher than that of the t-PA/tcu-PA hybrid, a difference comparable to that between scu-PA and tcu-PA.It is concluded that these t-PA/u-PA hybrid proteins combine fibrin-affinity of t-PA with the enzymatic properties of u-PA (either scu-PA or tcu-PA), resulting in improved fibrin-mediated plasminogen activation.
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Pannekok, H., A. J. Van Zonneveid, C. J. M. de vries, M. E. MacDonald, H. Veerman, and F. Blasi. "FUNCTIONAL PROPERTIES OF DELETION-MUTANTS OF TISSUE-TYPE PLASMINOGEN ACTIVATOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643724.
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Over the past twenty-five years, genetic methods have generated a wealth of information on the regulation and the structure-function relationship of bacterial genes.These methods are based on the introduction of random mutations in a gene to alter its function. Subsequently, genetic techniques cure applied to localize the mutation, while the nature of the impairedfunction could be determined using biochemical methods. Classic examples of this approach is now considered to be the elucidation of the structure and function of genes, constituting the Escherichia coli lactose (lac) and tryptophan (trp) operons,and the detailed establishment of the structure and function of the repressor (lacl) of the lac operon. Recombinant DNA techniques and the development of appropriate expression systems have provided the means both to study structure and functionof eukaryotic (glyco-) proteins and to create defined mutations with a predestinedposition. The rationale for the construction of mutant genes should preferentiallyrely on detailed knowledge of the three-dimensional structure of the gene product.Elegant examples are the application of in vitro mutagenesis techniques to substitute amino-acid residues near the catalytic centre of subtilisin, a serine proteasefrom Bacillus species and to substituteanamino acid in the reactive site (i.e. Pi residue; methionine) of α-antitrypsin, a serine protease inhibitor. Such substitutions have resulted into mutant proteins which are less susceptible to oxidation and, in some cases, into mutant proteins with a higher specific activity than the wild-type protein.If no data are available on the ternary structure of a protein, other strategies have to be developed to construct intelligent mutants to study the relation between the structure and the function of a eukaryotic protein. At least for a number of gene families, the gene structure is thought to be created by "exon shuffling", an evolutionary recombinational process to insert an exon or a set of exons which specify an additional structural and/or functional domain into a pre-existing gene. Both the structure of the tissue-type plasminogen activator protein(t-PA) and the t-PA gene suggest that this gene has evolved as a result of exon shuffling. As put forward by Gilbert (Science 228 (1985) 823), the "acid test"to prove the validity of the exon shuffling theory is either to delete, insert or to substitute exon(s) (i.e. in the corresponding cDNA) and toassay the properties of the mutant proteins to demonstrate that an exon or a set of adjacent exons encode (s) an autonomousfunction. Indeed, by the construction of specific deletions in full-length t-PA cDNA and expression of mutant proteins intissue-culture cells, we have shown by this approach that exon 2 of thet-PA gene encodes the function required forsecretion, exon 4 encodes the "finger" domain involved in fibrin binding(presumably on undegraded fibrin) and the set of exons 8 and 9 specifies kringle 2, containing a lysine-binding sit(LBS) which interacts with carboxy-terminal lysines, generated in fibrin after plasmic digestion. Exons 10 through 14 encode the carboxy-ter-minal light chain of t-PA and harbor the catalytic centre of the molecule and represents the predominant "target site" for the fast-acting endothelial plasminogen activator inhibitor (PAI-1).As a follow-up of this genetic approach to construct deletion mutants of t-PA, we also created substitution mutants of t-PA. Different mutants were constructed to substitute cDNA encoding thelight chain of t-PA by cDNA encoding the B-chain of urokinase (u-PA), in order to demonstrate that autonomous structural and functional domains of eitherone of the separate molecules are able toexert their intrinsic properties in a different context (C.J.M. de Vries et al., this volume). The possibilities and the limitations of this approach to study the structure and the function of t-PA and of other components of the fibrinolytic process will be outlined.
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Jackson, Craig M., George M. Brenckle, Philip J. Hogg, and Donald J. Winzor. "EVIDENCE FOR SELF-ASSOCIATION OF PROTHROMBIN FRAGMENT 1 IN THE ABSENCE OF CALCIUM IONS: IMPLICATIONS FOR THE INTERPRETATION OF COOPERATIVITY OF CALCIUM BINDING." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643933.
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The necessity to consider the binding of metal ion by prothrombin and its fragment 1 in terms of two entirely different mechanistic models has been removed. Cooperativity of Ca+T binding to prothrombin and prothrombin fragment 1 may reflect isomerization and/or self association of the protein. Sedimentation equilibrium studies have demonstrated that both prothrombin and its fragment 1 reversibly dimerize in the absence of Ca++.Based on this pre-existing equilibrium, a model for preferential binding of Ca++ to the dimer has been found capable of accounting quantitatively for the interaction of Ca2+ with fragment 1. This phenomenon is described by the relationship r ={pkA[A][S] (1 + kA[S])p-1 + qkc X [A]2[S](1 + kc [S])q-1}/[A] in which X (1,000 M-1) denotes the association constant for the pre-existing monomer-dimer equilibrium, and p, kA (10, 100 M-1) and q, kc (20, 2,000 M-1) are the respective stoichiometries and intrinsic binding constants for the interactions of Ca++ with monomeric and dimeric fragment 1, A. There is also evidence from exclusion chromatography and sedimentation velocity experiments that different isomeric states of prothrombin and its fragment 1 exist. It is therefore proposed that a model based on co-existence of isomeric and dimeric protein states will enable quantitative differences in the Ca++-mediated responses of fragment 1 and prothrombin to be rationalized solely in terms of differences in the relative magnitudes of equilibrium constants for the same interactions in the two systems.
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Orthner, Carolyn L., Prabir Bhattacharya, and Dudley K. Strikland. "PURIFICATION AND CHARACTERIZATION OF A PROTEIN C ACTIVATOR FROM THE VENOM OF AGKISTRODON CONTORTRIX CONTORTRIX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643813.
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There are two recent reports on the purification and properties of a protein C activator (PCA) from the venom of the Southern copperhead snalce. The purification of a 37,000 Mr nonenzymatic PCA (Martinoli and Stocker, Thrcmb. Res. 43, 253, 1976) as well as of a 20,000 Mr thrombin-like enzyme (Klein and Walker, Biochem. ,25, 4175, 1986) have been described. The purpose of this investigation was to purify and further characterize the PCA(s) from this vencm. A PCA has been isolated by sulphopropyl-Sephadex followed by gel filtration chromatography resulting in approximately a 100-fold purification with a 50% yield. PCA appeared as a single band on SDS-PAGE with an estimated Mr of 32,000 or 37,000 in the absence or presence of β-mercaptoethanol, respectively. High pressure gel permeation cinematography of PCA in Tris-buffered saline, pH 7.5 resulted in a single protein peak with a Mr of 39,000 which was coincident with activity. PCA was a potent activator of human protein C (PC) with a Km for PC of 0.6uM and a Vm of 0.02 sec-1. In addition, PCA catalyzed the arnidolysis of Tosyl-gly-pro-arg-p-nitroanilide (TGPRpNA) with a Km of 1.1 irM and a Vim of 66 sec-1. The rate of arnidolysis of five other pept idyl-arginyl-pNA substrates each tested at 1.0 mM was < 10% that of TGPRpNA. PCA was inhibited by nitrophenylguanidi-nobenzoate (NPGB), phenylmethylsulphonylflouride, D-phe-pro-arg-chloromethyi_ketone (PPACK) and soybean trypsin inhibitor indicating that PCA is a serine protease. The active site concentration of PCA as measured by NPGB titration was 90% that of the protein concentration. Measurement of the rate of PCA inhibition at varying levels of PPACK indicated that it had a Ki of 34uM .and an aUcylation rate constant of 0.09 min-1. PCA activation of PC was completely inhibited by CaC12 with an apparent Ki of 99uM. Since neither PCA arnidolysis of TGPRpNA nor inhibition by PPACK was affected by Ca2+, the effect of this metal was likely on the substrate PC. In summary, a PCA has been purified to homogeneity and has properties which are distinct from those reported. PCA premises to be a useful enzyme in studies of PC and its activation.
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Harrison, P., R. H. Saundry, and G. F. Savidge. "THE INFLUENCE OF L-LYSINE ON FACTOR VIII ELUTED FROM MATRIX BOUND DEXTRAN SULPHATE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644060.
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Factor VIII/vWF displays high affinity for matrix bound sulphate groups. Linear salt and pH gradient elution from Dextran Sulphate Sepharose at 4°C resulted in complete separation of the complex from major protein contaminants with typical yields of 70-90% vWF:Ag and vWF (RCoF). Elution in physiological calcium concentrations gave VIII and VIII:Ag yields of 35% and 65% respectively. Addition of L-Lysine (1.0M) to all buffers inhibited VIII/vWF binding, although lysine gradients (0-1.0M) gave comparable binding and elution profiles as C-1.0M NaCl, but with impaired resolution between protein moieties. However, in the presence of L-Lysine, yields of VIII and VIII:Ag were significantly improved to 80% and 100% respectively when assay standardizations with appropriate lysine concentrations were performed. Furthermore, the binding of fibrinogen could be inhibited by 0.15M L-Lysine, 0.075M NaCl in the equilibrating buffer.The presence of enzymic activity, as assessed by S-2222 and S-2238 in the eluting fractions could be abolished by the application of recryoprecipitated material pre-adsorbed with Al(OK)3 and celite. Incorporation of lysine to the buffers with the associated increase in yields further supports the potential viability of the separation principle for large scale purification of Factor VIII.
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GRUEL, Y., P. MOALIC, E. DUROUCHET, C. GUEROIS, B. DELAHOUSSE, and J. LEROY. "LEVELS OF TOTAL AND FREE PROTEIN S DURING NORMAL AND PATHOLOGICAL PREGNANCY AND IN POST-PARTUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644281.
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Levels of total and free Protein S (PS) were measured on plasmas from 28 women during normal (n = 15, mean age = 25) and pathological pregnancy (Hypertension or preeclampsia, n = 13, mean age = 27). Prepartum (PreP) samples were obtained in the third trimester between the 30th and the 40th weeks of gestation, and postpartum (PostP) blood collected in the 5 days after delivery. Total PS level was determined using Laurel 1 rocket immunoelectrophoresis (Diagnostica Stago, Asnifcres-France). Free PS was measured using the same method after precipitation of C4b-BP-Bound-PS by polyethylene glycol. C4b-Binding Protein (C4b-BP) determinations were conducted by Laurel 1 method as well. Results were expressed as a percentage (Mean ± SD) of a normal adult pool (n = 15).A significant decrease of free PS level was observed both in normal or pathological pregnancy and in postpartum. These data might be explained, by the increase of C4b-BP plasmatic level.*= p<0.05 (as compared to normal controls), **= p<0.01, ***= p<0.001 (Student´s t test).
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Fujikawa, K., T. Funakoshi, R. L. Heimark, and J. F. Tait. "HUMAN PLACENTAL ANTICOAGULANT PROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642949.
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Endothelium is important to maintain blood fluidity preventing coagulation. Glycosaminoglycan in the endothelial cell plasma membrane has been thought to prevent activation of blood coagulation. Heparin-like compound, which is a potent anticoagulant activity, has been localized on the surface of the cultured endothelial cells. Anticoagulant action associated with thrombomodulin, which is present in endothelial cells, is another mechanism to provide hemostatic nature of endothelial cells.We wondered whether any other intracellular protein(s) is involved in coagulation. We looked for such a protein(s) in cultured bovine aortic endothelial cells. We soon found an anticoagulant activity in the soluble fraction of endothelial cells and it was partially purified. This activity was adsorbed to DEAE-Sepharose and eluted from a gel filtration column in a molecular weight range of 30,000-40,000. However, limited amounts of the cells made it difficult to purify this activity. We then chose human placenta as a substitute source of this protein and have continued the purification of this anticoagulant activity.In this communication, we describe the isolation and characterization of a placental anticoagulant protein, called "PAP", which is silmilar or possible same as the endothelial anticoaguant protein. PAP was purified from the soluble fraction of human placenta by ammonium sulfate precipitation and column chromatography on DEAE-Sepharose, Sephadex G-75, and mono S (Pharmacia). Approximately 20 mg of the protein was purified from one placenta. The purified protein gave a single band by SDS polyacrylamide gel electrophoresis with a molecular weight of 36,500. This protein inhibited both kaolin- and thromboplastin-induced partial thromboplastin times of normal human plasma. It also inhibited the clotting time of platelet-rich plasma induced by factor Xa, but did not affect the thrombin activity of fibrinogen-fibrin conversion. The purified protein completely inhibited the prothrombin activation by reconstituted prothrombinase. The protein neither inhibited the amidolytic activity of factor Xa nor bound factor Xa. This protein specifically bound to phospholipid vesicles (20% phosphatidylserine and 80% phosphatidylcholine) in the presence of calcium ions. These results indicate that PAP inhibits coagulation through the binding to phospholipid vesicles. The study on the amino acid sequence of PAP is in progress in our laboratory. Surprisingly, the sequence analysis of the cyanogen bromide fragments revealed that PAP is a new member of the lipocortin or calpactin family. The sequences of several cyanogen bromide fragments of PAP aligns with the sequences of lipocortin I and II with over 50% identity.Since PAP interacts directly with phospholipid rather than factor Xa, other activation steps in the coagulation cascade, in which phospholipid is involved, are pro^|bly affected by PAP. These reactions are the activation of factor X by a complex of factor IXa-factor VIIIa-phospholipid-Ca++ and the activations of factor X and factor IX by a tissue factor-factor VIIa-Ca++ complex.Reutelingsperger et. al,, have reported the isolation of a novel inhibitor from arteries of human umbilical cord. This protein inhibited the prothrombin activation by prothrombinase. The authors proposed that the inhibition mechanism of this inhibitor was a competition with factor Xa for binding to phospholipid. This protein is very similar to PAP as to the mode of inhibition. The molecular weight of this inhibitor is 32,000, which is slightly smaller than PAP. With the limited chemical characterization of this protein, presently it is difficult to identify this inhibitor with PAP.At the present time, the physiological role and origin of PAP is not known. PAP may originate from the endothelium of placenta, because we have detected a PAP-like anticoagulant activity in bovine aortic endothelial cells. This activity and PAP were quite alike in the purification up to the gel filtration step. If PAP antibody recognizes the antigen in the endothelial cells, it is interesting to see whether PAP localizes on the surface or inside the cells. Nevertheless, if PAP is present in the endothelial cells, it may play an important role to maintain the hemostatic nature of endothelium. PAP may bind phospholipid components at injured sites, before coagulation factors come in contact with lipid components and initiate thrombolytic events.
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Farag, A. M., S. F. Bottoms, E. F. Mammen, M. Hosni, and A. Ali. "EFFECT OF ORAL CONTRACEPTIVES ON HEMOSTASIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644283.
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Retrospective statistical epidemiological studies have suggested a possible association between the ingestion of oral contraceptives (OC) and thromboembolic disease. Past analyses of the coagulation system have yielded controversial informationWe studied a cross section of 131 women taking different kinds of OC and 36 controls for changes in hemostasis. No significant differences were noted in the levels of fibrino- peptide A (RIA), platelet factor 4, 8 thromboglobulin (RIA), fibrinogen (Multistat III (MCA), clottable), antithrombin III (MCA, S-2238), α2 antiplasmin (MCA, S-2251), pre-kallikrein (MCA, S-2302) and fibronectin (MCA, immune turbi-dometric). However, plasminogen (MCA, S-2251) and protein C antigen (Laurell) levels were significantly elevated (p < 0.001 and p < 0.01), respectively)Canonical correlation analysis was used to examine correlations between hemostasis parameters measured and clinical risk factors, such as age, parity, weight, smoking, family history for thromboembolic diseases and estrogen-progesterone dose. There was a significantly negative correlation between family history for thromboembolisms and antithrombin III levels (p < 0.01). A positive correlation existed between obesity and fibrinogen and fibronectin levels (p < 0.001 for both). The hemostasis data seem to suggest that OC use does not introduce an imbalance in the hemostasis system which fosters "hypercoagulability", and that, if at all, possibly other risk factors determine the incidence of thromboembolisms in OC users. It is suggested that caution be exercised in the use of OCs in patients with a history of thromboembolic diseases and with obesity