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Academic literature on the topic 'HlyA'

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Published: 4 June 2021
Last updated: 18 February 2022

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Journal articles on the topic "HlyA"

1

Robertson, Kirstin P., C. Jeffrey Smith, Andrea M. Gough, and Edson R. Rocha. "Characterization of Bacteroides fragilis Hemolysins and Regulation and Synergistic Interactions of HlyA and HlyB." Infection and Immunity 74, no. 4 (April 2006): 2304–16. http://dx.doi.org/10.1128/iai.74.4.2304-2316.2006.

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ABSTRACT This study describes the presence of 10 hemolysin orthologs in the genome of the opportunistic human anaerobic pathogen Bacteroides fragilis, which is currently classified as a nonhemolytic bacterium. The hemolysins were designated HlyA through HlyI plus HlyIII. All cloned hemolysin genes were able to confer hemolytic activity to a nonhemolytic Escherichia coli strain on blood agar plates. Interestingly, HlyH was found to be present in the genome of the B. fragilis NCTC9343 strain but absent in strains 638R, YCH46, and Bacteroides thetaiotaomicron VPI-5482. The hemolysins HlyA, HlyB, and HlyIII were selected for further characterization. HlyA, HlyB, and HlyIII were cytolytic to erythrocytes on liquid hemolytic assay. When hlyA and hlyB were expressed together in a nonhemolytic E. coli strain, the strain showed enhanced hemolytic activity on blood agar plates. Further analysis revealed that HlyA and HlyB have synergistic hemolytic activity as detected by the liquid hemolytic assay. In addition, the two-component hemolysins HlyA and HlyB form a protein-protein complex in vivo as determined by bacterial two-hybrid system assay. The hlyB and hlyA genes are organized in an operon that is coordinately regulated by iron and oxygen. Northern blot hybridization analysis revealed that hlyBA were expressed as a bicistronic mRNA induced approximately 2.5-fold under low-iron conditions and repressed in iron-rich medium. The normal iron-regulated expression of hlyBA mRNA was lost in the furA mutant strain. In contrast, the hlyA gene was also expressed as a single mRNA in iron-rich medium, but its expression was reduced approximately threefold under low-iron conditions in a Fur-independent manner. This suggests that hlyA alone is regulated by an unidentified iron-dependent regulator. Moreover, the expression levels of hlyBA and hlyA were reduced about threefold following oxygen exposure and treatment with hydrogen peroxide. Taken together, these results suggest that iron and oxidative stress have an effect on the control of hlyBA and hlyA transcriptional levels. A hlyBA mutant was constructed, and its hemolytic activity was greatly diminished compared to those of the hlyIII mutant and parent strains. In addition, the hlyBA mutant had a significant modification in colony morphology and growth deficiency compared to the parent strain. The implications of these findings for the pathophysiology of B. fragilis in extraintestinal infections and competition in ecological systems for this organism are discussed.
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2

Pimenta, A. L., K. Racher, L. Jamieson, M. A. Blight, and I. B. Holland. "Mutations in HlyD, Part of the Type 1 Translocator for Hemolysin Secretion, Affect the Folding of the Secreted Toxin." Journal of Bacteriology 187, no. 21 (November 1, 2005): 7471–80. http://dx.doi.org/10.1128/jb.187.21.7471-7480.2005.

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ABSTRACT HlyD, a member of the membrane fusion protein family, is essential for the secretion of the RTX hemolytic toxin HlyA from Escherichia coli. Random point mutations affecting HlyA secretion were obtained, distributed in most periplasmic regions of the HlyD molecule. Analysis of the secretion phenotypes of different mutants allowed the identification of regions in HlyD involved in different steps of HlyA translocation. Four mutants, V349-I, T85-I, V334-I and L165-Q, were conditionally defective, a phenotype shown to be linked to the presence of inhibitory concentrations of Ca2+ in extracellular medium. Hly mutant T85-I was defective at an early stage in secretion, while mutants V334-I and L165-Q appeared to accumulate HlyA in the cell envelope, indicating a block at an intermediate step. Mutants V349-I, V334-I, and L165-Q were only partially defective in secretion, allowing significant levels of HlyA to be transported, but in the case of V349-I and L165-Q the HlyA molecules secreted showed greatly reduced hemolytic activity. Hemolysin molecules secreted from V349-I and V334-I are defective in normal folding and can be reactivated in vitro to the same levels as HlyA secreted from the wild-type translocator. Both V349-I and V334-I mutations mapped to the C-terminal lipoyl repeat motif, involved in the switching from the helical hairpin to the extended form of HlyD during assembly of the functional transport channel. These results suggest that HlyD is an integral component of the transport pathway, whose integrity is essential for the final folding of secreted HlyA into its active form.
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3

Sugamata, Yasuhiro, and Toshikazu Shiba. "Improved Secretory Production of Recombinant Proteins by Random Mutagenesis of hlyB, an Alpha-Hemolysin Transporter from Escherichia coli." Applied and Environmental Microbiology 71, no. 2 (February 2005): 656–62. http://dx.doi.org/10.1128/aem.71.2.656-662.2005.

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ABSTRACT Fusion proteins with an alpha-hemolysin (HlyA) C-terminal signal sequence are known to be secreted by the HlyB-HlyD-TolC translocator in Escherichia coli. We aimed to establish an efficient Hly secretory expression system by random mutagenesis of hlyB and hlyD. The fusion protein of subtilisin E and the HlyA signal sequence (HlyA218) was used as a marker protein for evaluating secretion efficiency. Through screening of more than 1.5 × 104 E. coli JM109 transformants, whose hlyB and hlyD genes had been mutagenized by error-prone PCR, we succeeded in isolating two mutants that had 27- and 15-fold-higher levels of subtilisin E secretion activity than the wild type did at 23°C. These mutants also exhibited increased activity levels for secretion of a single-chain antibody-HlyA218 fusion protein at 23 and 30°C but unexpectedly not at 37°C, suggesting that this improvement seems to be dependent on low temperature. One mutant (AE104) was found to have seven point mutations in both HlyB and HlyD, and an L448F substitution in HlyB was responsible for the improved secretion activity. Another mutant (AE129) underwent a single amino acid substitution (G654S) in HlyB. Secretion of c-Myc-HlyA218 was detected only in the L448F mutant (AE104F) at 23°C, whereas no secretion was observed in the wild type at any temperature. Furthermore, for the PTEN-HlyA218 fusion protein, AE104F showed a 10-fold-higher level of secretion activity than the wild type did at 37°C. This result indicates that the improved secretion activity of AE104F is not always dependent on low temperature.
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Stanley, Peter, Vassilis Koronakis, and Colin Hughes. "Acylation of Escherichia coli Hemolysin: A Unique Protein Lipidation Mechanism Underlying Toxin Function." Microbiology and Molecular Biology Reviews 62, no. 2 (June 1, 1998): 309–33. http://dx.doi.org/10.1128/mmbr.62.2.309-333.1998.

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SUMMARY The pore-forming hemolysin (HlyA) of Escherichia coli represents a unique class of bacterial toxins that require a posttranslational modification for activity. The inactive protoxin pro-HlyA is activated intracellularly by amide linkage of fatty acids to two internal lysine residues 126 amino acids apart, directed by the cosynthesized HlyC protein with acyl carrier protein as the fatty acid donor. This action distinguishes HlyC from all bacterial acyltransferases such as the lipid A, lux-specific, and nodulation acyltransferases, and from eukaryotic transferases such as N-myristoyl transferases, prenyltransferases, and thioester palmitoyltransferases. Most lipids directly attached to proteins may be classed as N-terminal amide-linked and internal ester-linked acyl groups and C-terminal ether-linked isoprenoid groups. The acylation of HlyA and related toxins does not equate to these but does appear related to a small number of eukaryotic proteins that include inflammatory cytokines and mitogenic and cholinergic receptors. While the location and structure of lipid moieties on proteins vary, there are common effects on membrane affinity and/or protein-protein interactions. Despite being acylated at two residues, HlyA does not possess a “double-anchor” motif and does not have an electrostatic switch, although its dependence on calcium binding for activity suggests that the calcium-myristoyl switch may have relevance. The acyl chains on HlyA may provide anchorage points onto the surface of the host cell lipid bilayer. These could then enhance protein-protein interactions either between HlyA and components of a host signal transduction pathway to influence cytokine production or between HlyA monomers to bring about oligomerization during pore formation.
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Masin, Jiri, Adriana Osickova, David Jurnecka, Nela Klimova, Humaira Khaliq, Peter Sebo, and Radim Osicka. "Retargeting from the CR3 to the LFA-1 receptor uncovers the adenylyl cyclase enzyme–translocating segment of Bordetella adenylate cyclase toxin." Journal of Biological Chemistry 295, no. 28 (May 11, 2020): 9349–65. http://dx.doi.org/10.1074/jbc.ra120.013630.

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The Bordetella adenylate cyclase toxin-hemolysin (CyaA) and the α-hemolysin (HlyA) of Escherichia coli belong to the family of cytolytic pore-forming Repeats in ToXin (RTX) cytotoxins. HlyA preferentially binds the αLβ2 integrin LFA-1 (CD11a/CD18) of leukocytes and can promiscuously bind and also permeabilize many other cells. CyaA bears an N-terminal adenylyl cyclase (AC) domain linked to a pore-forming RTX cytolysin (Hly) moiety, binds the complement receptor 3 (CR3, αMβ2, CD11b/CD18, or Mac-1) of myeloid phagocytes, penetrates their plasma membrane, and delivers the AC enzyme into the cytosol. We constructed a set of CyaA/HlyA chimeras and show that the CyaC-acylated segment and the CR3-binding RTX domain of CyaA can be functionally replaced by the HlyC-acylated segment and the much shorter RTX domain of HlyA. Instead of binding CR3, a CyaA1-710/HlyA411-1024 chimera bound the LFA-1 receptor and effectively delivered AC into Jurkat T cells. At high chimera concentrations (25 nm), the interaction with LFA-1 was not required for CyaA1-710/HlyA411-1024 binding to CHO cells. However, interaction with the LFA-1 receptor strongly enhanced the specific capacity of the bound CyaA1-710/HlyA411-1024 chimera to penetrate cells and deliver the AC enzyme into their cytosol. Hence, interaction of the acylated segment and/or the RTX domain of HlyA with LFA-1 promoted a productive membrane interaction of the chimera. These results help delimit residues 400–710 of CyaA as an “AC translocon” sufficient for translocation of the AC polypeptide across the plasma membrane of target cells.
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Russo, Thomas A., Zhengdong Wang, Bruce A. Davidson, Stacy A. Genagon, Janet M. Beanan, Ruth Olson, Bruce A. Holm, Paul R. Knight, Patricia R. Chess, and Robert H. Notter. "Surfactant dysfunction and lung injury due to theE. colivirulence factor hemolysin in a rat pneumonia model." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 3 (March 2007): L632—L643. http://dx.doi.org/10.1152/ajplung.00326.2006.

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This study tests the hypothesis that the virulence factor hemolysin (Hly) expressed by extraintestinal pathogenic Escherichia coli contributes to surfactant dysfunction and lung injury in a rat model of gram-negative pneumonia. Rats were instilled intratracheally with CP9 (wild type, Hly-positive), CP9 hlyA (Hly-minus), CP9 /pEK50 (supraphysiological Hly), or purified LPS. At 6 h postinfection, rats given CP9 had a decreased percentage content of large surfactant aggregates in cell-free bronchoalveolar lavage (BAL), decreased large aggregate surface activity, decreased PaO2/FiO2ratio, increased BAL albumin/protein levels, and increased histological evidence of lung injury compared with rats given CP9 hlyA or LPS. In addition, rats given CP9/ pEK50 or CP9 had decreased large aggregate surface activity, decreased PaO2/FiO2ratios, and increased BAL albumin/protein levels at 2 h postinfection compared with rats given CP9 hlyA. The severity of permeability lung injury based on albumin/protein levels in BAL at 2 h was ordered as CP9 /pEK50 > CP9 > CP9 hlyA > normal saline controls. Total lung titers of bacteria were increased at 6 h in rats given CP9 vs. CP9 hlyA, but bacterial titers were not significantly different at 2 h, indicating that increased surfactant dysfunction and lung injury were associated with Hly as opposed to bacterial numbers per se. Further studies in vitro showed that CP9 could directly lyse transformed pulmonary epithelial cells (H441 cells) but that indirect lysis of H441 cells secondary to Hly-induced neutrophil lysis did not occur. Together, these data demonstrate that Hly is an important direct mediator of surfactant dysfunction and lung injury in gram-negative pneumonia.
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Wang, Changying, Qianqian Li, Junqiang Lv, Xuan Sun, Yang Cao, Kaiyuan Yu, Chunhui Miao, Zhi-Song Zhang, Zhi Yao, and Quan Wang. "Alpha-hemolysin of uropathogenic Escherichia coli induces GM-CSF-mediated acute kidney injury." Mucosal Immunology 13, no. 1 (November 12, 2019): 22–33. http://dx.doi.org/10.1038/s41385-019-0225-6.

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Abstract Uropathogenic Escherichia coli (UPEC) is the leading cause of urinary tract infections (UTIs), inducing acute pyelonephritis and may result in permanent renal scarring and failure. Alpha-hemolysin (HlyA), a key UPEC toxin, causes serious tissue damage; however, the mechanism through which HlyA induces kidney injury remains unclear. In the present study, granulocyte-macrophage colony-stimulating factor (GM-CSF) secreted by renal epithelial cells was upregulated by HlyA in vitro and in vivo, which induced M1 macrophage accumulation in kidney, and ADAM10 was found involved in HlyA-induced GM-CSF. Macrophage elimination or GM-CSF neutralization protected against acute kidney injury in mice, and increased GM-CSF was detected in urine of patients infected by hlyA-positive UPEC. In addition, HlyA was found to promote UPEC invasion into renal epithelial cells by interacting with Nectin-2 in vitro. However, HlyA did not affect bacterial titers during acute kidney infections, and HlyA-induced invasion did not contribute to GM-CSF upregulation in vitro, which indicate that HlyA-induced GM-CSF is independent of bacteria invasion. The role of GM-CSF in HlyA-mediated kidney injury may lead to novel strategies to treat acute pyelonephritis.
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Zaitseva, J., S. Jenewein, C. Oswald, T. Jumpertz, I. B. Holland, and L. Schmitt. "A molecular understanding of the catalytic cycle of the nucleotide-binding domain of the ABC transporter HlyB." Biochemical Society Transactions 33, no. 5 (October 26, 2005): 990–95. http://dx.doi.org/10.1042/bst0330990.

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The ABC transporter (ATP-binding-cassette transporter) HlyB (haemolysin B) is the central element of a type I secretion machinery, dedicated to the secretion of the toxin HlyA in Escherichia coli. In addition to the ABC transporter, two other indispensable elements are necessary for the secretion of the toxin across two membranes in a single step: the transenvelope protein HlyD and the outer membrane protein TolC. Despite the fact that the hydrolysis of ATP by HlyB fuels secretion of HlyA, the essential features of the underlying transport mechanism remain an enigma. Similar to all other ABC transporters, ranging from bacteria to man, HlyB is composed of two NBDs (nucleotide-binding domains) and two transmembrane domains. Here we summarize our detailed biochemical, biophysical and structural studies aimed at an understanding of the molecular principles of how ATP-hydrolysis is coupled to energy transduction, including the conformational changes occurring during the catalytic cycle, leading to substrate transport. We have obtained individual crystal structures for each single ground state of the catalytic cycle. From these and other biochemical and mutational studies, we shall provide a detailed molecular picture of the steps governing intramolecular communication and the utilization of chemical energy, due to ATP hydrolysis, in relation to resulting structural changes within the NBD. These data will be summarized in a general model to explain how these molecular machines achieve translocation of molecules across biological membranes.
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Jumpertz, Thorsten, Christian Chervaux, Kathleen Racher, Maria Zouhair, Mark A. Blight, I. Barry Holland, and Lutz Schmitt. "Mutations affecting the extreme C terminus of Escherichia coli haemolysin A reduce haemolytic activity by altering the folding of the toxin." Microbiology 156, no. 8 (August 1, 2010): 2495–505. http://dx.doi.org/10.1099/mic.0.038562-0.

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Escherichia coli haemolysin A (HlyA), an RTX toxin, is secreted probably as an unfolded intermediate, by the type I (ABC transporter-dependent) pathway, utilizing a C-terminal secretion signal. However, the mechanism of translocation and post-translocation folding is not understood. We identified a mutation (hlyA99) at the extreme C terminus, which is dominant in competition experiments, blocking secretion of the wild-type toxin co-expressed in the same cell. This suggests that unlike recessive mutations which affect recognition of the translocation machinery, the hlyA99 mutation interferes with some later step in secretion. Indeed, the mutation reduced haemolytic activity of the toxin and the activity of β-lactamase when the latter was fused to a C-terminal 23 kDa fragment of HlyA carrying the hlyA99 mutation. A second mutant (hlyAdel6), lacking the six C-terminal residues of HlyA, also showed reduced haemolytic activity and neither mutant protein regained normal haemolytic activity in in vitro unfolding/refolding experiments. Tryptophan fluorescence spectroscopy indicated differences in structure between the secreted forms of wild-type HlyA and the HlyA Del6 mutant. These results suggested that the mutations affected the correct folding of both HlyA and the β-lactamase fusion. Thus, we propose a dual function for the HlyA C terminus involving an important role in post-translocation folding as well as targeting HlyA for secretion.
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Reimann, Sven, Gereon Poschmann, Kerstin Kanonenberg, Kai Stühler, Sander H. J. Smits, and Lutz Schmitt. "Interdomain regulation of the ATPase activity of the ABC transporter haemolysin B from Escherichia coli." Biochemical Journal 473, no. 16 (August 11, 2016): 2471–83. http://dx.doi.org/10.1042/bcj20160154.

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Type 1 secretion systems (T1SS) transport a wide range of substrates across both membranes of Gram-negative bacteria and are composed of an outer membrane protein, a membrane fusion protein and an ABC (ATP-binding cassette) transporter. The ABC transporter HlyB (haemolysin B) is part of a T1SS catalysing the export of the toxin HlyA in E. coli. HlyB consists of the canonical transmembrane and nucleotide-binding domains. Additionally, HlyB contains an N-terminal CLD (C39-peptidase-like domain) that interacts with the transport substrate, but its functional relevance is still not precisely defined. In the present paper, we describe the purification and biochemical characterization of detergent-solubilized HlyB in the presence of its transport substrate. Our results exhibit a positive co-operativity in ATP hydrolysis. We characterized further the influence of the CLD on kinetic parameters by using an HlyB variant lacking the CLD (HlyB∆CLD). The biochemical parameters of HlyB∆CLD revealed an increased basal maximum velocity but no change in substrate-binding affinity in comparison with full-length HlyB. We also assigned a distinct interaction of the CLD and a transport substrate (HlyA1), leading to an inhibition of HlyB hydrolytic activity at low HlyA1 concentrations. At higher HlyA1 concentrations, we observed a stimulation of the hydrolytic activities of both HlyB and HlyB∆CLD, which was completely independent of the interaction of HlyA1 with the CLD. Notably, all observed effects on ATPase activity, which were also analysed in detail by mass spectrometry, were independent of the HlyA1 secretion signal. These results assign an interdomain regulatory role for the CLD modulating the hydrolytic activity of HlyB.
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Dissertations / Theses on the topic "HlyA"

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González, Antonio Pablo. "IDENTIFICACIÓN DE LOS GENES: Stx1, Stx2, eaeA Y hlyA, EN CEPAS DE Escherichia coli AISLADAS DE CANALES Y CARNE PROCESADA DE OVINOS." Tesis de Licenciatura, Universidad Autónoma del Estado de México, 2018. http://hdl.handle.net/20.500.11799/94389.

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E. coli productora de toxina shiga (ECST) y E. coli enterohemorrágica (ECEH) pertenecen a los grupos patógenos de Escherichia coli causantes de enfermedades diarreicas. La presencia de ECST y ECEH en estas enfermedades diarreicas se atribuye principalmente al consumo de vegetales y carnes provenientes de bovinos y ovinos contaminados con estos grupos patógenos y que actualmente se encuentran dentro de las etiologías más importantes del grupo de Enfermedades Trasmitidas por Alimentos (ETA). ECST y ECEH presentan los genes Stx1, Stx2, eaeA y hlyA que codifican a proteínas con cualidades toxicas para el hombre ocasionando graves enfermedades como la colitis hemorrágica (CH), síndrome urémico hemolítico (SUH) y purpura trombocitopénica trombótica (PTT). Por lo tanto, el objetivo de esta investigación es identificar la presencia de los genes Stx1, Stx2, eaeA y hlyA en los aislamientos de E. coli obtenidos de canales de ovinos en rastro municipal de Capulhuac y en carne procesada de ovinos provenientes de la ciudad de Toluca. Se analizaron 71 aislados de E. coli para la identificación genes característicos de los grupos patógenos de ECST y ECEH. Los resultados encontrados indican: los 18 aislamientos de E. coli obtenidas de la carne procesada de ovinos no se identifica la presencia los genes analizados y, por otro lado, de los 53 aislados obtenidos de las canales de ovinos en el rastro municipal de Capulhuac, México, amplificaron los genes Stx1 en 3.7% (2/53), Stx2 en 5.6% (3/53), eaeA en 3.7% (2/53) y hlyA en 3.7% (2/53). De tal manera, que estas canales puede ser una fuente potencial de infección por E. coli productora de toxina shiga y E. coli enterohemorrágica.
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Holden, James Anthony, and jamesholden@netspace net au. "Vaccination Strategies for the Prevention of Swine Dysentery." RMIT University. Applied Sciences, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20070112.122102.

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The SmpA outer membrane lipoprotein of B. hyodysenteriae has several characteristics that indicate the potential to protect against swine dysentery (SD). It localises to the outer membrane and antibodies directed against SmpA can prevent the growth of B. hyodysenteriae in vitro. There is some variation observed in the distribution and expression of the SmpA lipoprotein, suggesting that vaccination with SmpA may not provide protection against challenge with a heterologous B. hyodysenteriae strain. This study has characterised the variation at the smpA locus, and in the process has identified a novel gene, smpB. There is very low similarity between smpB and smpA, with the exception of an identical lipoprotein signal sequence. This suggests that SmpB may be translocated to the outer membrane of B. hyodysenteriae in a similar fashion to SmpA. The results described in this thesis indicate that strains of B. hyodysenteriae harbour either smpA or smpB, but not both, explaining the earlier results of Turner et al. (1991). The presumed outer membrane location of SmpB lead to further investigations into its potential to protect mice from infection with B. hyodysenteriae. Swine Dysentery is a inflammatory disease of the swine colon. Therefore it is believed that a mucosal immune response may provide increased protection against challenge. In this study, vaccination of mice with recombinant SmpB elicited high levels of serum antibodies, induced the production of Interleukin-4 producing T lymphocytes and decreased the observed histological effects after challenge with virulent B. hyodysenteriae. In efforts to increase the protected conferred by vaccination with SmpB, recombinant Salmonella typhimurium STM-1 vaccines were created to express SmpB or deliver DNA vaccines encoding SmpB. Vaccination with these recombinant Salmonella vectors did not induce a measurable SmpB specific immune response. Macrophage survival and plasmid stability studies indicated that this was due to instability of the expression plasmids in STM-1. Although SmpB will only ever protect against strains of B. hyodysenteriae harbouring smpB, these results indicate that with further research, SmpB (and SmpA) may contribute to protection from SD. Toxin production is an important aspect of the pathogenesis of many pathogenic bacteria. Vaccination with attenuated toxins is commonly used to prevent disease. In this study, the B. hyodysenteriae â-haemolysin HlyA was used to vaccinate mice to determine the protection induced after challenge. Vaccination of mice with recombinant HlyA induced significant levels of serum antibodies and lowered the observed pathological effects after challenge of vaccinated mice with virulent B. hyodysenteriae. In an attempt to increase the mucosal immune response and therefore the protection afforded after vaccination with HlyA, recombinant S. typhimurium STM-1 strains were created to express HlyA or deliver DNA vaccines encoding HlyA. Similar to the recombinant STM-1 vaccines expressing SmpB, a HlyA specific immune response was not observed by ELISA or ELISPOT analysis. Plasmid stability trials revealed that the inability to induce a detectable HlyA specific immune response by recombinant STM-1 vaccination may be due to ins tability of the plasmids. Outer membrane proteins are often important components of vaccines against bacterial and viral pathogens. Considering the variation observed in the smpA locus in this study resulting in the identification of smpB, further investigation into the distribution and conservation of outer membrane encoding genes in B. hyodysenteriae strains was undertaken. In particular, the blpAEFG, vspABCD and vspEFGH clusters were analysed for their distribution. It was demonstrated that genes that are B. hyodysenteriae specific (vspABCD and vspEFGH) displayed higher levels of polymorphism than those that are distributed amongst non-pathogenic species, such as B. innocens (which contains blpAEFG). This suggests that the variation in the vspABCD and vspEFGH clusters amongst B. hyodysenteriae strains may be a result of the exposure to the host immune system. Further investigation was undertaken by PFGE analysis and 2D-gel electrophoresis, to analyse genomic and proteomic variation at a global level. Although strains of B. hyodyse nteriae produced several different electrophoretic types (ET) upon PFGE analysis, only limited correlation between the PFGE ET, the polymorphisms in vspABCD and vspEFGH and the presence of smpA/smpB were observed. 2D-gel electrophoresis analysis of outer membrane preparations of two B. hyodysenteriae strain revealed several distinct differences in the outer membrane between B. hyodysenteriae strains. The observed differences in the proteins contained in the outer membrane of B. hyodysenteriae is important for vaccine design, as the induction of cross protection between strains of B. hyodysenteriae is essential for a effective vaccine.
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Diabaté, Mamady. "Étude des relations fonctionnelles entre les toxines CNF1 et alpha-hémolysine (HlyA) des Escherichia coli uropathogènes." Nice, 2011. http://www.theses.fr/2011NICE4039.

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Le facteur cytotoxique nécrosant-1 (CNF1) et l’hémolysine-alpha (HlyA) sont les deux toxines majeures des Escherichia coli uropathogènes (UPEC), premier agent étiologique des infections du tractus urinaire (ITU) et principale cause de bactériémie à E. Coli. Comme plusieurs autres facteurs de virulence, ces toxines ont été associées à l’ITU en raison de leur grande prévalence dans les UPEC par rapport aux E. Coli fécaux, respectivement 30 % et 0. 9 % pour CNF1. Cependant, leurs rôles dans la physiopathologie de l’infection urinaire reste imprécis. Dans un modèle murin de bactériémie, nous avons pu montrer pour la première fois que CNF1 favorisait la réponse immunitaire innée de l’hôte entraînant l’élimination rapide des bactéries. Nous avons aussi montré que CNF1 présente un effet pro-inflammatoire aussi bien in vitro sur les monocytes qu’in vivo chez la souris. Un effet qui est au détriment de la survie des bactéries dans le sang. Nous montrons que HlyA présente un effet cytotoxique sur les monocytes. La mort des monocytes, induite par HlyA, empêche la production des cytokines pro-inflammatoires induites par CNF1. Nous avons relié cet effet au maintien des UPEC dans le sang. Dans le contexte de la bactériémie, ces deux toxines ont donc des effets opposés sur la survie des bactéries dans le sang. CNF1 apparaît donc comme un facteur d’avirulence dont l’effet est antagonisé par celui de HlyA. La sécrétion de CNF1 n’est pas connue, et on observe une grande divergence dans les résultats des quelques études faites sur ce sujet. Partant de l’observation du lien permanent du gène cnf1 au sein de l‘opéron hly dans les souches CNF1 (+), nous avons émis l’hypothèse que leur système de sécrétion pouvait être commun. Nos résultats montrant l’absence de CNF1 dans le périplasme nous a confortés dans l’idée que CNF1 pourrait être directement secrété dans le milieu extérieur par le système de sécrétion de type-1 décrit pour HlyA. Nous démontrons que l’absence d’HlyB (l’ATPase du système du système de sécrétion de HlyA) a un effet de blocage sur l’induction de mortalité des cellules THP-1 qu’induit CNF1 et inhibe la translocation d’une protéine de fusion CNF1-beta-lactamase dans le cytosol des THP-1. Sachant que la délétion d’HlyB n’affecte pas la production de CNF1, HlyB pourrait intervenir dans la sécrétion de CNF1. Ce travail a permis de mettre en évidence des interactions fonctionnelles entre deux facteurs de virulence toxiques des UPEC (CNF1 et HylA), et aussi le rôle de HlyB dans la translocation de CNF1 dans les THP-1
Cytotoxic necrotizing factor 1 (CNF1) and alpha-hemolysin (HlyA) are two major toxins of uropathogenic Escherichia coli (UPEC). UPEC are the major cause of urinary tract infection (UTI) and represent one of the main agents of bacteremia. These two toxins are usually associated to UTI because of their consistent presence in UPEC as compared to commensal strains of E. Coli. Nevertheless, their physiological involvement in UTI remains unclear. Using a mouse model of bacteremia, we showed that CNF1 by its pro-inflammatory property can trigger host immune responses, thus allowing bacterial clearing from the blood by phagocytic cells. We also demonstrated that HylA has a cytotoxic effect on monocytes. This cytotoxic effect will counteract the production of pro-inflammatory cytotoxines induced by CNF1, and will allow the persistence of bacteria in mouse blood. According to this observation, we concluded that during bacteremia, CNF1 and HlyA have an opposite effect on bacterial persistence in the blood. We have developed a technique that allowed us to observe the effect of CNF1 in vitro, by directly infecting monocytes with CNF1 producing UPEC. We thus demonstrated that CNF1 can induce monocytes death during infection. Using a plasmid which produced a chimeric protein (CNF1-bêta-lactamase), we demonstrated that CNF1 can translocate from the bacterial cytoplasmic domain to the monocyte cytosol during infection. This work evidenced a functional interplay between two major virulence factors (CNF1 and HylA) as well as the effect of CNF1 on monocytes
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Ha, Thi Quyen. "Analysis of gene encoding haemolysin A of Vibrio cholerae isolated in Vietnam." Technische Universität Dresden, 2018. https://tud.qucosa.de/id/qucosa%3A33123.

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Vibrio cholerae is the cholera causing agent, divided into two biotypes, including the classical biotype and ElTor biotype. Both of these biotypes caused cholera epidemics in the world. The classical biotype caused 6th cholera pandemic (from 1921 to 1961), and ElTor biotype caused 7th cholera pandemic (from 1961 to the 70s). Haemolysin A, a hemolytic protein of V. cholerae ElTor biotype, is encoded by the hlyA gene. This gene is often used for analyzing genetic relationship between strains in the same species or between species in the same Vibrio genus. Results of analyzing nucleotide and amino acid sequences of hlyA gene of V. cholerae strain causing cholera in Vietnam (named hlyA.VN) showed that: the hlyA.VN gene sequence was similar to the hlyA gene sequences of V. cholerae strains of the 6thand 7thcholera epidemics. The hlyA gene of the 6th cholera epidemic strain was deficient in 11 nuleotides (this deficiency leading to the loss of 4 amino acids in the haemolysin A protein) comparing to hlyA.VN gene and hlyA gene of the 7th cholera epidemic strain. The results of genetic distance analysis as well as phylogenetic tree construction also confirmed V. cholerae causing cholera in Vietnam was closely relationship to the strains causing cholera pandemics in the world. It is great significance for the surveillance of molecular epidemiology to prevent cholera effectively.
Vibrio cholerae là tác nhân gây bệnh tả, được chia thành hai typ sinh học, đó là typ sinh học cổ điển và typ sinh học ElTor. Cả hai typ này đã từng gây ra các đại dịch tả trên thế giới. Typ sinh học cổ điển đã từng gây ra đại dịch tả lần thứ 6 (từ năm 1921 đến 1961), còn typ sinh học ElTor đã từng gây ra đại dịch tả lần thứ 7 (từ 1961 đến những năm 70). Haemolysin A, một protein có chức năng làm tan máu của V. cholerae typ sinh học ElTor, được mã hóa bởi gen hlyA. Gene này thường được sử dụng cho các phân tích quan hệ di truyền giữa các chủng trong cùng một loài V. cholerae hay giữa các loài trong cùng một chi Vibrio. Kết quả phân tích trình tự nucleotide và axit amin gen hlyA của chủng V. cholerae gâybệnh ở Việt Nam (hlyA.VN) cho thấy: trình tự gen hlyA.VN có sự tương đồng lớn với trình tự gen hlyA của chủng gây đại dịch tả 6 và 7. Gen hlyA của chủng gây đại dịch tả 6 bị thiếu hụt 11 nuleotide (sự thiếu hụt này dẫn tới sự mất đi 4 axit amin trong phân tử haemolysin A) so với gen hlyA.VN và gene hlyA của chủng gây đại dịch tả 7. Kết quả phân tích khoảng cách di truyền cũng như xây dựng cây phát sinh chủng loại cũng đã khẳng định: chủng gây bệnh ở Việt Nam có quan hệ rất gần với các chủng gây đại dịch tả trên thế giới. Nhận định này có ý nghĩa rất lớn đối với công tác giám sát dịch tễ học phân tử để ngăn chặn bệnh tả hiệu quả.
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Guzmán-Verri, Caterina. "Virulence mechanisms of two Gram negative bacteria : studies on Escherichia coli hemolysin HlyA and on the interaction of Brucella abortus with non-phagocytic cells /." Stockholm : Karolinska Univ. Press, 2002. http://diss.kib.ki.se/2002/91-7349-114-4.

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Franco, Roger Teixeira. "Caracterização de amostras de Escherichia coli eae positivas isoladas de crianças com diarreia aguda e sem diarreia em Belo Horizonte: tipagem de intimina e pesquisa de hlyA, iha e toxB." Universidade Federal de Minas Gerais, 2012. http://hdl.handle.net/1843/ENMS-8RWQMM.

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Infectious diarrhea is still a main cause of morbidity and mortality among children from the less developed areas of the world. Among several etiologic agents, a group of diarrheagenic Escherichia coli (DEC) named attaching and effacing E. coli (AEEC), associated to the genesis of the intimin-mediated A/E lesion in enterocytes, should be mentioned. AEEC includes typical (tEPEC) and atypical (aEPEC) subgroups of enteropathogenic E. coli (EPEC) and the pathotype enterohemorrhagic E. coli (EHEC) that also expresses shiga toxin. All of them, mainly aEPEC, are genetically diverse, especially in regard to the expression of genetic markers of virulence. For these reasons, we carried out this investigation aiming to evaluate the distribution of intimin types and hlyA, iha, and toxB, that encode bacterial adhesins and toxins, in 561 AEEC strains. The strains were obtained from 110 children aged up to 69 months with acute diarrhea and without diarrhea, who searched for assistance at Hospital Infantil João Paulo II/FHEMIG, Belo Horizonte, MG, from 2004 to 2007. Beta was the most prevalent intimin genotype in both tEPEC and aEPEC. Gamma was the most common type among EHEC. Intimin kappa was not found in the population studied. Temporal shifts in the distribution of intimin genotypes were observed: type beta prevalence decreased steadly and epsilon intimin emerged from 2006 on. A higher prevalence of intimin iota was detected among children aged 13 to 24 months. Around 10% of AEEC strains could not have their intimin identified. Seasonality and association with gender and diarrhea were not observed. hlyA, iha and toxB were found in less than 50% of the AEEC strains, but were found to be harbored by all AEEC pathotypes. Our findings corroborate the existence of differences in geographic distribution of the virulence factors encoded by eae, hlyA, iha, and toxB among AEEC. They also support the hypothesis that this pathotype comprises a genetically diverse DEC group, specially the subtype aEPEC.
Diarreia infecciosa aguda continua sendo uma das principais causas de morbidade e mortalidade em crianças, especialmente nas regiões menos favorecidas do planeta. Entre os diferentes agentes etiológicos da doença, merece menção, pela prevalência elevada e gravidade da doença, o grupo de Escherichia coli diarreiogência (DEC) denominado attaching and effacing E. coli (AEEC), caracterizado pela formação da lesão A/E (attaching and effacing) nos enterócitos, mediada pela intimina. Este grupo inclui os subgrupos típico e atípico de E. coli enteropatogênica (EPEC) e o tipo patogênico denominado E. coli enteremorrágica (EHEC) que, além de intimina, expressa toxinas shiga. Estes patotipos apresentam grande diversidade genética, inclusive no que se refere à expressão de marcadores de virulência, razões pelas quais este estudo foi desenvolvido com o objetivo de avaliar a distribuição dos tipos genéticos de intimina e dos genes hlyA, iha e toxB, que codificam adesinas e toxina bacterianas. Foram estudadas 561 amostras de AEEC obtidas de 110 crianças com até 69 meses de idade, com diarreia aguda e sem diarreia, atendidos, entre 2004 e 2007, no Hospital Infantil João Paulo II/FEMIG, Belo Horizonte, MG. Intimina beta foi o tipo mais prevalente, detectada principalmente em EPEC típica e atípica. Intimina gama foi a mais comum em EHEC. Intimina kapa não foi detectada na população estudada. Foi observada variação temporal na distribuição dos tipos de intimina, com declínio de beta e emergência de épsilon ao longo do período de estudo. A detecção da intimina iota concentrou-se em crianças com idade entre 13 a 24 meses. Aproximadamente 10% das amostras de AEEC no nosso meio não tiveram sua intimina identificada. Nenhum tipo genético de intimina estava associado com sexo, estação do ano, e presença de diarreia. Os marcadores de virulência hlyA, iha e toxB foram detectados em menos da metade das amostras de AEEC, sendo carreados por todos os tipos patogênicos incluídos neste grupo de DEC. Nossos resultados confirmam a existência de diferenças geográficas na distribuição dos marcadores de virulência de AEEC e a grande diversidade genética deste grupo de DEC, especialmente aEPEC e podem contribuir para o delineamento de estratégias de prevenção e controle da diarreia associada a AEEC.
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Ping, Ivan Chang Kok. "HLA performance measurement." Thesis, Monterey, Calif. : Springfield, Va. : Naval Postgraduate School ; Available from National Technical Information Service, 2000. http://handle.dtic.mil/100.2/ADA376484.

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Thesis (M.S. in Modeling, Virtual Environments and Simulation (MOVES))--Naval Postgraduate School, March 2000.
Thesis advisor(s): Zyda, Michael ; Bachmann, Eric. "March 2000." Includes bibliographical references (p. 77). Also available in print.
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Lachaud, Laurence. "Reconnaissance allogénique HLA." Montpellier 1, 1995. http://www.theses.fr/1995MON11145.

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FODIL, NASSIMA. "Nouvelle diversite hla." Université Louis Pasteur (Strasbourg) (1971-2008), 2001. http://www.theses.fr/2001STR1A001.

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Au cours de ces 10 dernieres annees, de nombreux genes homologues aux molecules de classes i du complexe majeur d'histocompatibilite (cmh) ont ete mis en evidence. Ils exhibent, pour la plupart, une expression tissulaire restreinte et ne semblent pas avoir pour fonction la presentation peptidique aux cellules t. La famille des genes mic (mhc class i chain-related genes) a recemment ete caracterisee au sein meme de la region de classe i du cmh. Elle se compose de 2 genes fonctionnels (mica et micb) ainsi que de 5 pseudogenes (micc-g). Les travaux presentes dans cette these decrivent le polymorphisme inattendu des genes mica et micb, se rapprochant a terme de celui des genes classiques hla-a, -b et -c, les loci les plus polymorphes du genome humain. Nos investigations ont egalement permis de mettre en evidence un fort desequilibre de liaison entre mica et le gene hla le plus proche, hla-b. De part l'interaction de mica et micb avec certains recepteurs des cellules t et nk, l'evaluation de l'implication du gene mica dans 3 pathologies a caractere autoimmun a ete effectuee. Au vu des resultats obtenus, mica ne semble pas etre implique dans l'etiopathogenese de la sclerose en plaques et dans celle de la maladie de coeliaque, toutefois son role dans la physiopathologie de la maladie de behcet merite approfondissement sur le plan fonctionnel. Enfin, l'analyse phenotypique et genotypique des individus naturellement deficients en mica/b a permis de montrer qu'il n'y a aucune alteration du nombre des lymphocytes b, t et nk en comparaison avec les individus non-deletes ; l'analyse des pseudogenes mic n'indique aucune mutation gain de fonction. L'existence meme de ces individus devrait permettre de dissequer la fonction de ces molecules in vivo.
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Brown, Juliette. "HLA-DR and HLA-DQ polymorphism and associations in different populations." Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287875.

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Books on the topic "HlyA"

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Boegel, Sebastian, ed. HLA Typing. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8546-3.

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Hringnun hla mawi: Hla hmanga hringnun thlirna lehkhabu. Aizawl: Hriatpuia Pa, 2014.

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Honda, Yutaka, and Takeo Juji, eds. HLA in Narcolepsy. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83387-8.

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Lee, John, ed. The HLA System. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3454-8.

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Dupont, Bo, ed. Immunobiology of HLA. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1.

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Dupont, Bo, ed. Immunobiology of HLA. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0.

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Ping, Ivan Chang Kok. HLA performance measurement. Monterey, Calif: Naval Postgraduate School, 2000.

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Hmar hla suina. [Churachandpur, Manipur]: L. Rokung, 1985.

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International histocompatibility workshop and conference (12 1996 Saint-Malo, Ille-et-Vilaine / Paris). HLA, genetic diversity of HLA, functional and medical implication. Sèvres: EDK, 1997.

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Hla thu hman dan. Aizawl: Hausanga Hauzel, 2013.

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Book chapters on the topic "HlyA"

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Bodmer, Walter F. "HLA 1987." In Immunobiology of HLA, 1–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_1.

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Mervart, H. "HLA Subtypes." In Realm of Tolerance, 94–108. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74712-0_12.

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Stöcker, W. "HLA-Allele." In Springer Reference Medizin, 1125–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1459.

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Kleesiek, K., C. Götting, J. Diekmann, J. Dreier, and M. Schmidt. "HLA-Antikörper." In Springer Reference Medizin, 1126–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1460.

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Krüger, C., and W. Stöcker. "HLA-B27." In Springer Reference Medizin, 1128–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1462.

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Kleesiek, K., C. Götting, J. Diekmann, J. Dreier, and M. Schmidt. "HLA-Crossmatch." In Springer Reference Medizin, 1129. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1463.

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Renz, H., and B. Gierten. "HLA-DR." In Springer Reference Medizin, 1130–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1464.

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Stöcker, W. "HLA-Allele." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_1459-1.

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Kleesiek, K., C. Götting, J. Diekmann, J. Dreier, and M. Schmidt. "HLA-Antikörper." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1460-1.

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Krüger, C., and W. Stöcker. "HLA-B27." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_1462-1.

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Conference papers on the topic "HlyA"

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Wu, Lingwei, Quanjun Liu, Zhongwei Wu, and Zuhong Lu. "Detection of hlyA Gene of Listeria Monocytogenes with Electrochemical DNA Biosensor." In 2008 2nd International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2008. http://dx.doi.org/10.1109/icbbe.2008.95.

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Slukin, P. V., L. V. Kolupaeva, N. A. Slukina, N. N. Podgornaja, and N. K. Fursova. "VIRULENCE OF UROPATHOGENIC ESCHERICHIA COLI CARRYING HLYA AND CNF1 GENES FOR GALLERIA MELLONELLA LARVAE." In Molecular Diagnostics and Biosafety. Federal Budget Institute of Science 'Central Research Institute for Epidemiology', 2020. http://dx.doi.org/10.36233/978-5-9900432-9-9-241.

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Kieffer, N., M. Titeux, A. Henri, J. Breton-Gorius, and W. Vainchenker. "MEGAKARYOCYTIC ORIGIN OF PLATELET HLA CLASS I ANTIGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643546.

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The existence of HLA class I antigens on human platelets is well established. However, several authors have suggested that platelet HLA antigens are not integral membrane components but are acquired from soluble plasma sources and adsorbed to the platelet surface.In the present study, we used the monoclonal antibody W6/32, directed against a monomorphic epitope of the HLA class I antigen for the immunochemical characterization of platelet HLA. Immunoprecipitation experiments, performed after in vitro metabolic radiolabeling of human platelets revealed a band of molecular weight 44,000 identical to that precipitated from metabolic labeled U937 or HEL cells. When the same antibody was tested by indirected immunofluorescence in a double labeling technique on in vitro cultures of human megakaryocytes, performed in the absence of human serum in the culture medium, megakaryocytes identified by an anti-vWF MoAb revealed a membrane staining with W6/32 identical to that observed on other bone marrow cells, e.g. macrophages. Our results provide evidence that platelet HLA has a megaka-ryocytic origin and that residual biosynthesis of HLA antigen does still occur in circulating platelets. However, our results do not exclude the ability of human platelets to adsord circulating HLA class I antigen from plasma.
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Allen, Robert. "HLA." In Joint proceedings of the second international software architecture workshop (ISAW-2) and international workshop on multiple perspectives in software development (Viewpoints '96). New York, New York, USA: ACM Press, 1996. http://dx.doi.org/10.1145/243327.243626.

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Galli, Emanuele, Gaetano Cavarretta, and Salvatore Tucci. "HLA-OMNET++: An HLA Compliant Network Simulator." In 2008 12th IEEE International Symposium on Distributed Simulation and Real-Time Applications (DS-RT). IEEE, 2008. http://dx.doi.org/10.1109/ds-rt.2008.44.

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Liu, Pingan, Lei Li, Wei Heng, and Boyuan Wang. "HLDA based text clustering." In 2012 IEEE 2nd International Conference on Cloud Computing and Intelligence Systems (CCIS). IEEE, 2012. http://dx.doi.org/10.1109/ccis.2012.6664628.

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Silva, Marcio N. P., Luís Cristóvão M. S. Pôrto, Leandro A. J. Marzulo, and Alexandre C. Sena. "Estudo e Implementação de um Sistema Customizável para Controle Laboratorial para o Processo de Tipificação HLA." In Anais do Simpósio Brasileiro de Computação Aplicada à Saúde. Sociedade Brasileira de Computação - SBC, 2019. http://dx.doi.org/10.5753/sbcas.2019.6247.

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Uma compatibilidade favorável entre doador/receptor diminui con- sideravelmente a chance de rejeição em transplantes. Nos humanos o grupa- mento gênico do DNA responsável pelo sistema imune é denominado HLA. Tes- tes laboratoriais foram desenvolvidos para identificar esse grupamento e um deles é a tipificação HLA. Essas avaliações precisam ser realizadas por labo- ratórios especializados e nesse contexto o Laboratório de Histocompatibilidade e Criopreservação da Universidade do Estado do Rio de Janeiro (HLA-UERJ) tem posição de destaque no setor. O processo como um todo é complexo e ex- tenso, envolvendo diversas equipes e setores do laboratório, com uma intensa troca de informações. Os dados tratados são extremamente importantes o que demanda um rı́gido controle para garantir a rastreabilidade e confiabilidade dos resultados. Nesse contexto, o objetivo deste trabalho é mapear todo o pro- cesso de tipificação HLA e apresentar e implementar um sistema customizável para gerenciamento de processos laboratoriais.
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Reisner, H. M., E. A. Reisner, D. D. Kostyu, B. C. Lubahn, C. McMillan, and G. C. White. "POSSIBLE ASSOCIATION OF HLA AND Gm WITH THE ALLOIMMUNE RESPONSE TO FVIII." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644021.

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Between 5 and 15% of individuals with severe hemophilia A are at risk of developing inhibitors (alloantibodies) to FVIII. Genetic factors are important in determining risk, but the nature of these factors is poorly defined. The human immune response to a wide variety of antigens has been associated with the HLA and/or Gm loci. Hence, we have investigated polymorphisms at these two loci in hemophilia A patients with and without inhibitors.DATA SET: To date 127 hemophiliacs have been Gm or HLA typed. Forty-eight are inhibitor positive (I+) based on positive FVIII neutralization assays. This represents about 70% of all I+ hemophiliacs seen at UNC. To prevent familial bias, one member of each of 14 pairs of close relatives was randomly removed from the Data Set without regard to inhibitor status (Data Set 1). Twenty non-white individuals were also removed to constitute Data Set 2. GM TYPING: Samples were typed for Gm antigens 1, 3 and 5. Phenotype frequencies in Data Sets 1 and 2 did not deviate from expected values. I+ hemophiliacs showed an excess of Gm 1 in both Data Sets which was of possible significance (p = .13 and .21 respectively by chi square). Reanalysis of Data Set 2 to include only I- individuals without evidence of either circulating VIII:C or VIII:CAg (N=58) yields a p of .12. HLA TYPING: Analysis on 77 individuals in Data Set 2 (21 I+, 56 I-) has been done. In preliminary typing of HLA A, B, C, DR and DQ no significant differences in antigen frequency were found between the I+ and I- groups. INTERACTION BETWEEN HLA AND GM: A significant excess of Gm 1 I+ individuals was found among all HLA-A2 positive hemophiliacs (N=45, p=.034 by Fisher’s exact test. This was not significant after correction for multiple comparisons). This suggestion of an interaction between HLA-A2 and Gm 1 in determining alloreactivity to FVIII will require further prospective evaluation for confirmation.
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Pereira, J., C. Cretney, and R. H. Aster. "VARIABLE EXPRESSION OF ALLOANTIGENS IN PLATELET COHORTS OF DIFFERENT MEAN DENSITY:AN EFFECT OF AGING IN VIVO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644158.

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Platelets differ widely in size and density, but the relationship of this heterogeneity to platelet age and function is not established. Published evidence suggests that platelet alloantigens of the HLA and PlA systems may be acquired by or releasedfrom platelets in the circulation. We therefore studied expression of HLA, PlAl, and other markers in platelet cohorts of high density (HD) and low density (LD) separated on a linear, isoosmotic arabinogalactan gradient. HD and LD cohorts contained 11-14% of total platelets and did not differ significantly in mean cell volume. Alloantibodies reactive with antigens P1A1, Baka, and HLA-A2 were used to saturate alloantigen sites. Surface markers were quantified (Human Immunol. 15:251, 1986) with radiolabeled monoclonalprobes specific for HLA A, B, C antigens (W6/32), the Fc fragment of IgG (Hb-43) and the glycoprotein IIb/IIIa complex (AP-2).As shown in the Table, HD platelets carry significantly more PlAl (located on GPIIIa) and significantly less HLA than LD platelets. However, HD and LD cohorts express the same number of GPIIb/IIIa and Baka (located on GPIIb) molecules. These findings are consistent with preferential loss of HLA molecules from HD- platelets in the circulation or acquisition by LD platelets. The variable expression of P1A1 in HD and LD cohorts is apparently due to a conformational change in GPIIIa, rather than acquisition or loss of the GPIIIa molecule, because total GPIIb/IIIa was thesame in the two platelet populations. Whether antigen differences in HD and LD platelets are determined at the time of platelet production or result from aging of platelets in the circulation is under investigation.
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Paunic, Vanja, Michael Steinbach, Vipin Kumar, and Martin Maiers. "Prediction of HLA Genes from SNP Data and HLA Haplotype Frequencies." In 2012 IEEE 12th International Conference on Data Mining Workshops. IEEE, 2012. http://dx.doi.org/10.1109/icdmw.2012.74.

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Reports on the topic "HlyA"

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O'Day, Stephen C., and John W. McMaster. The ACETEF HLA Interface. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada375781.

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GOTTLIEB, ERIC JOSEPH, MICHAEL J. MCDONALD, and FRED J. OPPEL, III. Umbra's High Level Architecture (HLA) Interface. Office of Scientific and Technical Information (OSTI), April 2002. http://dx.doi.org/10.2172/800785.

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Spellman, Stephen. HLA Typing for Bone Marrow Transplantation. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada546709.

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Black, Jerry. Data Collection in an HLA Federation. Fort Belvoir, VA: Defense Technical Information Center, March 1999. http://dx.doi.org/10.21236/ada378558.

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Setterholm, Michelle, Judy W. Davis, and Steve M. Spellman. HLA Typing for Bone Marrow Transplantation. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada473611.

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Coppo, Patricia A., Judy W. Davis, and Steve M. Spellman. HLA Typing for Bone Marrow Transplantation. Fort Belvoir, VA: Defense Technical Information Center, January 2007. http://dx.doi.org/10.21236/ada462775.

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Paterson, Daniel J., Eric Anschuetz, Mark Biddle, Dave Kotick, and Thai Nguyen. Architecture Issues for DIS-TO-HLA Conversion. Fort Belvoir, VA: Defense Technical Information Center, December 1997. http://dx.doi.org/10.21236/ada332944.

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Dingel, Juergen, David Garlan, and Craig A. Damon. A Feasibility Study of the HLA Bridge. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada461048.

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Silbert, Mark, William Schibler, and Gordon Curran. Using HLA to Transmit Real-Time Sensor Imagery. Fort Belvoir, VA: Defense Technical Information Center, January 2000. http://dx.doi.org/10.21236/ada389159.

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Layman, Gene, Zach Furness, John Daly, and Jennie Womble. C4I-Simulation Interoperability Using the DII COE and HLA. Fort Belvoir, VA: Defense Technical Information Center, May 2001. http://dx.doi.org/10.21236/ada461964.

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