36 results on '"Sanderson-Smith, Martina L."'
Search Results
2. Safety and Efficacy of Using Nuts to Improve Bowel Health in Hemodialysis Patients
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Lambert, Kelly, Bird, Luke, Borst, Addison C., Fuller, Andrew, Wang, Yanan, Rogers, Geraint B., Stanford, Jordan, Sanderson-Smith, Martina L., Williams, Jonathan G., McWhinney, Brett C., Neale, Elizabeth P., Probst, Yasmine, and Lonergan, Maureen
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- 2020
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3. An optimised GAS-pharyngeal cell biofilm model
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Vyas, Heema K. N., McArthur, Jason D., and Sanderson-Smith, Martina L.
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- 2021
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4. Immune Cross-Opsonization Within emm Clusters Following Group A Streptococcus Skin Infection : Broadening the Scope of Type-Specific Immunity
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Frost, Hannah R., Laho, Delphine, Sanderson-Smith, Martina L., Licciardi, Paul, Donath, Susan, Curtis, Nigel, Kado, Joseph, Dale, James B., Steer, Andrew C., and Smeesters, Pierre R.
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- 2017
5. Prophage exotoxins enhance colonization fitness in epidemic scarlet fever-causing Streptococcus pyogenes
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Brouwer, Stephan, Barnett, Timothy C., Ly, Diane, Kasper, Katherine J., De Oliveira, David M. P., Rivera-Hernandez, Tania, Cork, Amanda J., McIntyre, Liam, Jespersen, Magnus G., Richter, Johanna, Schulz, Benjamin L., Dougan, Gordon, Nizet, Victor, Yuen, Kwok-Yung, You, Yuanhai, McCormick, John K., Sanderson-Smith, Martina L., Davies, Mark R., and Walker, Mark J.
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- 2020
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6. Streptococcus pyogenes emm98.1 variants activate inflammatory caspases in human neutrophils.
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Williams, Jonathan G., Sluyter, Ronald, and Sanderson-Smith, Martina L.
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- 2023
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7. Biological functions of GCS3, a novel plasminogen-binding protein of Streptococcus dysgalactiae ssp. equisimilis
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Bergmann, René, Dinkla, Katrin, Patric Nitsche-Schmitz, D., Graham, Rikki M.A., Lüttge, Melanie, Sanderson-Smith, Martina L., Nerlich, Andreas, Rohde, Manfred, and Chhatwal, Gursharan S.
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- 2011
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8. Effects on human plasminogen conformation and activation rate caused by interaction with VEK-30, a peptide derived from the group A streptococcal M-like protein (PAM)
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Figuera-Losada, Mariana, Ranson, Marie, Sanderson-Smith, Martina L., Walker, Mark J., Castellino, Francis J., and Prorok, Mary
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- 2010
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9. DNase Sda1 provides selection pressure for a switch to invasive group A streptococcal infection
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Walker, Mark J, Hollands, Andrew, Sanderson-Smith, Martina L, Cole, Jason N, Kirk, Joshua K, Henningham, Anna, McArthur, Jason D, Dinkla, Katrin, Aziz, Ramy K, Kansal, Rita G, Simpson, Amelia J, Buchanan, John T, Chhatwal, Gursharan S, Kotb, Malak, and Nizet, Victor
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- 2007
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10. The plasminogen-binding group A streptococcal M protein-related protein Prp binds plasminogen via arginine and histidine residues
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Sanderson-Smith, Martina L., Dowton, Mark, Ranson, Marie, and Walker, Mark J.
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Thrombolytic drugs -- Research ,Arginine -- Research ,Streptococcus pyogenes -- Genetic aspects ,Streptococcus pyogenes -- Research ,Binding proteins -- Research ,Histidine -- Research ,Biological sciences - Abstract
The migration of the human pathogen Streptococcus pyogenes (group A streptococcus) from localized to deep tissue sites may result in severe invasive disease, and sequestration of the host zymogen plasminogen appears crucial for virulence. Here, we describe a novel plasminogen-binding M protein, the plasminogen-binding group A streptococcal M protein (PAM)-related protein (Prp). Prp is phylogenetically distinct from previously described plasminogen-binding M proteins of group A, C, and G streptococci. While competition experiments indicate that Prp binds plasminogen with a lower affinity than PAM (50% effective concentration = 0.34 [micro]M), Prp nonetheless binds plasminogen with high affinity and at physiologically relevant concentrations of plasminogen ([K.sub.d] = 7.8 nM). Site-directed mutagenesis of the putative plasminogen binding site indicates that unlike the majority of plasminogen receptors, Prp does not interact with plasminogen exclusively via lysine residues. Mutagenesis to alanine of lysine residues [Lys.sup.96] and [Lys.sup.101] reduced but did not abrogate plasminogen binding by Prp. Plasminogen binding was abolished only with the additional mutagenesis of [Arg.sup.107] and [His.sup.108] to alanine. Furthermore, mutagenesis of [Arg.sup.107] and [His.sup.108] abolished plasminogen binding by Prp despite the presence of [Lys.sup.96] and [Lys.sup.101] in the binding site. Thus, binding to plasminogen via arginine and histidine residues appears to be a conserved mechanism among plasminogen-binding M proteins.
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- 2007
11. Characterizing the role of tissue-type plasminogen activator in a mouse model of Group A streptococcal infection
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Ly, Diane, Donahue, Deborah, Walker, Mark J., Ploplis, Victoria A., McArthur, Jason D., Ranson, Marie, Castellino, Francis J., and Sanderson-Smith, Martina L.
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- 2019
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12. Streptococcus pyogenes M1T1 Variants Induce an Inflammatory Neutrophil Phenotype Including Activation of Inflammatory Caspases.
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Williams, Jonathan G., Ly, Diane, Geraghty, Nicholas J., McArthur, Jason D., Vyas, Heema K. N., Gorman, Jody, Tsatsaronis, James A., Sluyter, Ronald, and Sanderson-Smith, Martina L.
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STREPTOCOCCUS pyogenes ,CASPASES ,PHENOTYPES ,REACTIVE oxygen species - Abstract
Invasive infections due to group A Streptococcus (GAS) advance rapidly causing tissue degradation and unregulated inflammation. Neutrophils are the primary immune cells that respond to GAS. The neutrophil response to GAS was characterised in response to two M1T1 isolates; 5448 and animal passaged variant 5448AP. Co-incubation of neutrophils with 5448AP resulted in proliferation of GAS and lowered the production of reactive oxygen species when compared with 5448. Infection with both strains invoked neutrophil death, however apoptosis was reduced in response to 5448AP. Both strains induced neutrophil caspase-1 and caspase-4 expression in vitro , with inflammatory caspase activation detected in vitro and in vivo. GAS infections involving strains such as 5448AP that promote an inflammatory neutrophil phenotype may contribute to increased inflammation yet ineffective bacterial eradication, contributing to the severity of invasive GAS infections. [ABSTRACT FROM AUTHOR]
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- 2021
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13. Bacterial plasminogen receptors: mediators of a multifaceted relationship
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Sanderson-Smith, Martina L., De Oliveira, David M.P., Ranson, Marie, and McArthur, Jason D.
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Zymogens -- Physiological aspects -- Health aspects ,Thrombolytic drugs -- Dosage and administration ,Microbiological chemistry -- Research ,Biotechnology industry ,High technology industry ,Physiological aspects ,Research ,Dosage and administration ,Health aspects - Abstract
Multiple species of bacteria are able to sequester the host zymogen plasminogen to the cell surface. Once localised to the bacterial surface, plasminogen can act as a cofactor in adhesion, or, following activation to plasmin, provide a source of potent proteolytic activity. Numerous bacterial plasminogen receptors have been identified, and the mechanisms by which they interact with plasminogen are diverse. Here we provide an overview of bacterial plasminogen receptors and discuss the diverse role bacterial plasminogen acquisition plays in the relationship between bacteria and the host., 1. Introduction Recruitment of plasminogen to the bacterial cell surface is emerging as a central theme in host/pathogen interactions. The glycoprotein plasminogen is found in plasma and extracellular fluids at [...]
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- 2012
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14. Validation of an automated colony counting system for group A Streptococcus Infectious Diseases
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Frost, Hannah R. C., Tsoi, Shu Ki, Baker, Ciara A, Laho, Delphine, Sanderson-Smith, Martina L, Steer, Andrew C, and Smeesters, Pierre
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Automated ,Automation ,Colony counting ,Colony Count, Microbial -- methods ,Streptococcus pyogenes -- growth & development -- isolation & purification ,Group A Streptococcus ,Temperature ,Humans ,Reproducibility of Results ,Biological Assay ,Sciences bio-médicales et agricoles ,Biologie ,TTC - Abstract
Background: The practice of counting bacterial colony forming units on agar plates has long been used as a method to estimate the concentration of live bacteria in culture. However, due to the laborious and potentially error prone nature of this measurement technique, an alternative method is desirable. Recent technologic advancements have facilitated the development of automated colony counting systems, which reduce errors introduced during the manual counting process and recording of information. An additional benefit is the significant reduction in time taken to analyse colony counting data. Whilst automated counting procedures have been validated for a number of microorganisms, the process has not been successful for all bacteria due to the requirement for a relatively high contrast between bacterial colonies and growth medium. The purpose of this study was to validate an automated counting system for use with group A Streptococcus (GAS). Results: Methods: Twenty-one different GAS strains, representative of major emm-types, were selected for assessment. In order to introduce the required contrast for automated counting, 2,3,5-triphenyl-2H-tetrazolium chloride (TTC) dye was added to Todd-Hewitt broth with yeast extract (THY) agar. Growth on THY agar with TTC was compared with growth on blood agar and THY agar to ensure the dye was not detrimental to bacterial growth. Automated colony counts using a ProtoCOL 3 instrument were compared with manual counting to confirm accuracy over the stages of the growth cycle (latent, mid-log and stationary phases) and in a number of different assays. The average percentage differences between plating and counting methods were analysed using the Bland-Altman method. Conclusions: Results: A percentage difference of ±10 % was determined as the cut-off for a critical difference between plating and counting methods. All strains measured had an average difference of less than 10 % when plated on THY agar with TTC. This consistency was also observed over all phases of the growth cycle and when plated in blood following bactericidal assays. Agreement between these methods suggest the use of an automated colony counting technique for GAS will significantly reduce time spent counting bacteria to enable a more efficient and accurate measurement of bacteria concentration in culture., SCOPUS: ar.j, info:eu-repo/semantics/published
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- 2016
15. Human glycan expression patterns influence Group A streptococcal colonization of epithelial cells.
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De Oliveira, David M. P., Everest-Dass, Arun, Hartley-Tassell, Lauren, Day, Christopher J., Indraratna, Anuk, Brouwer, Stephan, Cleary, Ailish, Kautto, Liisa, Gorman, Jody, Packer, Nicolle H., Jennings, Michael P., Walker, Mark J., and Sanderson-Smith, Martina L.
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- 2019
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16. Group A Streptococcus Modulates Host Inflammation by Manipulating Polymorphonuclear Leukocyte Cell Death Responses.
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Tsatsaronis, James a., Ly, Diane, Pupovac, aleta, Goldmann, Oliver, Rohde, Manfred, Taylor, Jude M., Walker, Mark J., Medina, Eva, and Sanderson-Smith, Martina L.
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- 2015
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17. Preferential Acquisition and Activation of Plasminogen Glycoform II by PAM Positive Group A Streptococcal Isolates.
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De Oliveira, David M. P., Law, Ruby H. P., Ly, Diane, Cook, Simon M., Quek, Adam J., McArthur, Jason D., Whisstock, James C., and Sanderson-Smith, Martina L.
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- 2015
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18. Molecular Markers for the Study of Streptococcal Epidemiology.
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McMillan, David J., Sanderson-Smith, Martina L., Smeesters, Pierre Robert, and Sriprakash, Kadaba S.
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- 2013
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19. Host Responses to Group A Streptococcus: Cell Death and Inflammation.
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Tsatsaronis, James A., Walker, Mark J., and Sanderson-Smith, Martina L.
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STREPTOCOCCUS ,INFLAMMATION ,CELL death ,LEUCOCYTES ,EPITHELIAL cells ,APOPTOSIS - Abstract
Infections caused by group A Streptococcus (GAS) are characterized by robust inflammatory responses and can rapidly lead to life-threatening disease manifestations. However, host mechanisms that respond to GAS, which may influence disease pathology, are understudied. Recent works indicate that GAS infection is recognized by multiple extracellular and intracellular receptors and activates cell signalling via discrete pathways. Host leukocyte receptor binding to GAS-derived products mediates release of inflammatory mediators associated with severe GAS disease. GAS induces divergent phagocyte programmed cell death responses and has inflammatory implications. Epithelial cell apoptotic and autophagic components are mobilized by GAS infection, but can be subverted to ensure bacterial survival. Examination of host interactions with GAS and consequences of GAS infection in the context of cellular receptors responsible for GAS recognition, inflammatory mediator responses, and cell death mechanisms, highlights potential avenues for diagnostic and therapeutic intervention. Understanding the molecular and cellular basis of host symptoms during severe GAS disease will assist the development of improved treatment regimens for this formidable pathogen. [ABSTRACT FROM AUTHOR]
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- 2014
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20. Site-restricted plasminogen activation mediated by group A streptococcal streptokinase variants.
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COOK, Simon M., SKORA, Amanda, WALKER, Mark J., SANDERSON-SMITH, Martina L., and MCARTHUR, Jason D.
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STREPTOCOCCUS pyogenes ,PLASMINOGEN activators ,STREPTOKINASE ,THROMBOLYTIC therapy ,FIBRINOGEN ,PLASMINOGEN - Abstract
SK (streptokinase) is a secreted plasminogen activator and virulence factor of GAS (group A Streptococcus). Among GAS isolates, SK gene sequences are polymorphic and are grouped into two sequence clusters (cluster type-1 and cluster type- 2) with cluster type-2 being further classified into subclusters (type-2a and type-2b). In the present study, we examined the role of bacterial and host-derived cofactors in SK-mediated plasminogen activation. All SK variants, apart from type-2b, can form an activator complex with Glu-Plg (Glu-plasminogen). Specific ligand-binding-induced conformational changes in Glu- Plg mediated by fibrinogen, PAM (plasminogen-binding group A streptococcal M protein), fibrinogen fragment D or fibrin, were required for type-2b SK to form a functional activator complex with Glu-Plg. In contrast with type-1 and type-2a SK, type-2b SK activator complexes were inhibited by a2-antiplasmin unless bound to fibrin or to the GAS cell-surface via PAMin combination with fibrinogen. Taken together, these data suggest that type-2b SK plasminogen activation may be restricted to specific microenvironments within the host such as fibrin deposits or the bacterial cell surface through the action of a2-antiplasmin. We conclude that phenotypic SK variation functionally underpins a pathogenic mechanismwhereby SK variants differentially focus plasminogen activation, leading to specific niche adaption within the host. [ABSTRACT FROM AUTHOR]
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- 2014
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21. Plasmin(ogen) Acquisition by Group A Streptococcus Protects against C3b-Mediated Neutrophil Killing.
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Ly, Diane, Taylor, Jude M., Tsatsaronis, James a., Monteleone, Mercedes M., Skora, amanda S., Donald, Cortny a., Maddocks, Tracy, Nizet, Victor, West, Nicholas P., Ranson, Marie, Walker, Mark J., Mcarthur, Jason D., and Sanderson-Smith, Martina L.
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- 2014
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22. A Key Role for the Urokinase Plasminogen Activator (uPA) in Invasive Group A Streptococcal Infection.
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Sanderson-Smith, Martina L., Zhang, Yueling, Ly, Diane, Donahue, Deborah, Hollands, Andrew, Nizet, Victor, Ranson, Marie, Ploplis, Victoria A., Walker, Mark J., and Castellino, Francis J.
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UROKINASE , *PLASMINOGEN activators , *STREPTOCOCCAL diseases , *BACTERIAL diseases , *PATHOGENIC microorganisms - Abstract
Recruitment of the serine protease plasmin is central to the pathogenesis of many bacterial species, including Group A streptococcus (GAS), a leading cause of morbidity and mortality globally. A key process in invasive GAS disease is the ability to accumulate plasmin at the cell surface, however the role of host activators of plasminogen in this process is poorly understood. Here, we demonstrate for the first time that the urokinase-type plasminogen activator (uPA) contributes to plasmin recruitment and subsequent invasive disease initiation in vivo. In the absence of a source of host plasminogen activators, streptokinase (Ska) was required to facilitate cell surface plasmin acquisition by GAS. However, in the absence of Ska, host activators were sufficient to promote cell surface plasmin acquisition by GAS strain 5448 during incubation with plasminogen or human plasma. Furthermore, GAS were able mediate a significant increase in the activation of zymogen pro-uPA in human plasma. In order to assess the contribution of uPA to invasive GAS disease, a previously undescribed transgenic mouse model of infection was employed. Both C57/black 6J, and AlbPLG1 mice expressing the human plasminogen transgene, were significantly more susceptible to invasive GAS disease than uPA−/− mice. The observed decrease in virulence in uPA−/−mice was found to correlate directly with a decrease in bacterial dissemination and reduced cell surface plasmin accumulation by GAS. These findings have significant implications for our understanding of GAS pathogenesis, and research aimed at therapeutic targeting of plasminogen activation in invasive bacterial infections. [ABSTRACT FROM AUTHOR]
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- 2013
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23. Streptococcal collagen-like protein A and general stress protein 24 are immunomodulating virulence factors of group A Streptococcus.
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Tsatsaronis, James A., Hollands, Andrew, Cole, Jason N., Maamary, Peter G., Gillen, Christine M., Ben Zakour, Nouri L., Kotb, Malak, Nizet, Victor, Beatson, Scott A., Walker, Mark J., and Sanderson-Smith, Martina L.
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SYSTEMS biology ,NATURAL immunity ,DEVELOPING countries ,STREPTOCOCCUS ,SEROTYPES - Abstract
In Western countries, invasive infections caused by M1T1 serotype group A Streptococcus (GAS) are epidemiologically linked to mutations in the control of virulence regulatory 2-component operon (covRS). In indigenous communities and developing countries, severe GAS disease is associated with genetically diverse non-M1T1 GAS serotypes. Hypervirulent M1T1 covRS mutant strains arise through selection by human polymorphonuclear cells for increased expression of GAS virulence factors such as the DNase Sda1, which promotes neutrophil resistance. The GAS bacteremia isolate NS88.2 (emm 98.1) is a covS mutant that exhibits a hypervirulent phenotype and neutrophil resistance yet lacks the phage-encoded Sda1. Here, we have employed a comprehensive systems biology (genomic, transcriptomic, and proteomic) approach to identify NS88.2 virulence determinants that enhance neutrophil resistance in the non-M1T1 GAS genetic background. Using this approach, we have identified streptococcal collagen-like protein A and general stress protein 24 proteins as NS88.2 determinants that contribute to survival in whole blood and neutrophil resistance in non-M1T1 GAS. This study has revealed new factors that contribute to GAS pathogenicity that may play important roles in resisting innate immune defenses and the development of human invasive infections. [ABSTRACT FROM AUTHOR]
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- 2013
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24. Parameters Governing Invasive Disease Propensity of Non-M1 Serotype Group A Streptococci.
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Maamary, Peter G., Sanderson-Smith, Martina L., Aziz, Ramy K., Hollands, Andrew, Cole, Jason N., McKay, Fiona C., McArthur, Jason D., Kirk, Joshua K., Cork, Amanda J., Keefe, Rachael J., Kansal, Rita G., Sun, Hongmin, Taylor, William L., Chhatwal, Gursharan S., Ginsburg, David, Nizet, Victor, Kotb, Malak, and Walker, Mark J.
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- 2010
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25. Allelic variants of streptokinase from Streptococcus pyogenes display functional differences in plasminogen activation.
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McArthur, Jason D., McKay, Fiona C., Ramachandran, Vidiya, Shyam, Priya, Cork, Amanda J., Sanderson-Smith, Martina L., Cole, Jason N., Ringdahl, Ulrika, Sjöbring, Ulf, Ranson, Marie, and Walker, Mark J.
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STREPTOKINASE ,STREPTOCOCCUS pyogenes ,PLASMINOGEN activators ,FIBRINOGEN ,MICROBIAL virulence - Abstract
A common mammalian defense mechanism employed to prevent systemic dissemination of invasive bacteria involves occlusion of local microvasculature and encapsulation of bacteria within fibrin networks. Acquisition of plasmin activity at the bacterial cell surface circumvents this defense mechanism, allowing invasive disease initiation. To facilitate this process, S. pyogenes secretes streptokinase, a plasminogen-activating protein. Streptokinase polymorphism exhibited by S. pyogenes isolates is well characterized. However, the functional differences displayed by these variants and the biological significance of this variation has not been elucidated. Phylogenetic analysis of ska sequences from 28 S. pyogenes isolates revealed 2 main sequence clusters (clusters 1 and 2). All strains secreted streptokinase, as determined by Western blotting, and were capable of acquiring cell surface plasmin activity after incubation in human plasma. Whereas culture supernatants from strains containing cluster 1 ska alleles also displayed soluble plasminogen activation activity, supernatants from strains containing cluster 2 ska alleles did not. Furthermore, plasminogen activation activity in culture supernatants from strains containing cluster 2 ska alleles could only be detected when plasminogen was prebound with fibrinogen. This study indicates that variant streptokinase proteins secreted by S. pyogenes isolates display differing plasminogen activation characteristics and may therefore play distinct roles in disease pathogenesis. [ABSTRACT FROM AUTHOR]
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- 2008
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26. The Maintenance of High Affinity Plasminogen Binding by Group A Streptococcal Plasminogen-binding M-Iike Protein Is Mediated by Arginine and Histidine Residues within the a1 and a2 Repeat Domains.
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Sanderson-Smith, Martina L., Walker, Mark J., and Ranson, Marie
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PLASMINOGEN , *RADIOGENETICS , *FIBRINOLYTIC agents , *MUTAGENESIS , *GENETIC mutation , *BIOCHEMISTRY - Abstract
Subversion of the plasminogen activation system is implicated in the virulence of group A streptococci (GAS). GAS displays receptors for the human zymogen plasminogen on the cell surface, one of which is the plasminogen-binding group A streptococcal M-like protein (PAM). The plasminogen binding domain of PAM is highly variable, and this variation has been linked to host selective immune pressure. Site-directed mutagenesis of full-length PAM protein from an invasive GAS isolate was undertaken to assess the contribution of residues in the a1 and a2 repeat domains to plasminogen binding function. Mutagenesis to alanine of key plasminogen binding lysine residues in the a1 and a2 repeats (Lys98 and Lys111) did not abrogate plasminogen binding by PAM nor did additional mutagenesis of Arg101 and His102 and Glu104, which have previously been implicated in plasminogen binding. Plasminogen binding was only abolished with the additional mutagenesis of Arg114 and His115 to alanine. Furthermore, mutagenesis of both arginine (Arg101 and Arg114) and histidine (His102 and His115) residues abolished interaction with plasminogen despite the presence of Lys98 and Lys111 in the binding repeats. This study shows for the first time that residues Arg101, Arg114, His102, and His115 in both the a1 and a2 repeat domains of PAM can mediate high affinity plasminogen binding. These data suggest that highly conserved arginine and histidine residues may compensate for variation elsewhere in the a1 and a2 plasminogen binding repeats, and may explain the maintenance of high affinity plasminogen binding by naturally occurring variants of PAM. [ABSTRACT FROM AUTHOR]
- Published
- 2006
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27. Assessing the Role of Pharyngeal Cell Surface Glycans in Group A Streptococcus Biofilm Formation.
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Vyas, Heema K. N., Indraratna, Anuk D., Everest-Dass, Arun, Packer, Nicolle H., De Oliveira, David M. P., Ranson, Marie, McArthur, Jason D., Sanderson-Smith, Martina L., and Reffuveille, Fany
- Subjects
BIOFILMS ,CELL membranes ,GLYCANS ,GLYCAN structure ,STREPTOCOCCUS ,SIALIC acids - Abstract
Group A Streptococcus (GAS) causes 700 million infections and accounts for half a million deaths per year. Antibiotic treatment failure rates of 20–40% have been observed. The role host cell glycans play in GAS biofilm formation in the context of GAS pharyngitis and subsequent antibiotic treatment failure has not been previously investigated. GAS serotype M12 GAS biofilms were assessed for biofilm formation on Detroit 562 pharyngeal cell monolayers following enzymatic removal of all N-linked glycans from pharyngeal cells with PNGase F. Removal of N-linked glycans resulted in an increase in biofilm biomass compared to untreated controls. Further investigation into the removal of terminal mannose and sialic acid residues with α1-6 mannosidase and the broad specificity sialidase (Sialidase A) also found that biofilm biomass increased significantly when compared to untreated controls. Increases in biofilm biomass were associated with increased production of extracellular polymeric substances (EPS). Furthermore, it was found that M12 GAS biofilms grown on untreated pharyngeal monolayers exhibited a 2500-fold increase in penicillin tolerance compared to planktonic GAS. Pre-treatment of monolayers with exoglycosidases resulted in a further doubling of penicillin tolerance in resultant biofilms. Lastly, an additional eight GAS emm-types were assessed for biofilm formation in response to terminal mannose and sialic acid residue removal. As seen for M12, biofilm biomass on monolayers increased following removal of terminal mannose and sialic acid residues. Collectively, these data demonstrate that pharyngeal cell surface glycan structures directly impact GAS biofilm formation in a strain and glycan specific fashion. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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28. Trigger for group A streptococcal M1T1 invasive disease.
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Cole, Jason N., McArthur, Jason D., McKay, Fiona C., Sanderson-Smith, Martina L., Cork, Amanda J., Ranson, Marie, Rohde, Manfred, Itzek, Andreas, Hongmin Sun, Ginsburg, David, Kotb, Malak, Nizet, Victor, Chhatwal, G. S., and Walker, Mark J.
- Subjects
STREPTOCOCCAL diseases ,CYSTEINE proteinases ,MICROBIAL virulence ,PLASMINOGEN ,TRANSGENIC mice - Abstract
The article presents a study which investigated the trigger factor for group A streptococcal M1T1 invasive disease. The characterization and M1T1 5448 and cysteine protease SpeB is discussed. The progression of the virulence of the wild-type strain in humanized plasminogen transgenic mice is examined. A description of SpeB activity of 5448 in vivo isolates is provided.
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- 2006
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29. Development and optimization of ciprofloxacin-loaded gelatin microparticles by single-step spray-drying technique.
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Silva, Dina M., Vyas, Heema Kumari Nilesh, Sanderson-Smith, Martina L., and Sencadas, Vitor
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CIPROFLOXACIN , *MECHANICAL loads , *GELATIN , *SPRAY drying , *DRUG delivery systems , *PHARMACODYNAMICS - Abstract
Polymeric particles are a versatile class of local or systemic drug delivery systems, used to improve drugs pharmacokinetics and pharmacodynamics along with patient compliance. Herein, we report a rapid, scalable, and optimized method to encapsulate ciprofloxacin (CPx), a poor water soluble antimicrobial agent, in gelatin microparticles by single step processing via spray-drying of an aqueous solution. The developed particles show mainly a wrinkle morphology with a unimodal distribution, with mean diameters ranging between 2 and 4 μm, depending on the processing conditions. The encapsulation of 1, 2 and 5 wt% CPx narrows the size distribution (1–3 μm). In vitro release experiments showed that up to 80% of encapsulated drug is released during the first 6 h, and the release kinetics was best fitted with the Korsmeyer-Peppas model, explained by the superimposition of drug diffusion and polymer chain relaxation. The minimal inhibitory concentrations against S. aureus and E. coli , obtained from pure and encapsulated ciprofloxacin, demonstrated that the spray-drying process does not inhibit the drug's bioactivity or the process feasibility. Thus, spray-drying of protein-drug particle systems is an advantageous method to produce microparticles with potential to lung delivery systems. [ABSTRACT FROM AUTHOR]
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- 2018
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30. Streptococcus pyogenes emm 98.1 variants activate inflammatory caspases in human neutrophils.
- Author
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Williams JG, Sluyter R, and Sanderson-Smith ML
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- Humans, Streptococcus pyogenes genetics, Caspases genetics, Bacterial Proteins genetics, Virulence, Neutrophils, Streptococcal Infections
- Abstract
Abbreviations: CovRS, control of virulence regulatory system; GAS, Group A Streptococcus; PMN, polymorphonuclear leukocyte.
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- 2023
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31. Anti-persister efficacy of colistin and meropenem against uropathogenic Escherichia coli is dependent on environmental conditions.
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Urbaniec J, Getino M, McEwan TB, Sanderson-Smith ML, McFadden J, Hai F, La Ragione R, Hassan MM, and Hingley-Wilson S
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- Humans, Colistin pharmacology, Meropenem pharmacology, Meropenem therapeutic use, Anti-Bacterial Agents pharmacology, Anti-Bacterial Agents therapeutic use, Bacteria genetics, Uropathogenic Escherichia coli genetics, Urinary Tract Infections drug therapy, Urinary Tract Infections microbiology, Escherichia coli Infections drug therapy, Escherichia coli Infections microbiology
- Abstract
Antibiotic persistence is a phenomenon observed when genetically susceptible cells survive long-term exposure to antibiotics. These 'persisters' are an intrinsic component of bacterial populations and stem from phenotypic heterogeneity. Persistence to antibiotics is a concern for public health globally, as it increases treatment duration and can contribute to treatment failure. Furthermore, there is a growing array of evidence that persistence is a 'stepping-stone' for the development of genetic antimicrobial resistance. Urinary tract infections (UTIs) are a major contributor to antibiotic consumption worldwide, and are known to be both persistent (i.e. affecting the host for a prolonged period) and recurring. Currently, in clinical settings, routine laboratory screening of pathogenic isolates does not determine the presence or the frequency of persister cells. Furthermore, the majority of research undertaken on antibiotic persistence has been done on lab-adapted bacterial strains. In the study presented here, we characterized antibiotic persisters in a panel of clinical uropathogenic Escherichia coli isolates collected from hospitals in the UK and Australia. We found that a urine-pH mimicking environment not only induces higher levels of antibiotic persistence to meropenem and colistin than standard laboratory growth conditions, but also results in rapid development of transient colistin resistance, regardless of the genetic resistance profile of the isolate. Furthermore, we provide evidence for the presence of multiple virulence factors involved in stress resistance and biofilm formation in the genomes of these isolates, whose activities have been previously shown to contribute to the formation of persister cells.
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- 2023
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32. Investigation of Group A Streptococcal Interactions with Host Glycan Structures Using High-Throughput Techniques: Glycan Microarray Analysis Using Recombinant Protein and Whole Cells.
- Author
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Indraratna A, De Oliveira DMP, Hartley-Tassell LE, Day CJ, Walker MJ, Jennings MP, and Sanderson-Smith ML
- Subjects
- Bacterial Adhesion physiology, Host-Pathogen Interactions physiology, Lectins metabolism, Microarray Analysis, High-Throughput Screening Assays methods, Polysaccharides metabolism, Streptococcus pyogenes metabolism
- Abstract
Glycans, also known as carbohydrates, are abundant upon cell surfaces, where they often mediate host-pathogen interactions. The specific recognition of host glycans by pathogenic lectins is an important process that allows the adherence of bacteria to the host epithelial surface in many species, including Group A Streptococcus (GAS). Glycan microarrays present a sensitive, high-throughput approach for identifying novel lectin-glycan interactions and can be applied in the context of whole bacteria or purified bacterial proteins.
- Published
- 2020
- Full Text
- View/download PDF
33. Blood Group Antigen Recognition via the Group A Streptococcal M Protein Mediates Host Colonization.
- Author
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De Oliveira DM, Hartley-Tassell L, Everest-Dass A, Day CJ, Dabbs RA, Ve T, Kobe B, Nizet V, Packer NH, Walker MJ, Jennings MP, and Sanderson-Smith ML
- Subjects
- Antigens, Bacterial genetics, Bacterial Outer Membrane Proteins genetics, Carrier Proteins genetics, DNA Mutational Analysis, Epithelial Cells chemistry, Protein Binding, Antigens, Bacterial metabolism, Bacterial Adhesion, Bacterial Outer Membrane Proteins metabolism, Blood Group Antigens metabolism, Carrier Proteins metabolism, Epithelial Cells microbiology, Polysaccharides metabolism, Streptococcus pyogenes physiology
- Abstract
Streptococcus pyogenes (group A streptococcus [GAS]) is responsible for over 500,000 deaths worldwide each year. The highly virulent M1T1 GAS clone is one of the most frequently isolated serotypes from streptococcal pharyngitis and invasive disease. The oral epithelial tract is a niche highly abundant in glycosylated structures, particularly those of the ABO(H) blood group antigen family. Using a high-throughput approach, we determined that a strain representative of the globally disseminated M1T1 GAS clone 5448 interacts with numerous, structurally diverse glycans. Preeminent among GAS virulence factors is the surface-expressed M protein. M1 protein showed high affinity for several terminal galactose blood group antigen structures. Deletion mutagenesis shows that M1 protein mediates glycan binding via its B repeat domains. Association of M1T1 GAS with oral epithelial cells varied significantly as a result of phenotypic differences in blood group antigen expression, with significantly higher adherence to those cells expressing H antigen structures compared to cells expressing A, B, or AB antigen structures. These data suggest a novel mechanism for GAS attachment to host cells and propose a link between host blood group antigen expression and M1T1 GAS colonization., Importance: There has been a resurgence in group A streptococcal (GAS) invasive disease, which has been paralleled by the emergence of the highly virulent M1T1 GAS clone. Intensive research has focused on mechanisms that contribute to the invasive nature of this serotype, while the mechanisms that contribute to host susceptibility to disease and bacterial colonization and persistence are still poorly understood. The M1T1 GAS clone is frequently isolated from the throat, an environment highly abundant in blood group antigen structures. This work examined the interaction of the M1 protein, the preeminent GAS surface protein, against a wide range of host-expressed glycan structures. Our data suggest that susceptibility to infection by GAS in the oral tract may correlate with phenotypic differences in host blood group antigen expression. Thus, variations in host blood group antigen expression may serve as a selective pressure contributing to the dissemination and overrepresentation of M1T1 GAS., (Copyright © 2017 De Oliveira et al.)
- Published
- 2017
- Full Text
- View/download PDF
34. Disease manifestations and pathogenic mechanisms of Group A Streptococcus.
- Author
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Walker MJ, Barnett TC, McArthur JD, Cole JN, Gillen CM, Henningham A, Sriprakash KS, Sanderson-Smith ML, and Nizet V
- Subjects
- Animals, Anti-Bacterial Agents pharmacology, Anti-Bacterial Agents therapeutic use, Disease Models, Animal, Drug Resistance, Bacterial, Host-Pathogen Interactions, Humans, Streptococcal Infections epidemiology, Streptococcal Infections mortality, Streptococcal Vaccines administration & dosage, Streptococcal Vaccines immunology, Streptococcus pyogenes genetics, Virulence, Virulence Factors genetics, Streptococcal Infections microbiology, Streptococcal Infections pathology, Streptococcus pyogenes pathogenicity, Virulence Factors metabolism
- Abstract
Streptococcus pyogenes, also known as group A Streptococcus (GAS), causes mild human infections such as pharyngitis and impetigo and serious infections such as necrotizing fasciitis and streptococcal toxic shock syndrome. Furthermore, repeated GAS infections may trigger autoimmune diseases, including acute poststreptococcal glomerulonephritis, acute rheumatic fever, and rheumatic heart disease. Combined, these diseases account for over half a million deaths per year globally. Genomic and molecular analyses have now characterized a large number of GAS virulence determinants, many of which exhibit overlap and redundancy in the processes of adhesion and colonization, innate immune resistance, and the capacity to facilitate tissue barrier degradation and spread within the human host. This improved understanding of the contribution of individual virulence determinants to the disease process has led to the formulation of models of GAS disease progression, which may lead to better treatment and intervention strategies. While GAS remains sensitive to all penicillins and cephalosporins, rising resistance to other antibiotics used in disease treatment is an increasing worldwide concern. Several GAS vaccine formulations that elicit protective immunity in animal models have shown promise in nonhuman primate and early-stage human trials. The development of a safe and efficacious commercial human vaccine for the prophylaxis of GAS disease remains a high priority.
- Published
- 2014
- Full Text
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35. Molecular markers for the study of streptococcal epidemiology.
- Author
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McMillan DJ, Sanderson-Smith ML, Smeesters PR, and Sriprakash KS
- Subjects
- Humans, Molecular Epidemiology, Multilocus Sequence Typing, Streptococcus pyogenes pathogenicity, Virulence Factors genetics, Streptococcal Infections epidemiology, Streptococcus pyogenes genetics
- Abstract
Diseases caused by Streptococcus pyogenes (Group A streptococcus, GAS) range from superficial infections such as pharyngitis and impetigo to potentially fatal rheumatic heart disease and invasive disease. Studies spanning emm-typing surveillance to population genomics are providing new insights into the epidemiology, pathogenesis, and biology of this organism. Such studies have demonstrated the differences that exist in the epidemiology of streptococcal disease between developing and developed nations. In developing nations, where streptococcal disease is endemic, the diversity of GAS emm-types circulating is much greater than that found in developed nations. An association between emm-type and disease, as observed in developed countries is also lacking. Intriguingly, comparative genetic studies suggest that emm-type is not always a good predictor of the evolutionary relatedness of geographically distant isolates. A view of GAS as a highly dynamic organism, in possession of a core set of virulence genes that contribute to host niche specialization and common pathogenic processes, augmented by accessory genes that change the relative virulence of specific lineages is emerging. Our inability to definitively identify genetic factors that contribute to specific disease outcome underscores the complex nature of streptococcal diseases.
- Published
- 2013
- Full Text
- View/download PDF
36. Plasminogen binding by group A streptococcal isolates from a region of hyperendemicity for streptococcal skin infection and a high incidence of invasive infection.
- Author
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McKay FC, McArthur JD, Sanderson-Smith ML, Gardam S, Currie BJ, Sriprakash KS, Fagan PK, Towers RJ, Batzloff MR, Chhatwal GS, Ranson M, and Walker MJ
- Subjects
- Bacterial Outer Membrane Proteins metabolism, Bacterial Proteins genetics, Carrier Proteins genetics, Fibrinogen metabolism, Humans, Incidence, Molecular Sequence Data, Northern Territory epidemiology, Sequence Analysis, DNA, Skin Diseases, Bacterial microbiology, Streptococcal Infections microbiology, Streptococcus pyogenes metabolism, Antigens, Bacterial, Bacterial Proteins metabolism, Carrier Proteins metabolism, Endemic Diseases, Plasminogen metabolism, Skin Diseases, Bacterial epidemiology, Streptococcal Infections epidemiology, Streptococcus pyogenes isolation & purification
- Abstract
Reports of resurgence in invasive group A streptococcal (GAS) infections come mainly from affluent populations with infrequent exposure to GAS. In the Northern Territory (NT) of Australia, high incidence of invasive GAS disease is secondary to endemic skin infection, serotype M1 clones are rare in invasive infection, the diversity and level of exposure to GAS strains are high, and no particular strains dominate. Expression of a plasminogen-binding GAS M-like protein (PAM) has been associated with skin infection in isolates elsewhere (D. Bessen, C. M. Sotir, T. M. Readdy, and S. K. Hollingshead, J. Infect. Dis. 173:896-900, 1996), and subversion of the host plasminogen system by GAS is thought to contribute to invasion in animal models. Here, we describe the relationship between plasminogen-binding capacity of GAS isolates, PAM genotype, and invasive capacity in 29 GAS isolates belonging to 25 distinct strains from the NT. In the presence of fibrinogen and streptokinase, invasive isolates bound more plasminogen than isolates from uncomplicated infections (P < or = 0.004). Only PAM-positive isolates bound substantial levels of plasminogen by a fibrinogen-streptokinase-independent pathway (direct binding). Despite considerable amino acid sequence variation within the A1 repeat region of PAM where the plasminogen-binding domain maps, the critical lysine residue was conserved.
- Published
- 2004
- Full Text
- View/download PDF
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