Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity. - sprookjes - yvandenbroek - TriplyDB

Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

http://www.wikidata.org/entity/Q33862671

about

Bacillus anthracis factors for phagosomal escape Crystal structure of an efficacious gonococcal adherence inhibitor: an enolase from Lactobacillus gasseri Minor Role of Plasminogen in Complement Activation on Cell Surfaces.The interaction of canine plasminogen with Streptococcus pyogenes enolase: they bind to one another but what is the nature of the structures involved?Whole proteome analysis of mouse lymph nodes in cutaneous anthrax Multiple activities of LigB potentiate virulence of Leptospira interrogans: inhibition of alternative and classical pathways of complement.Clostridium difficile spore-macrophage interactions: spore survival.Effects of a skin neuropeptide (substance p) on cutaneous microflora.Evasion and interactions of the humoral innate immune response in pathogen invasion, autoimmune disease, and cancer The Exosporium Layer of Bacterial Spores: a Connection to the Environment and the Infected Host Bacterial plasminogen receptors utilize host plasminogen system for effective invasion and dissemination.Protease-dependent mechanisms of complement evasion by bacterial pathogens.Cooperative plasminogen recruitment to the surface of Streptococcus canis via M protein and enolase enhances bacterial survival.Effect of Substance P in Staphylococcus aureus and Staphylococcus epidermidis Virulence: Implication for Skin Homeostasis Bacterial plasminogen receptors: mediators of a multifaceted relationship.Bacteria under stress by complement and coagulation.Interaction of spirochetes with the host fibrinolytic system and potential roles in pathogenesis.Bacterial pathogens activate plasminogen to breach tissue barriers and escape from innate immunity.Riemerella anatipestifer extracellular protease S blocks complement activation via the classical and lectin pathways.Ser/Thr protein kinase PrkC-mediated regulation of GroEL is critical for biofilm formation in Bacillus anthracis.Recombinant GroEL enhances protective antigen-mediated protection against Bacillus anthracis spore challenge.Immunohaemostasis: a new view on haemostasis during sepsis.Clostridium sordellii outer spore proteins maintain spore structural integrity and promote bacterial clearance from the gastrointestinal tract.

P2860

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P2860

Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

http://www.wikidata.org/entity/Q33862671

description

2011 nî lūn-bûn

@nan

2011 թուականի Մարտին հրատարակուած գիտական յօդուած

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2011 թվականի մարտին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

@zh-hk

2011年論文

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2011年論文

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2011年论文

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name

Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

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Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

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type

label

Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

@ast

Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

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prefLabel

Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

@ast

Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

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JOURNAL.PONE.0018119

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Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

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Aarthi Narayanan

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Bradford Gutting

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Charles L Bailey

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Dhritiman V Mukherjee

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Fatah Kashanchi

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Jessica H Tonry

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Myung-Chul Chung

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Ryan S Mackie

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Serguei G Popov

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Taissia G Popova

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P2860

Borrelia recurrentis employs a novel multifunctional surface protein with anti-complement, anti-opsonic and invasive potential to escape innate immunity

Mycobacterial protein HbhA binds human complement component C3

Surface-associated plasminogen binding of Cryptococcus neoformans promotes extracellular matrix invasion

alpha-enolase, a novel strong plasmin(ogen) binding protein on the surface of pathogenic streptococci

Surface localized and extracellular Glyceraldehyde-3-phosphate dehydrogenase of Bacillus anthracis is a plasminogen binding protein

A novel mechanism for the acquisition of virulence by a human influenza A virus

Germination of Bacillus anthracis spores within alveolar macrophages.

Proteomic profiling and identification of immunodominant spore antigens of Bacillus anthracis, Bacillus cereus, and Bacillus thuringiensis.

Primary involvement of pharynx and peyer's patch in inhalational and intestinal anthrax.

Complement evasion by human pathogens.

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scholarly article

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10.1371/JOURNAL.PONE.0018119

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