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Literature DB >> 24150653

The role of the TLR-dependent signaling pathway in the mechanism of phagocyte protection by exogenous heat shock protein HSP70 from the endotoxin action.

O Yu Antonova¹, M M Yurinskaya, M B Evgen'ev, M G Vinokurov.

Abstract

Entities: Gene

Mesh：

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Year: 2013 PMID： 24150653 DOI： 10.1134/S0012496613050037

Source DB: PubMed Journal: Dokl Biol Sci ISSN： 0012-4966

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13 in total

1. Exogenous mammalian extracellular HSP70 reduces endotoxin manifestations at the cellular and organism levels.

Authors: Elena Rozhkova; Marina Yurinskaya; Olga Zatsepina; David Garbuz; Vadim Karpov; Sergei Surkov; Arkady Murashev; Vladimir Ostrov; Boris Margulis; Mikhail Evgen'ev; Maxim Vinokurov
Journal: Ann N Y Acad Sci Date: 2010-06 Impact factor: 5.691

2. Circulating endotoxemia: a novel factor in systemic inflammation and cardiovascular disease in chronic kidney disease.

Authors: Christopher W McIntyre; Laura E A Harrison; M Tarek Eldehni; Helen J Jefferies; Cheuk-Chun Szeto; Stephen G John; Mhairi K Sigrist; James O Burton; Daljit Hothi; Shvan Korsheed; Paul J Owen; Ka-Bik Lai; Philip K T Li
Journal: Clin J Am Soc Nephrol Date: 2010-09-28 Impact factor: 8.237

3. The structural basis of lipopolysaccharide recognition by the TLR4-MD-2 complex.

Authors: Beom Seok Park; Dong Hyun Song; Ho Min Kim; Byong-Seok Choi; Hayyoung Lee; Jie-Oh Lee
Journal: Nature Date: 2009-03-01 Impact factor: 49.962

Review 4. Crosstalk in NF-κB signaling pathways.

Authors: Andrea Oeckinghaus; Matthew S Hayden; Sankar Ghosh
Journal: Nat Immunol Date: 2011-07-19 Impact factor: 25.606

5. Exogenous heat shock protein HSP70 protects human blood phagocytes at the action of different chemotypes of lipopolysaccharide.

Authors: O Yu Antonova; M M Yurinskaya; M B Evgen'ev; A V Suslikov; M G Vinokurov
Journal: Dokl Biol Sci Date: 2013-01-06

Review 6. Endotoxin elimination in sepsis: physiology and therapeutic application.

Authors: Klaus Buttenschoen; Peter Radermacher; Hendrik Bracht
Journal: Langenbecks Arch Surg Date: 2010-06-27 Impact factor: 3.445

Review 7. The role of toll-like receptor-4 in the development of multi-organ failure following traumatic haemorrhagic shock and resuscitation.

Authors: Lee J McGhan; Dawn E Jaroszewski
Journal: Injury Date: 2012-02 Impact factor: 2.586

8. Exercise-induced extracellular 72 kDa heat shock protein (Hsp72) stimulates neutrophil phagocytic and fungicidal capacities via TLR-2.

Authors: Esther Giraldo; Leticia Martin-Cordero; Juan Jose Garcia; Mathias Gehrmann; Mathias Gerhmann; Gabriele Multhoff; Eduardo Ortega
Journal: Eur J Appl Physiol Date: 2009-09-22 Impact factor: 3.078

The role of the TLR-dependent signaling pathway in the mechanism of phagocyte protection by exogenous heat shock protein HSP70 from the endotoxin action.

1. Exogenous mammalian extracellular HSP70 reduces endotoxin manifestations at the cellular and organism levels.

2. Circulating endotoxemia: a novel factor in systemic inflammation and cardiovascular disease in chronic kidney disease.

3. The structural basis of lipopolysaccharide recognition by the TLR4-MD-2 complex.

Review 4. Crosstalk in NF-κB signaling pathways.

5. Exogenous heat shock protein HSP70 protects human blood phagocytes at the action of different chemotypes of lipopolysaccharide.

Review 6. Endotoxin elimination in sepsis: physiology and therapeutic application.

Review 7. The role of toll-like receptor-4 in the development of multi-organ failure following traumatic haemorrhagic shock and resuscitation.

8. Exercise-induced extracellular 72 kDa heat shock protein (Hsp72) stimulates neutrophil phagocytic and fungicidal capacities via TLR-2.

9. TAK-242 selectively suppresses Toll-like receptor 4-signaling mediated by the intracellular domain.

10. Binding of different forms of lipopolysaccharide and gene expression in bovine blood neutrophils.

1. Influence of encapsulated heat shock protein HSP70 on the basic functional properties of blood phagocytes.

2. Exogenous heat shock protein HSP70 reduces response of human neuroblastoma cells to lipopolysaccharide.