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Journal ArticleDOI

Pulmonary hemorrhage induced by jararhagin, a metalloproteinase from Bothrops jararaca snake venom

TLDR
Despite the fact that jararhagin is complexed by plasma proteins after iv injection, its hemorrhagic activity was not inhibited by the plasma proteinase inhibitor alpha(2)-macroglobulin, and was only partially reduced by normal mouse serum, suggesting that resistance to inhibition may contribute to its ability to cause pulmonary hemorrhage.
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This article is published in Toxicology and Applied Pharmacology.The article was published on 2003-11-15. It has received 61 citations till now. The article focuses on the topics: Jararhagin & Batimastat.

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Journal ArticleDOI

Hemorrhage induced by snake venom metalloproteinases: biochemical and biophysical mechanisms involved in microvessel damage.

TL;DR: It is proposed that SVMP-induced hemorrhage occurs in vivo by a 'two-step' mechanism, whereby SVMPs degrade basement membrane and adhesion proteins, thus weakening the capillary wall and perturbing the interactions between endothelial cells and the basement membrane.
Journal ArticleDOI

Snake venom metalloproteinases.

TL;DR: This chapter discusses the multiple activities of the SVMPs, which have fibrin(ogen)olytic activity, act as prothrombin activators, activate blood coagulation factor X, possess apoptotic activity, inhibit platelet aggregation, are pro-inflammatory and inactivate blood serine proteinase inhibitors.
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Key events in microvascular damage induced by snake venom hemorrhagic metalloproteinases

TL;DR: Evidence gathered support a two-step model for the pathogenesis of SVMP-induced hemorrhage: initially, hemorrhagic SVMPs bind to and hydrolyze components of the BM and associated extracellular matrix proteins that play a key role in the mechanical stability of BM.
Journal ArticleDOI

Experimental pathology of local tissue damage induced by Bothrops asper snake venom

TL;DR: The search for novel toxin inhibitors represents a potential avenue for improving the treatment of this serious aspect of snakebite envenomation, as muscle tissue regeneration after venom-induced pathological effects is often impaired, thus resulting in permanent tissue loss and dysfunction.
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Hemorrhage Caused by Snake Venom Metalloproteinases: A Journey of Discovery and Understanding

TL;DR: Experimental evidence suggests that degradation of type IV collagen, and perhaps also perlecan, is the key event in the onset of microvessel damage, and it is necessary to study this phenomenon from a holistic, systemic perspective in which the action of other venom components is also taken into consideration.
References
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Journal ArticleDOI

Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4

TL;DR: Using an improved method of gel electrophoresis, many hitherto unknown proteins have been found in bacteriophage T4 and some of these have been identified with specific gene products.
Journal Article

Cleavage of structural proteins during the assemble of the head of bacterio-phage T4

U. K. Laemmli
- 01 Jan 1970 - 
TL;DR: Using an improved method of gel electrophoresis, many hitherto unknown proteins have been found in bacteriophage T4 and some of these have been identified with specific gene products as mentioned in this paper.
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Astacins, serralysins, snake venom and matrix metalloproteinases exhibit identical zinc-binding environments (HEXXHXXGXXH and Met-turn) and topologies and should be grouped into a common family, the 'metzincins'

TL;DR: X‐ray crystal structures of two zinc endopeptidases, astacin from crayfish and adamalysin II from snake venom, reveal a strong overall topological equivalence and virtually identical extended HEXXHXXGXXH zinc‐binding segments, but in addition a methionine‐containing turn of similar conformation (the ‘Met‐turn’), which forms a hydrophobic basis for the zinc ion and the three liganding histidine residues.
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Snake venoms and the hemostatic system

TL;DR: This review is focused on those venom constituents which affect the blood coagulation pathway, endothelial cells, and platelets, and contains a large number of disintegrins, which act as fibrinogen receptor (integrin GPIIb/IIIa) antagonists.
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Integration of endothelial cells in multicellular spheroids prevents apoptosis and induces differentiation

TL;DR: The findings indicate that polarized surface EC differentiate to become independent of exogenous survival factors and demonstrate that spheroid cell culture systems are useful not just for the study of tumor cells and embryonic stem cells but also for the analysis of differentiated functions of nontransformed cells.
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