Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.3389/fmicb.2018.01341 http://scihub22266oqcxt.onion/10.3389/fmicb.2018.01341 C6036244!6036244!30013522     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Microbiol 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=30013522|t=2018. Amastigote Synapse: The Tricks of Trypanosoma cruzi Extracellular Amastigotes |pdf=|usr=}}{{30013522}} gab.com Text Amastigote Synapse: The Tricks of Trypanosoma cruzi Extracellular Amastigotes JO: Front Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=30013522 #FOAvip To complete its life cycle within the mammalian host, Trypanosoma cruzi, the agent of Chagas? disease, must enter cells. Trypomastigotes originating from the insect vector (metacyclic) or from infected cells (bloodstream/tissue culture-derived) are the classical infective forms of the parasite and enter mammalian cells in an actin-independent manner. By contrast, amastigotes originating from the premature rupture of infected cells or transformed from swimming trypomastigotes (designated extracellular amastigotes, EAs) require functional intact microfilaments to invade non-phagocytic host cells. Earlier work disclosed the key features of EA-HeLa cell interplay: actin-rich protrusions called ?cups? are formed at EA invasion sites on the host cell membrane that are also enriched in actin-binding proteins, integrins and extracellular matrix elements. In the past decades we described the participation of membrane components and secreted factors from EAs as well as the actin-regulating proteins of host cells involved in what we propose to be a phagocytic-like mechanism of parasite uptake. Thus, regarding this new perspective herein we present previously described EA-induced ?cups? as parasitic synapse since they can play a role beyond its architecture function. In this review, we focus on recent findings that shed light on the intricate interaction between extracellular amastigotes and non-phagocytic HeLa cells. Twit Text FOAVip Amastigote Synapse: The Tricks of Trypanosoma cruzi Extracellular Amastigotes ????Front Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=30013522 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30013522 #FOAvip English Wikipedia <ref>{{Cite pmid|30013522}}</ref> Amastigote Synapse: The Tricks of Trypanosoma cruzi Extracellular Amastigotes #MMPMID30013522 Bonfim-Melo A; Ferreira ER; Florentino PTV; Mortara RA Front Microbiol 2018[]; 9 (ä): ä PMID30013522show ga To complete its life cycle within the mammalian host, Trypanosoma cruzi, the agent of Chagas? disease, must enter cells. Trypomastigotes originating from the insect vector (metacyclic) or from infected cells (bloodstream/tissue culture-derived) are the classical infective forms of the parasite and enter mammalian cells in an actin-independent manner. By contrast, amastigotes originating from the premature rupture of infected cells or transformed from swimming trypomastigotes (designated extracellular amastigotes, EAs) require functional intact microfilaments to invade non-phagocytic host cells. Earlier work disclosed the key features of EA-HeLa cell interplay: actin-rich protrusions called ?cups? are formed at EA invasion sites on the host cell membrane that are also enriched in actin-binding proteins, integrins and extracellular matrix elements. In the past decades we described the participation of membrane components and secreted factors from EAs as well as the actin-regulating proteins of host cells involved in what we propose to be a phagocytic-like mechanism of parasite uptake. Thus, regarding this new perspective herein we present previously described EA-induced ?cups? as parasitic synapse since they can play a role beyond its architecture function. In this review, we focus on recent findings that shed light on the intricate interaction between extracellular amastigotes and non-phagocytic HeLa cells. äAmastigote Synapse: The Tricks of Trypanosoma cruzi Extracellular Amas(epmc).pdf DeepDyve Pubget Overpricing