作者: Nobuko Yoshida
DOI: 10.1590/S0001-37652006000100010
关键词: Tyrosine kinase 、 Cruzipain 、 Cell adhesion 、 Signal transduction 、 Trypanosoma cruzi 、 Cell biology 、 Cell 、 Biology 、 Phospholipase C 、 Internalization
摘要: Establishment of infection by Trypanosoma cruzi, the agent Chagasdisease, depends on a series events involving interactions diverse parasite molecules with host components. Here we focus mechanisms target cell invasion metacyclic trypomastigotes (MT) and mammalian tissue culture (TCT). During MT or TCT internalization, signal transduction pathways are activated both in cell, leading to Ca 2+ mobilization. For adhesion, engage surface glycoproteins, such as gp82 gp35/50, which signal-inducing molecules. In T. cruzi isolates that enter cells gp82-mediated manner, protein tyrosine kinase well phospholipase C activated, is released from IP3-sensitive stores, whereas attach mainly through signaling pathway adenylate cyclase appears be stimulated, release acidocalciosomes. addition, isolate-dependent inhibitory signals, mediated MT-specific gp90, may triggered parasite. The repertoire implicated includes glycoproteins gp85 family, members containing binding sites for laminin cytokeratin 18, enzymes cruzipain, trans-sialidase, an oligopeptidase B generates -agonist precursor molecule.