{"title":"锥虫的凋亡样死亡:寻找可能的途径和涉及的基因。","authors":"Ali Ouaissi","doi":"10.1186/1475-9292-2-5","DOIUrl":null,"url":null,"abstract":"<p><p>Members of the Trypanosomatidae family comprises species that are causative of important human diseases such as Chagas'disease, Leishmaniasis and sleeping sickness. A wealth of evidence has accumulated that illustrates the ability of these unicellular organisms to undergo, with or without induction (stress conditions), a cell death with some features resembling apoptosis-like phenomenon. However, despite the apparent phenotypic similarities between the apoptosis-like death of kinetoplastids and mammalian nucleated cell programmed cell death (PCD), the pathways seem to differ significantly. This review analyses some of the current data related to the cell death in trypanosomatids. Special attention is given to members of conserved protein families demonstrating remarkable diversity and plasticity of function [i.e. elongation factor-1 subunits alpha and gamma; and the Silent Information Regulator (SIR2)-related gene, showed to be associated with resistance to apoptosis-like death in Leishmania]. The elucidation of the molecular events which tightly regulated the processes of growth arrest, differentiation and death of Trypanosoma cruzi, Leishmania spp and African trypanosomes, might allow not only to define a more comprehensive view of the cell death machinery in term of evolutionary origin but may also be useful to identify new target molecules for chemotherapeutic drug development and therapeutic intervention.</p>","PeriodicalId":17853,"journal":{"name":"Kinetoplastid Biology and Disease","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2003-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1475-9292-2-5","citationCount":"35","resultStr":"{\"title\":\"Apoptosis-like death in trypanosomatids: search for putative pathways and genes involved.\",\"authors\":\"Ali Ouaissi\",\"doi\":\"10.1186/1475-9292-2-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Members of the Trypanosomatidae family comprises species that are causative of important human diseases such as Chagas'disease, Leishmaniasis and sleeping sickness. A wealth of evidence has accumulated that illustrates the ability of these unicellular organisms to undergo, with or without induction (stress conditions), a cell death with some features resembling apoptosis-like phenomenon. However, despite the apparent phenotypic similarities between the apoptosis-like death of kinetoplastids and mammalian nucleated cell programmed cell death (PCD), the pathways seem to differ significantly. This review analyses some of the current data related to the cell death in trypanosomatids. Special attention is given to members of conserved protein families demonstrating remarkable diversity and plasticity of function [i.e. elongation factor-1 subunits alpha and gamma; and the Silent Information Regulator (SIR2)-related gene, showed to be associated with resistance to apoptosis-like death in Leishmania]. The elucidation of the molecular events which tightly regulated the processes of growth arrest, differentiation and death of Trypanosoma cruzi, Leishmania spp and African trypanosomes, might allow not only to define a more comprehensive view of the cell death machinery in term of evolutionary origin but may also be useful to identify new target molecules for chemotherapeutic drug development and therapeutic intervention.</p>\",\"PeriodicalId\":17853,\"journal\":{\"name\":\"Kinetoplastid Biology and Disease\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2003-06-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1186/1475-9292-2-5\",\"citationCount\":\"35\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Kinetoplastid Biology and Disease\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1186/1475-9292-2-5\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Kinetoplastid Biology and Disease","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1186/1475-9292-2-5","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Apoptosis-like death in trypanosomatids: search for putative pathways and genes involved.
Members of the Trypanosomatidae family comprises species that are causative of important human diseases such as Chagas'disease, Leishmaniasis and sleeping sickness. A wealth of evidence has accumulated that illustrates the ability of these unicellular organisms to undergo, with or without induction (stress conditions), a cell death with some features resembling apoptosis-like phenomenon. However, despite the apparent phenotypic similarities between the apoptosis-like death of kinetoplastids and mammalian nucleated cell programmed cell death (PCD), the pathways seem to differ significantly. This review analyses some of the current data related to the cell death in trypanosomatids. Special attention is given to members of conserved protein families demonstrating remarkable diversity and plasticity of function [i.e. elongation factor-1 subunits alpha and gamma; and the Silent Information Regulator (SIR2)-related gene, showed to be associated with resistance to apoptosis-like death in Leishmania]. The elucidation of the molecular events which tightly regulated the processes of growth arrest, differentiation and death of Trypanosoma cruzi, Leishmania spp and African trypanosomes, might allow not only to define a more comprehensive view of the cell death machinery in term of evolutionary origin but may also be useful to identify new target molecules for chemotherapeutic drug development and therapeutic intervention.