Abstract:
:The inhibition of apoptosis by Toxoplasma gondii is governed by its modulation of several signaling cascades including the NFkappaappaB and JNK pathways. This is evident in the dysregulation of JNK activation following treatment with UV and TNFalpha, both apoptogenic stimuli. Infection-mediated interference with the JNK cascade was found to be highly reproducible in HeLa cells. In light of emerging evidence regarding cross talk between the JNK and NFkappaB cascades, we examined the impact of infection in wild type and RelA/p65-/- mouse embryonic fibroblasts (MEF). Remarkably, parasite infection failed to significantly impact both UV and TNFalpha-mediated JNK phosphorylation in both cell lines suggesting a cell type specific effect. Furthermore siRNA-mediated knockdown of RelA/p65 failed to impact the parasite mediated effects on stimulus dependent activation of JNK in HeLa cells. Finally, the infection mediated suppression of JNK phosphorylation in HeLa cells did not result in decreased JNK kinase activity. Rather, the reduced levels of phospho-JNK in infected cells correlated with increased phosphatase activity noted by the partial rescue of the phenotype following treatment with okadaic acid. Taken together the results indicate that manipulation of the JNK pathway does not involve NFkappaB and is furthermore not a central component of the parasite enforced block of apoptosis. It further highlights the complexity of these systems and the danger of extrapolating results both within and across pathogen-host cell systems based on limited studies.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Carmen JC,Southard RC,Sinai APdoi
10.1016/j.yexcr.2008.09.019subject
Has Abstractpub_date
2008-12-10 00:00:00pages
3724-36issue
20eissn
0014-4827issn
1090-2422pii
S0014-4827(08)00387-Xjournal_volume
314pub_type
杂志文章abstract::Tunicamycin, an inhibitor of one of the earliest steps in the synthesis of N-linked oligosaccharides, prevents bud formation and growth in Saccharomyces cerevisiae cells that are either growing exponentially or recovering from different cell cycle arrests at start. Analysis of tunicamycin-treated cells by flow microfl...
journal_title:Experimental cell research
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journal_title:Experimental cell research
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journal_title:Experimental cell research
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journal_title:Experimental cell research
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journal_title:Experimental cell research
pub_type: 杂志文章
doi:10.1006/excr.1998.4175
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journal_title:Experimental cell research
pub_type: 杂志文章
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journal_title:Experimental cell research
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doi:10.1016/0014-4827(92)90294-i
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journal_title:Experimental cell research
pub_type: 杂志文章
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journal_title:Experimental cell research
pub_type: 杂志文章
doi:10.1016/0014-4827(87)90172-8
更新日期:1987-08-01 00:00:00
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journal_title:Experimental cell research
pub_type: 杂志文章
doi:10.1016/j.yexcr.2008.07.021
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journal_title:Experimental cell research
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doi:10.1016/j.yexcr.2010.09.008
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doi:10.1016/j.yexcr.2005.03.006
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更新日期:2020-05-15 00:00:00
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journal_title:Experimental cell research
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doi:10.1006/excr.1996.0133
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journal_title:Experimental cell research
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journal_title:Experimental cell research
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更新日期:2004-11-15 00:00:00
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journal_title:Experimental cell research
pub_type: 杂志文章
doi:10.1016/j.yexcr.2007.04.014
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abstract::Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresis...
journal_title:Experimental cell research
pub_type: 杂志文章
doi:10.1016/j.yexcr.2019.111597
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