Human-Gyrovirus-Apoptin Triggers Mitochondrial Death Pathway—Nur77 is Required for Apoptosis Triggering
| العنوان: | Human-Gyrovirus-Apoptin Triggers Mitochondrial Death Pathway—Nur77 is Required for Apoptosis Triggering |
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| المؤلفون: | Joerg Stetefeld, Joanna Rzeszowska-Wolny, Mayur V. Jain, Artur Cieślar-Pobuda, Wiem Chaabane, Saeid Ghavami, Marek J. Łos, Mohamed El-Gazzah, Mehrdad Rafat |
| المصدر: | Neoplasia: An International Journal for Oncology Research, Vol 16, Iss 9, Pp 679-693 (2014) Neoplasia (New York, N.Y.) |
| بيانات النشر: | Elsevier BV, 2014. |
| سنة النشر: | 2014 |
| مصطلحات موضوعية: | Cytoplasm, Cancer Research, TMRM, Tetramethylrhodamine methyl ester perchlorate0, HGV-Apoptin, Human gyrovirus apoptin, Apoptosis, MOMP, Mitochondrial outer membrane permeabilization, Mitochondrial apoptosis-induced channel, AIF, Nur77, Annan medicinsk grundvetenskap, AIF, Apoptosis inducing factor, Nuclear Receptor Subfamily 4, Group A, Member 1, Gyrovirus, BCL-XL, B-cell lymphoma extra-large, DISC, Death-inducing signal complex, FADD, Other Basic Medicine, Membrane Potential, Mitochondrial, biology, Apoptosis Inducing Factor, Cytochromes c, virus diseases, Receptors, Death Domain, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, mitochondrial pathway, Mitochondria, Cell biology, Protein Transport, Proto-Oncogene Proteins c-bcl-2, Caspases, Apoptosis-inducing factor, Signal Transduction, CAV-Apoptin, Chicken anemia virus apoptin, Programmed cell death, cyt c, cytochrome c, caspase, Bcl-xL, Models, Biological, lcsh:RC254-282, Article, Cell Line, Viral Proteins, death receptors, Humans, 7AAD, 7-amino-actinomycin D, FADD, Fas-associated death domain, Death domain, Intrinsic apoptosis, MEF, Mouse embryonic fibroblast, cytc, digestive system diseases, Apoptin, biology.protein, Apoptosome |
| الوصف: | The human gyrovirus derived protein Apoptin (HGV-Apoptin) a homologue of the chicken anemia virus Apoptin (CAV-Apoptin), a protein with high cancer cells selective toxicity, triggers apoptosis selectively in cancer cells. In this paper, we show that HGV-Apoptin acts independently from the death receptor pathway as it induces apoptosis in similar rates in Jurkat cells deficient in either FADD (fas-associated death domain) function or caspase-8 (key players of the extrinsic pathway) and their parental clones. HGV-Apoptin induces apoptosis via the activation of the mitochondrial intrinsic pathway. It induces both mitochondrial inner and outer membrane permebilization, characterized by the loss of the mitochondrial potential and the release into cytoplasm of the pro-apoptotic molecules including apoptosis inducing factor and cytochrome c. HGV-Apoptin acts via the apoptosome, as lack of expression of apoptotic protease-activating factor 1 in murine embryonic fibroblast strongly protected the cells from HGV-Apoptin–induced apoptosis. Moreover, QVD-oph a broad-spectrum caspase inhibitor delayed HGV-Apoptin–induced death. On the other hand, overexpression of the anti-apoptotic BCL-XL confers resistance to HGV-Apoptin–induced cell death. In contrast, cells that lack the expression of the pro-apoptotic BAX and BAK are protected from HGV-Apoptin induced apoptosis. Furthermore, HGV-Apoptin acts independently from p53 signal but triggers the cytoplasmic translocation of Nur77. Taking together these data indicate that HGV-Apoptin acts through the mitochondrial pathway, in a caspase-dependent manner but independently from the death receptor pathway. |
| وصف الملف: | application/pdf |
| تدمد: | 1476-5586 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4ff91e1764b6bc1727600d6c646b3f55Test https://doi.org/10.1016/j.neo.2014.08.001Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....4ff91e1764b6bc1727600d6c646b3f55 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14765586 |
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