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Human-Gyrovirus-Apoptin Triggers Mitochondrial Death Pathway—Nur77 is Required for Apoptosis Triggering:
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet. Tunis University, Tunisia.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet. Silesian University of Technology, Gliwice, Poland.
Tunis University, Tunisia.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet.
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2014 (engelsk)Inngår i: Neoplasia, ISSN 1522-8002, E-ISSN 1476-5586, Vol. 16, nr 9, s. 679-693Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

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, trigger 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-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 (AIF) and cytochrome c. HGV-Apoptin acts via the apoptosome, as lack of expression of APAF1 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 this data indicate that HGV-Apoptin acts through the mitochondrial pathway, in a caspase-dependent manner but independently from the death receptor pathway.

sted, utgiver, år, opplag, sider
Elsevier, 2014. Vol. 16, nr 9, s. 679-693
Emneord [en]
Apoptin, death receptors, mitochondrial pathway, cytc, AIF, caspase, Nur77
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-109684DOI: 10.1016/j.neo.2014.08.001ISI: 000342079000001PubMedID: 25246270OAI: oai:DiVA.org:liu-109684DiVA, id: diva2:740593
Tilgjengelig fra: 2014-08-25 Laget: 2014-08-25 Sist oppdatert: 2018-01-11bibliografisk kontrollert

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14_Chaabane_HGyVapoptin_NeoplasiaGalley.pdf(2602 kB)235 nedlastinger
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Chaabane, WiemCieślar-Pobuda, ArturJain, Mayur V.Rafat, MehrdadLos, Marek

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