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001-es BibID:	BIBFORM086717
Első szerző:	Golda Mária (molekuláris biológus)
Cím:	Study of the Retrotransposon-Derived Human PEG10 Protease / Mária Golda, János András Mótyán, Mohamed Mahdi, József Tőzsér
Dátum:	2020
Megjegyzések:	Paternally expressed gene 10 (PEG10) is a human retrotransposon-derived imprinted gene. Previous works have demonstrated that a mutation in the coding sequence of this gene is lethal with regard to embryological age due to defects of placental development. In addition, PEG10 is implicated in several malignancies, such as pancreatic cancer and hepatocellular carcinoma. The PEG10 gene encodes two protein isoforms, which are translated by a typical retroviral frameshift mechanism. The Gag-like protein (RF1PEG10) is encoded by reading frame 1, whilst reading frames 1 and 2 accounts for the Gag-Pol-like polyprotein (RF1/RF2PEG10). The protease (PR) domain of RF2PEG10 contains an -Asp-Ser-Gly- sequence, which refers to the conservative -Asp-Ser/Thr-Gly- active-site motif of retroviral aspartic proteases. The function of the aspartic protease domain of RF2PEG10 remains unclear. In order to further investigate the function of the PEG10 protease (PRPEG10), a frameshift mutant was generated (fsRF1/RF2PEG10) for comparison with the RF1/RF2PEG10 form. To study the effects of PRPEG10 on cellular proliferation and viability, mammalian HEK293T and HaCaT cells were transfected with plasmids encoding for either the frameshift mutant (fsRF1/RF2PEG10) or a PR active-site (D370A) mutant fsRF1/RF2PEG10. Based on our findings, an fsRF1/RF2PEG10 overexpression resulted in an increased cellular proliferation, compared to the mutant form. Interestingly, transfection with fsRF1/RF2PEG10 had a detrimental effect on cell viability. We hypothesize that PRPEG10 may play a cardinal role in the function of this retroviral remnant, possibly implicated in cellular proliferation and the inhibition of apoptosis.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idézhető absztrakt folyóiratcikk PEG10 paternally expressed gene 10 cell viability cell proliferation cis protease activity ubiquitination homology modeling retroviral-like protease retrotransposon protease
Megjelenés:	Proceedings. - 50 : 1 (2020), p. 110. -
További szerzők:	Mótyán János András (1981-) (biokémikus, molekuláris biológus) Mahdi, Mohamed (1979-) (orvos, tudományos segédmunkatárs) Tőzsér József (1959-) (molekuláris biológus, biokémikus, vegyész)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00044 GINOP K-101591 OTKA NKFIH-1150-6/2019 Egyéb NKFI-125238 Egyéb
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