P
Peter Polčic
Researcher at Comenius University in Bratislava
Publications - 24
Citations - 5887
Peter Polčic is an academic researcher from Comenius University in Bratislava. The author has contributed to research in topics: Mitochondrion & Bcl-2 family. The author has an hindex of 12, co-authored 23 publications receiving 5379 citations. Previous affiliations of Peter Polčic include Oregon Health & Science University.
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BH3‐only proteins Noxa, Bik, Bmf, and Bid activate Bax and Bak indirectly when studied in yeast model
Gabriela Gérecová,Jana Kopanicová,Petra Jaká,Lucia Běhalová,Barbora Juhásová,Ingrid Bhatia-Kiššová,Michael Forte,Peter Polčic,Marek Mentel +8 more
TL;DR: It is reported that the cell death-promoting activity of BH3-only proteins Bik, Bmf, Noxa, and tBid can only be reconstituted in yeast when both multidomain proapoptotic and antiap optotic Bcl-2 family proteins are present.
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Adenine nucleotide transport via Sal1 carrier compensates for the essential function of the mitochondrial ADP/ATP carrier
TL;DR: It is shown that adenine nucleotide transport activity related to Sal1p can be demonstrated in isolated mitochondria as well as in intact cells under conditions when Aac2-mediated exchange is not functional.
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Yeast as a tool for studying proteins of the Bcl-2 family
TL;DR: This review focuses on using yeast expressing mammalian proteins of the Bcl-2 family as a tool to investigate mechanisms, by which these proteins permeabilize mitochondrial membranes, mechanisms,By which pro- and antiapoptotic members of this family interact, and involvement of other cellular components in the regulation of programmed cell death by Bcl -2 family proteins.
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BH3-only protein Bim inhibits activity of antiapoptotic members of Bcl-2 family when expressed in yeast.
Barbora Juhásová,Marek Mentel,Ingrid Bhatia-Kiššová,Igor Zeman,Jordan Kolarov,Michael Forte,Peter Polčic +6 more
TL;DR: It is reported that cell death promoting activity of BH3‐only protein Bim can be reconstituted in yeast when both Bax and antiapoptotic protein Bcl‐XL are present, suggesting that Bim likely activates Bax indirectly by inhibiting antiapopotic proteins.
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Alterations in mitochondrial morphology of Schizosaccharomyces pombe induced by cell-death promoting agents.
TL;DR: Aberrant mitochondrial morphology generated by either Bax or acetic acid was not accompanied with the loss of mitochondrial genome (mtDNA), indicating that alterations of mitochondrial morphology following death stimuli follow different mechanisms than those involved in mitochondrial inheritance mutants.