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Wyszukujesz frazę "Biogenesis" wg kryterium: Temat


Wyświetlanie 1-4 z 4
Tytuł:
Prohibitins and Ras2 protein cooperate in the maintenance of mitochondrial function during yeast aging.
Autorzy:
Kirchman, Paul
Miceli, Michael
West, Roger
Jiang, James
Kim, Sangkyu
Jazwinski, S
Powiązania:
https://bibliotekanauki.pl/articles/1043375.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
ROS
retrograde response
Saccharomyces cerevisiae
longevity
mitochondrial biogenesis
Opis:
The yeast Saccharomyces cerevisiae has a finite replicative life span. Yeasts possess two prohibitins, Phb1p and Phb2p, in similarity to mammalian cells. These proteins are located in the inner mitochondrial membrane, where they are involved in the processing of newly-synthesized membrane proteins. We demonstrate that the elimination of one or both of the prohibitin genes in yeast markedly diminished the replicative life span of cells that lack fully-functional mitochondria, while having no effect on cells with functioning mitochondria. This deleterious effect was suppressed by the deletion of the RAS2 gene. The expression of PHB1 and PHB2 declined gradually up to 5-fold during the life span. Cells in which PHB1 was deleted in conjunction with the absence of a mitochondrial genome displayed remarkable changes in mitochondrial morphology, distribution, and inheritance. This loss of mitochondrial integrity was not seen in cells devoid of PHB1 but possessing an intact mitochondrial genome. In a subset of the cells, the changes in mitochondrial integrity were associated with increased production of reactive oxygen species, which co-localized with the altered mitochondria. The mitochondrial deficits described above were all suppressed by deletion of RAS2. Our data, together with published information, are interpreted to provide a unified view of the role of the prohibitins in yeast aging. This model posits that the key initiating event is a decline in mitochondrial function, which leads to progressive oxidative damage that is exacerbated in the absence of the prohibitins. This aggravation of the initial damage is ameliorated by the suppression of the production of mitochondrial proteins in the absence of Ras2p signaling of mitochondrial biogenesis.
Źródło:
Acta Biochimica Polonica; 2003, 50, 4; 1039-1056
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Nuclear and mitochondrial genome responses in HeLa cells treated with inhibitors of mitochondrial DNA expression
Autorzy:
Piechota, Janusz
Szczęsny, Roman
Wolanin, Kamila
Chlebowski, Aleksander
Bartnik, Ewa
Powiązania:
https://bibliotekanauki.pl/articles/1041204.pdf
Data publikacji:
2006
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
thiamphenicol
mtDNA depletion
HeLa
dideoxycytidine
mitochondrial biogenesis
ethidium bromide
Opis:
The influence of mutations in the mitochondrial DNA (mtDNA) on the bioenergetic metabolism of the cell is still poorly understood. Many of the mutations in the mtDNA affect the expression of the mitochondrial genome. Investigations on cells from patients are not easy, especially as the mitochondrial DNA is heteroplasmic and this state is changed in culture. Moreover, the nuclear background and the mitochondrial haplotype may affect the behaviour of cells. Transfer of patient mitochondria to rho zero cell lines is also not optimal as these cells in general have many nuclear changes which may also affect cell behaviour. Thus, we decided to use inhibitors of mitochondrial genome expression, such as thiamphenicol, ethidium bromide and dideoxycytidine to investigate the bioenergetic metabolism of HeLa cells. We found that oxidative phosphorylation and glycolysis participate equally in ATP production in HeLa cells and that decreased activity of the respiratory chain leads to increased glycolysis and the reduction of cell growth. Insufficient ATP production in the oxidative phosphorylation process was not compensated by increased proliferation of the mitochondria. However, we were able to show that there are some mechanisms compensating limited expression of the mitochondrial genome within the mitochondria. Experiments with dideoxycytidine revealed that 10-fold decrease of the mtDNA copy number resulted in almost normal activity of cytochrome c oxidase. We found that mtDNA depletion is compensated mostly on the level of RNA metabolism in the mitochondria. Thus, our results are in agreement with the hypothesis that transcription initiation rather than mtDNA copy number is a rate limiting factor for expression of the mitochondrial genome.
Źródło:
Acta Biochimica Polonica; 2006, 53, 3; 485-495
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Discrete dynamic system oriented on the formation of prebiotic dipeptides from Rodes experiment
Autorzy:
Polanco, Carlos
Samaniego, José
Buhse, Thomas
Castañón González, Jorge
Powiązania:
https://bibliotekanauki.pl/articles/1039201.pdf
Data publikacji:
2014
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
origins of life
biogenesis
dipeptides
salt-induced peptide formation
Opis:
This work attempts to rationalize the possible prebiotic profile of the first dipeptides of about 4 billion years ago based on a computational discrete dynamic system that uses the final yields of the dipeptides obtained in Rode's experiments of salt-induced peptide formation (Rode et al., 1999, Peptides 20: 773-786). The system built a prebiotic scenario that allowed us to observe that (i) the primordial peptide generation was strongly affected by the abundances of the amino acid monomers, (ii) small variations in the concentration of the monomers have almost no effect on the final distribution pattern of the dipeptides and (iii) the most plausible chemical reaction of prebiotic peptide bond formation can be linked to Rode's hypothesis of a salt-induced scenario. The results of our computational simulations were related to former simulations of the Miller, and Fox & Harada experiments on amino acid monomer and oligomer generation, respectively, offering additional information to our approach.
Źródło:
Acta Biochimica Polonica; 2014, 61, 4; 717-726
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
MicroRNA biogenesis: Epigenetic modifications as another layer of complexity in the microRNA expression regulation
Autorzy:
Bhat, Susheel
Jarmolowski, Artur
Szweykowska-Kulińska, Zofia
Powiązania:
https://bibliotekanauki.pl/articles/1038729.pdf
Data publikacji:
2016
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
microRNA
microRNA biogenesis
m6A modification
m6A RNA methyltransferase
Opis:
Since their discovery, microRNAs have led to a huge shift in our understanding of the regulation of key biological processes. The discovery of epigenetic modifications that affect microRNA expression has added another layer of complexity to the already tightly controlled regulatory machinery. Modifications like uridylation, adenylation and RNA editing have been shown to have variable effects on miRNA biogenesis and action. Methylation of the N6 adenosine has been studied extensively in mRNA. Presence of the N6-methyl-adenosine (m6A) mark and its critical importance in miRNA biogenesis in animals adds to our understanding of the regulatory mechanisms, while its effect on miRNA biogenesis in plants is yet to be understood.
Źródło:
Acta Biochimica Polonica; 2016, 63, 4; 717-723
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-4 z 4

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