| 1. |
- Andersson, SGE, et al.
(author)
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Genomic evolution drives the evolution of the translation system
- 1995
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In: BIOCHEMISTRY AND CELL BIOLOGY-BIOCHIMIE ET BIOLOGIE CELLULAIRE. - : NATL RESEARCH COUNCIL CANADA. - 0829-8211. ; 73:11-12, s. 775-787
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Journal article (other academic/artistic)abstract
- Our thesis is that the characteristics of the translational machinery and its organization are selected in part by evolutionary pressure on genomic traits have nothing to do with translation per se. These genomic traits include size, composition, and arch
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| 2. |
- Bandura, L, et al.
(author)
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Differential effects of selenite and selenate on human melanocytes, keratinocytes, and melanoma cells
- 2005
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In: Biochemistry and cell biology = Biochimie et biologie cellulaire. - : Canadian Science Publishing. - 0829-8211. ; 83:2, s. 196-211
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Journal article (peer-reviewed)abstract
- Among the substances that attracted the attention of oncologists in recent years are selenium-containing compounds, both inorganic and organic. Several epidemiological studies have shown an inverse correlation between selenium intake and cancer incidence. In the experiments reported here, we compared the effects of 2 inorganic selenium- containing salts that differed in the level of selenium oxidation, selenite IV and selenate VI. We tested the effects of these 2 compounds on cell survival and growth, cell cycle processing, cell morphology, cytoskeleton, and lipid peroxidation in 3 human skin cell types: normal keratinocytes, melanocytes, and human melanoma cell line HTB140. The different effects of selenite and selenate on the viability, growth, and morphology of normal cells and tumor cells are reported and provide a base for future research and treatment of some neoplastic diseases. The attention is paid to cell apoptosis induced by selenite and not by selenate, and the effects of tested substances on thioredoxin reductase system are postulated.Key words: selenium, cell viability and growth, apoptosis, lipid oxidation, thioredixin reductase system, human skin cells, human melanoma.
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| 3. |
- Dayeh, Tasnim, et al.
(author)
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Does epigenetic dysregulation of pancreatic islets contribute to impaired insulin secretion and type 2 diabetes?
- 2015
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In: Biochemistry and Cell Biology. - : Canadian Science Publishing. - 1208-6002 .- 0829-8211. ; 93:5, s. 511-521
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Research review (peer-reviewed)abstract
- β cell dysfunction is central to the development and progression of type 2 diabetes (T2D). T2D develops when β cells are not able to compensate for the increasing demand for insulin caused by insulin resistance. Epigenetic modifications play an important role in establishing and maintaining β cell identity and function in physiological conditions. On the other hand, epigenetic dysregulation can cause a loss of β cell identity, which is characterized by reduced expression of genes that are important for β cell function, ectopic expression of genes that are not supposed to be expressed in β cells, and loss of genetic imprinting. Consequently, this may lead to β cell dysfunction and impaired insulin secretion. Risk factors that can cause epigenetic dysregulation include parental obesity, an adverse intrauterine environment, hyperglycemia, lipotoxicity, aging, physical inactivity, and mitochondrial dysfunction. These risk factors can affect the epigenome at different time points throughout the lifetime of an individual and even before an individual is conceived. The plasticity of the epigenome enables it to change in response to environmental factors such as diet and exercise, and also makes the epigenome a good target for epigenetic drugs that may be used to enhance insulin secretion and potentially treat diabetes.
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| 4. |
- Ehrenberg, Måns, et al.
(author)
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tRNA-ribosome interactions
- 1995
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In: Biochemistry and Cell Biology. - 0829-8211 .- 1208-6002. ; 73:11-12, s. 1049-1054
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Research review (peer-reviewed)abstract
- Direct measurements of the rates of dissociation of dipeptidyl-tRNA from the ribosome show that hyperaccurate SmP and SmD ribosomes have unstable A-site binding of peptidyl-tRNA, while P-site binding is extremely stable in relation to the wild type. Error-prone Ram ribosomes, on the other hand, have stable A-site and unstable P-site binding of peptidyl-tRNA. At least for these mutant ribosomes, we conclude that stabilization of peptidyl-tRNA in one site destabilizes binding in the other. Elongation factor Tu (EF-Tu) undergoes a dramatic structural transition from its GDP-bound form to its active GTP-bound form, in which it binds aa-tRNA (aminoacyl-tRNA) in ternary complex. The effects of substitution mutations at three sites in domain I of EF-Tu, Gln124, Leu120, and Tyr160, all of which point into the domain I-domain III interface in both the GTP and GDP conformations of EF-Tu, were examined. Mutations at each position cause large reductions in aa-tRNA binding. An attractive possibility is that the mutations alter the domain I-domain III interface such that the switching of EF-Tu between different conformations is altered, decreasing the probability of aa-tRNA binding. We have previously found that two GTPs are hydrolyzed per peptide bond on EF-Tu, the implication being that two molecules of EF-Tu may interact on the ribosome to catalyze the binding of a single aa-tRNA to the A-site. More recently we found that ribosomes programmed with mRNA constructs other than poly(U), including the sequence AUGUUUACG, invariably use two GTPs per peptide bond in EF-Tu function. Other experiments measuring the protection of aa-tRNA from deacylation or from RNAse A attack show that protection requires two molecules of EF-Tu, suggesting an extended ternary complex. To remove remaining ambiguities in the interpretion of these experiments, we are making direct molecular weight determinations with neutron scattering and sedimentation-diffusion techniques.
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| 5. |
- Florian, Paula, et al.
(author)
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Endocytosis and trafficking of human lactoferrin in macrophage-like human THP-1 cells (1).
- 2012
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In: Biochemistry and cell biology = Biochimie et biologie cellulaire. - : Canadian Science Publishing. - 1208-6002. ; 90:3, s. 449-55
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Journal article (peer-reviewed)abstract
- Different cell types have been reported to internalize lactoferrin (Lf) by specific or nonspecific receptors. Our studies focused on the endocytic pathway of human Lf in macrophage-like THP-1 cells. Lactoferrin was found to be internalized by THP-1 cells differentiated with phorbol myristate acetate. Incubation of cells with chlorpromazine and dansylcadaverine, inhibitors of clathrin-dependent endocytosis, led to a 50% inhibition of Lf internalization compared with untreated cells. Bafilomycin A1 and NH(4)Cl treatment also resulted in 40%-60% inhibition, respectively, suggesting that the internalization of Lf may partly be mediated by acidic endosome-like organelles. Endocytic uptake of Lf was also cholesterol-dependent, as shown by methyl-β-cyclodextrin or nystatin treatment of the cells prior to internalization. Partial colocalization of Lf and EEA-1, a marker specific for early endosomes, could be observed. Colocalization of Lf with a specific endoplasmic reticulum marker was also detected. Our results suggest that Lf is internalized mainly by the clathrin-dependent pathway in THP-1 cells and targets the ER. The physiological consequences of this intracellular trafficking will be the subject of future investigations.
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| 6. |
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| 7. |
- Navakauskiene, Ruta, et al.
(author)
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Translocation of transcription regulators into the nucleus during granulocyte commitment of HL-60 cells
- 2003
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In: Biochemistry and Cell Biology. - : Canadian Science Publishing. - 0829-8211 .- 1208-6002. ; 81:4, s. 285-295
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Journal article (peer-reviewed)abstract
- Expression of transcription factors required for lineage commitment of differentiating cells (C/EBPβ and c-Myb) and for survival of differentiated cells (STATs and NFκB) was examined in the HL-60 cell line. Differentiation was induced by treating the cells with retinoic acid. c-Myb expression in the nucleus restored at the precommitment stage (18 h) what concurred with the highest nuclear level of C/EBPβ, which suggests a combinatorial interaction of these transcription factors in the granulocytic signalling pathway. Expression of STAT5a and STAT5b varied during differentiation, whereas no significant changes were seen in STAT3 levels. Increased cytosolic level of NFκB p65 during precommitment and commitment stages of granulocytic differentiation coincided with augmentation of the STAT5a protein level, which could be evidence of their possible cooperation during granulocytic-lineage commitment of HL-60 cells. Our results suggest that the studied transcription factors cooperatively promote signalling in the differentiating promyelocytic HL-60 cell line in response to retinoic acid.
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| 8. |
- Pocock, Tessa, et al.
(author)
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Excitation pressure regulates the activation energy for recombination events in the photosystem II reaction centres of Chlamydomonas reinhardtii
- 2007
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In: Biochemistry and Cell Biology. - 0829-8211 .- 1208-6002. ; 85:6, s. 721-729
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Journal article (peer-reviewed)abstract
- Using in vivo thermoluminescence, we examined the effects of growth irradiance and growth temperature on charge recombination events in photosystem IT reaction centres of the model green alga Chlamydomonas reinhardtii. We report that growth at increasing irradiance at either 29 or 15 degrees C resulted in comparable downward shifts in the temperature peak maxima (T-M) for S(2)Q(B)(-) charge pair recombination events, with minimal changes in S(2)Q(A)(-) recombination events. This indicates that such growth conditions decrease the activation energy required for S(2)QB(-) charge pair recombination events with no concomitant change in the activation energy for S(2)Q(A)(-) recombination events. This resulted in a decrease in the Delta T-M between S(2)Q(A)(-) and S(2)Q(B)(-) recombination events, which was reversible when shifting cells from low to high irradiance and back to low irradiance at 29 degrees C. We interpret these results to indicate that the redox potential of Q(B) was modulated independently of Q(A), which consequently narrowed the redox potential gap between Q(A) and Q(B) in photosystem II reaction centres. Since a decrease in the Delta T-M between S(2)Q(A)(-) and S(2)Q(B)(-) recombination events correlated with growth at increasing excitation pressure, we conclude that acclimation to growth under high excitation pressure narrows the redox potential gap between Q(A) and Q(B) in photosystem 11 reaction centres, enhancing the probability for reaction center quenching in C. reinhardtii. We discuss the molecular basis for the modulation of the redox state of Q(B), and suggest that the potential for reaction center quenching complements antenna quenching via the xanthophyll cycle in the photoprotection of C. reinhardtii from excess light.
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| 9. |
- Rundquist, Ingemar, et al.
(author)
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Analyses of linker histone - chromatin interactions in situ
- 2006
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In: Biochemistry and Cell Biology. - 0829-8211 .- 1208-6002. ; 84:4, s. 427-436
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Journal article (peer-reviewed)abstract
- Recent studies, using cytometric techniques based on fluorescence microscopy, have provided new information on how linker histones interact with chromatin in vivo or in situ. In particular, the use of green fluorescent proteins (GFPs) has enabled detailed studies of how individual H1 subtypes, and specific motifs in them, interact with chromatin in vivo. Furthermore, the development of cytochemical methods to study the interaction between linker histones and chromatin using DNA-binding fluorochromes as indirect probes for linker histone affinity in situ, in combination with highly sensitive and specific analytical methods, has provided additional information on the interactions between linker histones and chromatin in several cell systems. Such results verified that linker histones have a substantially higher affinity for chromatin in mature chicken erythrocytes than in frog erythrocytes, and they also indicated that the affinity decreased during differentiation of the frog erythrocytes. Furthermore, in cultured human fibroblasts, the linker histones showed a relatively high affinity for chromatin in interphase, whereas it showed a significantly lower affinity in highly condensed metaphase chromosomes. This method also enables the analysis of linker histone affinity for chromatin in H1-depleted fibroblasts reconstituted with purified linker histones. No consistent correlation between linker histone affinity and chromatin condensation has so far been detected.
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| 10. |
- Tritto, Simona, et al.
(author)
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Osmotic water permeability of rat intestinal brush border membrane vesicles : involvement of aquaporin-7 and aquaporin-8 and effect of metal ions
- 2007
-
In: Biochemistry and Cell Biology. - : Canadian Science Publishing. - 0829-8211 .- 1208-6002. ; 85:6, s. 675-684
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Journal article (peer-reviewed)abstract
- Water channels AQP7 and AQP8 may be involved in transcellular water movement in the small intestine. We show that both AQP7 and AQP8 mRNA are expressed in rat small intestine. Immunoblot and immunohistochemistry experiments demonstrate that AQP7 and AQP8 proteins are present in the apical brush border membrane of intestinal epithelial cells. We investigated the effect of several metals and pH on the osmotic water permeability (Pf) of brush border membrane vesicles (BBMVs) and of AQP7 and AQP8 expressed in a cell line. Hg2+, Cu2+, and Zn2+ caused a significant decrease in the BBMV Pf, whereas Ni2+ and Li+ had no effect. AQP8-transfected cells showed a reduction in Pf in the presence of Hg2+ and Cu2+, whereas AQP7-transfected cells were insensitive to all tested metals. The Pf of both BBMVs and cells transfected with AQP7 and AQP8 was not affected by pH changes within the physiological range, and the Pf of BBMVs alone was not affected by phlorizin or amiloride. Our results indicate that AQP7 and AQP8 may play a role in water movement via the apical domain of small intestine epithelial cells. AQP8 may contribute to the water-imbalance-related clinical symptoms apparent after ingestion of high doses of Hg2+ and Cu2+.
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