1,720,972 research outputs found
Regulation of cytochrome c oxidase and FoF1-ATPase subunits expression in rat brain during aging
No full textIn the present study we analyzed the age-dependent changes of mRNA levels for cytochrome c oxidase and FoF1-ATP synthase subunits in rat cerebral cortex and cerebellum. To establish whether the regulation of expression is transcriptional or post-transcriptional, the results were compared to those related to protein subunits levels, of the same enzymatic complexes, previously observed. The different patterns of age-related changes of mRNA subunits, in particular the lower increments, compared with those related to protein subunits, indicate that post-transcriptional mechanisms of regulation might be involved in the coordinated expression of the various subunits of each complex. Northern blotting analyses of RNA from the cerebellum of rats at the various ages, showed also differences in age-dependent patterns of transcription between cerebral cortex and cerebellum. Moreover, the major age-dependent changes of mitochondrial-encoded subunits, compared with the nuclear-encoded ones, previously observed at proteins level, occur also during transcriptio
Age-related chances of mitochondrial cytochrome C oxidase and F(0)F(1)-ATP synthase subunit contents in rat cerebral cortex
No full textThe levels of subunits I, II/III, and IV of cytochrome c oxidase and of subunits alpha. beta and gamma of F(0)F(1)-ATP synthase in inner mitochondrial membrane proteins purified from cerebral cortex of rat at 2, 6, 12, 18, 24, 26 months of age were analyzed by Western blot. Age-related changes in the content of subunits, encoded either in mitochondrial or nuclear DNA, were observe
Superoxide dismutase and cytochrome oxidase activities in light and heavy synaptic mitochondria from rat cerebral cortex during aging
No full textThe specific activities of superoxide dismutase (SOD) and cytochrome oxidase (COX) in light and heavy synaptic mitochondria from rat cerebral cortex at different ages (4, 8, 12, 16, 20, and 24 months) have been measured. The specific activity of COX was significantly higher in light synaptic mitochondria than in heavy ones at all ages examined. However, no significant difference during aging was shown. A marked decrease of SOD in light and heavy synaptic mitochondria during aging was observe
Effect of hypoxia on protein composition of synaptic plasma membranes from cerebral cortex during aging
No full textThe effect of hypoxia on the protein composition of synaptic plasma membranes (SPM) isolated from cerebral cortex of rats at 4, 12, and 24 months of age was investigated. The proteins were separated by SDS polyacrylamide gel electrophoresis and the percent content was evaluated by measuring the optical density of the stained gels. After hypoxic treatment various proteins showed significant changes. Some proteins were only affected at 4 and 12 months of age and not at 24 months. The various modified proteins may be identified according to their molecular weight, as follows: the 18 kDa protein with calmodulin; the 23 kDa protein with D3 subunits; the 28 kDa protein could contain the delta subunit of the Ca2+ channel. The changes in the amount of some SPM proteins during hypoxia is consistent with the alteration in membrane polarization and neurotransmission observed in this condition. The effect of aging at the synaptosomal level seems to be a selective process; after hypoxia the age-related changes of many proteins are more pronounce
Effect of hypoxia on mitochondrial protein composition of cerebral cortex during aging
No full textThe effect of hypoxia on the protein composition of mitochondria from cerebral cortex of rats at 4, 12, and 24 months of age was investigated. The proteins were separated by electrophoresis on SDS polyacrylamide gels and the percent content was evaluated by measuring the optical density of the stained gels. The results demonstrate that hypoxic treatment causes a decrease in the amount of some proteins as follows: the 90 and the 16 kDa Mw proteins at 4 months; the 82 and the 79 kDa Mw proteins at 24 months; the 52-49, 35 and 20 kDa at all ages investigated; the 44 kDa protein at 4 and 12 months and the 28 kDa protein at 4 and 24 months of age. Our results show that hypoxic conditions affect mitochondrial protein composition to a greater extent than aging alon
Structural features of the rat GFAP gene and identification of a novel alternative transcript
No full textThe glial fibrillary acidic protein (GFAP) is expressed in a cell-specific manner and represents the major subunit of intermediate filaments of astroglial cells. The knowledge of the gene structure is an important step for further understanding the mechanisms of cell-specific expression. In the present study, we report the complete sequence of the rat GFAP gene and provide evidence for the existence, in the rat brain, of a novel alternative transcript. Since three different transcripts, indicated as GFAP alpha, beta, and gamma, have been previously reported (Feinstein et al, [1992] J. Neurosci. Res. 32:1-14; Zelenika et al. [1995] Mol. Brain Res. 30:251-258), we called this novel mRNA isoform GFAP delta. It is generated by the alternative splicing of a novel exon located in the classic seventh intron. This alternative exon (called VII+) contains a 101-bp coding sequence in frame with exon VII and interrupted by a stop codon TAA at position +5451. Therefore, the novel GFAP delta transcript encodes for an hypothetical GFAP where the forty-two carboxyterminal amino acids encoded by exon VIII and IX are replaced by thirty-three amino acids encoded by exon VII+. Northern blot analysis with a specific probe for exon VII+ revealed a 4.2-kb mRNA, expressed in several brain areas, but absent in extracerebral tissues (lung, heart, kidney, liver, spleen). The previously discovered GFAP isoforms (alpha, beta, and gamma) produce hypothetical translation products differing in the aminoterminal Head domain. The present data suggest, for the first time, the possible existence of GFAP isoforms differing in the carboxy-terminal Tail domai
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