Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.9.3.1 (cytochrome oxidase)
8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intracellular redox conditions influence the activity of several transcription factors leading to a modulation of the expression of the genes controlled by these factors. We examined the changes in cell transcription patterns after oxidative stress induced by diethylmaleate (DEM). Using the differential display technique we identified several differentially expressed sequence tags, four of which are identical or highly homologous to sequences contained in the human cDNAs encoding vimentin, c-fos, cytochrome oxidase IV and ribosomal protein L4; another one corresponds to a transcript of the mitochondrial genome of unknown function. The remaining five cDNAs are not recorded in any sequence data bank. One of these, named Rox3, lights up two mRNA species of approximately 3400 and 3600 bp, significantly increased after treatment with DEM or with other oxidizing agents. This increase appears precociously after exposure to DEM and it is completely prevented by pretreatment with N-acetylcysteine. The Rox3 fragment was used to screen a cDNA library; one fully sequenced clone showed 100% homology with the putative human guanine nucleotide regulatory protein nep1.
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PMID:Differentially expressed mRNAs as a consequence of oxidative stress in intact cells. 755 93

We have evaluated the pattern of c-fos expression induced in the rat spinal cord, caudal brainstem and cerebellum by a behavior that is associated with non-noxious inputs transmitted over large-diameter primary afferent fibers, namely walking for 1 h on a rotating rod. Walking on the rotating rod induced a large increase in the number of Fos-like immunoreactive neurons in regions of the cervical and lumbar spinal cord gray matter that contain neurons that respond to non-noxious stimuli: the inner part of the substantia gelatinosa (lamina IIi), the nucleus proprius and the medial parts of laminae V and VI. We also observed considerable labeling in lamina VII and in ventral horn motoneurons. We did not record an increased number of Fos-like immunoreactive neurons in lamina I, in the outer substantia gelatinosa (lamina IIo), or in the lateral, reticulated portion of lamina V, regions that contain neurons predominantly responsive to noxious stimulation. Unilateral sensory deafferentation of the forelimb, by multiple dorsal rhizotomies, significantly decreased the number of Fos-like immunoreactive neurons in the ipsilateral spinal cord, suggesting that afferent input contributed to the walking-induced pattern of labeling. In rats that walked on the Rota-Rod, we also recorded increased labeling in the dorsal column nuclei. Unilateral cervical deafferentation reduced the labeling in the cuneate nucleus; this reduction was paralleled by decreased cytochrome oxidase activity. Finally, we found that there was a significant increase in the number of Fos-like immunoreactive neurons in the cerebellum of rats that walked on the Rota-Rod. Northern blot analysis revealed that the increase in Fos-like immunoreactivity was associated with an increase in c-fos messenger RNA. The pattern of labeling observed in the rats that walked on the Rota-Rod was distinct from that observed when rats are exposed to a noxious stimulus [Presley et al. (1990) J. Neurosci. 10, 323-335]. This result reinforces the conclusion that by monitoring the evoked expression of the c-fos proto-oncogene, it is possible to identify unique populations of neurons that are specifically related to the modality of the stimulus or to behaviour occurring during the stimulus presentation.
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PMID:Walking evokes a distinctive pattern of Fos-like immunoreactivity in the caudal brainstem and spinal cord of the rat. 815 39

Electrical stimulation of neonatal cardiac myocytes produces hypertrophy and cellular maturation with increased mitochondrial content and activity. To investigate the patterns of gene expression associated with these processes, cardiac myocytes were stimulated for varying times up to 72 hr in serum-free culture. The mRNA contents for genes associated with transcriptional activation [c-fos, c-jun, JunB, nuclear respiratory factor 1 (NRF-1)], mitochondrial proliferation [cytochrome c (Cyt c), cytochrome oxidase], and mitochondrial differentiation [carnitine palmitoyltransferase I (CPT-I) isoforms] were measured. The results establish a temporal pattern of mRNA induction beginning with c-fos (0.25-3 hr) and followed sequentially by c-jun (0.5-3 hr), JunB (0.5-6 hr), NRF-1 (1-12 hr), Cyt c (12-72 hr), and muscle-specific CPT-I (48-72 hr). Induction of the latter was accompanied by a marked decrease in the liver-specific CPT-I mRNA, thus supporting the developmental fidelity of this pattern of gene regulation. Consistent with a transcriptional mechanism, electrical stimulation increased c-fos, beta-myosin heavy chain, and Cyt c promoter activities. These increases coincided with a rise in their respective endogenous gene transcripts. NRF-1, cAMP response element, and Sp-1 site mutations within the Cyt c promoter reduced luciferase expression in both stimulated and nonstimulated myocytes. Mutations in the NRF-1 and CRE sites inhibited the induction by electrical stimulation (5-fold and 2-fold, respectively) whereas mutation of the Sp-1 site maintained or increased the fold induction. This finding is consistent with the appearance of NRF-1 and fos/jun mRNAs prior to that of Cyt c and suggests that induction of these transcription factors is a prerequisite for the transcriptional activation of Cyt c expression. These results support a regulatory role for NRF-1 and possibly AP-1 in the initiation of mitochondrial proliferation.
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PMID:Electrical stimulation of neonatal cardiomyocytes results in the sequential activation of nuclear genes governing mitochondrial proliferation and differentiation. 932 21

The hypothesis that oxidative stress induced by acute, sublethal, gossypol treatment induces transcription of stress genes in a rodent liver cell line was tested. In northern blot analysis of gossypol-treated cells, there was a dose-dependent increase in c-fos, a component of the redox-regulated transcription factor activator protein-1 (AP-1). Induction of c-fos was biphasic. A rapid 3.33+/-1.37 fold induction in c-fos was detected after treatment with 5 micromol/L gossypol for 30 min. Additionally, treatment with 5 micromol/L gossypol for 12 h caused a 2.66+/-0.67 fold increase in c-fos expression. PCR-based subtractive hybridization was used to generate a subtracted complementary DNA (cDNA) pool representing mRNA species increased in response to gossypol exposure. Several thousand clones were grown from bacteria transformed with the subtracted cDNA pool. After screening and confirmation by northern blotting, five clones were confirmed to be induced by gossypol. Sequence analysis confirmed that four of these clones contained DNA sequences from cytochrome-c oxidase subunit II (COX II), and one contained a DNA sequence from cytochrome-c oxidase subunit I (COX I). A five-fold induction (5.13+/-1.39 fold) in COX II occurred after 1 h of gossypol exposure, and a three-fold induction (3.24 fold) in COX I occurred after 3 h of gossypol exposure. These studies provide further evidence that mitochondria are a major site of the cytotoxic action of gossypol based upon an adaptive response to gossypol involving the upregulation of genes from the mitochondrial genome.
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PMID:Induction of c-fos, and cytochrome c oxidase subunits I and II by gossypol acetic acid in rat liver cells. 987 31

Hypoxic induction of c-fos was studied in rat brains as a function of the cerebral oxygenation state using near-infrared spectroscopy by which the hemoglobin oxygenation state and redox state of mitochondrial cytochrome oxidase could be monitored noninvasively. Following reoxygenation after hypoxia, the expression of c-fos and MAP2 mRNAs was followed by reverse transcription-coupled PCR. The expression of MAP2 remained unchanged throughout all the conditions from 21 to 8% FiO2. Under mildly hypoxia conditions, c-fos mRNA was not induced. Hemoglobin was partially deoxygenated but cytochrome oxidase remained fully oxidized. Severe hypoxia, where cytochrome oxidase was reduced, caused a significant induction of c-fos mRNA At this stage, the oxygen concentration in cerebral tissue fell to < 10(-7) M. These data suggest that the decline in oxidative phosphorylation might be a trigger for the induction of c-fos mRNA.
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PMID:c-fos expression and redox state of cytochrome oxidase of rat brain in hypoxia. 1067 75

To study the mechanism of pulmonary edema after seawater drowning (PE-SWD), the indexes of blood-gas and acid-base in rabbits artery blood were measured by the blood-gas analyser. The activity of Na(+)-K(+)-ATPase, cytochrome oxidase(CYTO) and alkaline phospharase(ALP) in the lungs were measured and analysed by computer image system. C-fos mRNA and Fos protein in the lungs were respectively determined by situ hybrioization and immunohisto chemical techniques. The distribution of phospholipid and Ca2+ of rabbits lungs was quantitatively analysed by ultrastructural location method. The results showed that, five parameters of PaO2, oxygen saturation(SaO2), pH, actual bicarbonite(AB) and base excess(BE) and the activity of Na(+)-K(+)-ATPase and CYTO decreased remarkably in PE-SWD. Both c-fos mRNA and Fos protein expression in pulmonary epithelial cells in PE-SWD were significantly elevated compared with the normal controls(P < 0.01). The phospholipids products in the pulmonary alveolar type II epithelial cells were decreased, however, the Ca2+ precipitate pellets inside the lung capillary endothelial cells and the pulmonary alveolar type I and II epithelial cells increased obviously. The arthors suggest that the injuny action of the seawater, hypoxia and metabolic acidosis may be the mian three mechanisms of the pulmonary edema induced seawater drowning. The lowering activity of Na(+)-K(+)-ATPase and CYTO in the lungs and calcium overload in the cells are not only evil consequence resulted from above three factors, but also the importent causes leading to the worse of PE-SWD. The transmiting line of Ca(2+)-fos may be also a key link to bring about the worse of PE-SWD.
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PMID:[Study on the mechanism of pulmonary edema after seawater drowning in rabbit]. 1255 79

Our aim was to determine the molecular targets involved in the antiproliferative effects of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), in a normal murine mammary epithelial cell line, HC11. Among the early response genes analyzed, c-myc, junB, junD, c-jun, c-fos, fosB, fra, as well as max, mad1-4, sin3, only c-jun and fra-2 mRNAs were up-regulated after 1,25(OH)(2)D(3) exposure. Cyclin C was reduced and cyclin A2 and E were slightly enhanced; however, cyclins D1, D3, B1, B2, F, G1, G2, I and H, as well as TGF beta 1, TGF beta 3, T beta RI and T beta RII transcripts were not modulated by 1,25(OH)(2)D(3). Although p27(KIP1) protein content was unchanged, enhancement of p21(WAF1/CIP1) low basal levels in cell extracts and IGFBP-3 abundance on the culture medium was detected after 1,25(OH)(2)D(3) induction. Using differential display analysis, we identified eight down-modulated clones in exposed cells: 26S proteasome non-ATPase subunit Pad1, ubiquitin-conjugating enzyme Ube2i, extracellular proteinase inhibitor Expi or Wdnm1, cytochrome-c oxidase Cox7c, microtubule-associated protein-1 light chain-3 (Map1lc3), nascent-associated complex alpha Naca, transforming acidic coiled-coil Tacc3, stearoyl-CoA desaturase (Scd), keratin 6 alpha, and 1 up-regulated, fork head transcription factor Hfh-1L. Hence, the antiproliferative effect of 1,25(OH)(2)D(3) seems associated to enhancement of c-jun, Fra-2, IGFBP3 and p21(WAF1/CIP1). Decreased Pad1 and Ube2i might account for increased stability of cell cycle inhibitory proteins while reduced Wdnm1, Tacc3 and Scd might be secondary to accumulation of cells in G0/G1 phase.
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PMID:Molecular targets of 1,25(OH)2D3 in HC11 normal mouse mammary cell line. 1264 25

Hypoxic induction of c-fos was studied in rat brains as a function of the cerebral oxygenation state using near-infrared spectroscopy by which the hemoglobin oxygenation state and redox state of mitochondrial cytochrome oxidase can be monitored noninvasively. Following reoxygenation after hypoxia, the expression of c-fos and MAP2 mRNAs was determined by reverse transcription-coupled PCR. The expression of MAP2 remained unchanged throughout all conditions from 21 to 8% FiO2. Under the mildly hypoxic conditions, c-fos mRNA was not induced. Hemoglobin was partially deoxygenated but cytochrome oxidase remained fully oxidized. Severe hypoxia, where cytochrome oxidase was reduced, caused a significant induction of c-fos mRNA. At this stage, the oxygen concentration in cerebral tissue fell to lower than 10(-7) M. These data suggest that the decline in oxidative phosphorylation might be a trigger for the induction of c-fos mRNA.
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PMID:Relationship between the gene expression of c-fos and degree of hypoxia in rat brain, as revealed by near-infrared spectroscopy. 1456 59

Functional neuroanatomical tools have played an important role in proposing which structures underlie brain stimulation reward circuitry. This review focuses on studies employing metabolic markers of neuronal and glial activation, including 2-deoxyglucose, cytochrome oxidase, and glycogen phosphorylase, and a marker of cellular activation, the immediate early gene c-fos. The principles underlying each method, their application to the study of brain stimulation reward, and their strengths and limitations are described. The usefulness of this strategy in identifying candidate structures, and the degree of overlap in the patterns of activation arising from different markers is addressed in detail. How these data have contributed to an understanding of the organization of reward circuitry and directed our thinking towards an alternative framework of neuronal arrangement is discussed in the final section.
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PMID:Tracing the neuroanatomical profiles of reward pathways with markers of neuronal activation. 1565 86

Visual inputs from the 2 eyes in most primates activate alternating bands of cortex in layer 4C of primary visual cortex, thereby forming the well-studied ocular dominance columns (ODCs). In addition, the enzymatic reactivity of cytochrome oxidase (CO) reveals "blob" structures within the supragranular layers of ODCs. Here, we present evidence for compartments within ODCs that have not been clearly defined previously. These compartments are revealed by the activity-dependent mRNA expression of immediate-early genes (IEGs), zif268 and c-fos, after brief periods of monocular inactivation (MI). After a 1-3-h period of MI produced by an injection of tetrodotoxin, IEGs were expressed in a patchy pattern that included infragranular layers, as well as supragranular layers, where they corresponded to the CO blobs. In addition, the expressions of IEGs in layer 4C were especially high in narrow zones along boundaries of ODCs, referred to here as the "border strips" of the ODCs. After longer periods of MI (>5 h), the border strips were no longer apparent. When either eyelid was sutured, changes in IEG expression were not evident in layer 4C; however, the patchy pattern of the expression in the infragranular and supragranular layers remained. These changes of IEG expression after MI indicate that cortical circuits involving the CO blobs of the supragranular layers include aligned groups of neurons in the infragranular layers and that the border strip neurons of layer 4C are highly active for a 3-h period after MI.
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PMID:Expression of immediate-early genes reveals functional compartments within ocular dominance columns after brief monocular inactivation. 1958 97


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