Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

High-resolution digital photography and graphical image analyses systems have been used to define external morphometric characters of shell deformations in four populations of the Baltic clam Macoma balthica from the Gulf of Gdansk (southern Baltic Sea). The proposed shell deformation indices (SDI), which were based on the relationship of selected dimensions in the posterior and the anterior part of the shell, showed at least three morphological features that provide a distinctive diagnosis of "regular" and "deformed" clams: the presence of flexure on the posterior side (SDI1), elongated posterior region (SDI2), and shell growth (SDI3). The degree and prevalence of deformed clams varied locally over space. Increase in percentage contribution of aberrated shells with depth, corresponding to oxygen depletion profile in the Gulf, suggests low oxygen concentrations as the main agent exerting a deforming influence. The observed morphological aberrations developed with age (size) of a bivalve, suggesting a long-term effect of causal factors, and were accompanied by lightening shell weight, possibly due to decalcification of previously deposited calcareous material during anaerobic metabolism. It is hypothesized that hypoxic/anoxic conditions and a subsequent presence of hydrogen sulfide on a deep organic-rich sea bottom induce shell form alterations that enable the pumping of oxygenated water from above the anoxic layer. Such a morphological modification highlights the functional significance of shell deformations in protective response to the ambient low-oxygen concentrations. Sediment organotin concentrations fall within moderate to high contamination range and, therefore, may also have an adverse impact on the shell form. DNA analyses of the fragment of mitochondrial gene cytochrome oxidase I (COI, 393 base pairs) showed homogenous genetic structure of regular and deformed clams, indicating that shell deformations in M. balthica are primarily driven by acclimatization to the ambient environmental conditions.
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PMID:Shell deformations in the Baltic clam Macoma balthica from southern Baltic Sea (the Gulf of Gdansk): hypotheses on environmental effects. 1848 51