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okadaic acid/рак

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The concept of the okadaic acid class of tumor promoters is revived in endogenous protein inhibitors of protein phosphatase 2A, SET and CIP2A, in human cancers.

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OBJECTIVE The okadaic acid class of tumor promoters, which are inhibitors of protein phosphatases 1 and 2A (PP1 and PP2A), induced tumor promotion in mouse skin, rat glandular stomach, and rat liver. Endogenous protein inhibitors of PP2A, SET and CIP2A, were up-regulated in various human cancers, so

Different sensitivities of p42 mitogen-activated protein kinase to phorbol ester and okadaic acid tumor promoters among cell types.

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The operational equivalence of different types of tumor promoters was studied by comparing immediate, early, and late effects of okadaic acid (OA) and 12-O-tetradecanoylphorbol-13-acetate (TPA) on the phosphorylation state of p42 mitogen-activated protein kinase isoform (ERK2) in eight different

Rapid induction of the Grp78 gene by cooperative actions of okadaic acid and heat-shock in 9L rat brain tumor cells--involvement of a cAMP responsive element-like promoter sequence and a protein kinase A signaling pathway.

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We have demonstrated that treatment with 200 nM okadaic acid (OA) for 1 h followed by a 15-min heat shock (HS) at 45 degrees C (termed OA-->HS treatment) leads to a rapid transactivation of grp78, the gene for the 78-kDa glucose-regulated protein, in 9L rat brain tumor cells. The level of Grp78 mRNA

The tumour promoter okadaic acid inhibits reticulocyte-lysate protein synthesis by increasing the net phosphorylation of elongation factor 2.

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Okadaic acid, a tumour promoter which potently inhibits protein phosphatases, inhibited translation in the reticulocyte-lysate cell-free system. Inhibition was dose-dependent, with half-maximal effects occurring at 20-40 nM-okadaic acid. Inhibition of translation by okadaic acid resulted in the

Nonphorbol tumor promoters okadaic acid and calyculin-A induce membrane translocation of protein kinase C.

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The cell-permeable inhibitors of type 1 and 2A protein phosphatases, okadaic acid and calyculin-A, induced a redistribution of protein kinase C (PKC) activity and immunoreactivity (40 to 60%) from cytosol to membrane in some cell types. Calyculin-A was 100-fold more potent than okadaic acid and

Okadaic acid induces down-modulation and shedding of tumor necrosis factor receptors. Comparison with another tumor promoter, phorbol ester.

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Protein kinase C modulates the receptor for tumor necrosis factor (TNF) in wide variety of different cell types. However, there is no information about the role of phosphatases in the regulation of the TNF receptor. In this report, we investigated the effect of okadaic acid, an inhibitor of

A dominant negative c-jun specifically blocks okadaic acid-induced skin tumor promotion.

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Okadaic acid (OA) is a prototypical non-phorbol ester skin tumor-promoting agent that works by inhibiting protein phosphatases, leading to an increase in protein phosphorylation. Increased protein phosphorylation can lead to stimulated signaling through various signal transduction pathways. One or

Differentiation induction in human breast tumor cells by okadaic acid and related inhibitors of protein phosphatases 1 and 2A.

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Okadaic acid (OA), an inhibitor of protein phosphatases 1 and 2A, induces differentiation in human MCF-7, AU-565, and MB-231 breast tumor cells. In MCF-7 cells, OA elicited within 5 min an increase in the levels of a set of phosphorylated cellular proteins, within hours expression of the early

Gene amplification and multidrug resistance induced by the phosphatase-inhibitory tumor promoter, okadaic acid.

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The mechanism by which tumor promoters contribute to cellular transformation and tumorigenesis is not completely understood. To investigate further the molecular events involved in these processes, we used okadaic acid, a non-phorbol ester type tumor promoter that specifically inhibits certain

[(-)-Epigallocatechin gallate, the main constituent of Japanese green tea, inhibits tumor promotion of okadaic acid].

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(-)-Epigallocatechin gallate (EGCG), the main constituent of green tea, inhibited a tumor promoting activity of okadaic acid in a two-stage carcinogenesis experiment on mouse skin. The group treated with a single application of 100 micrograms 7, 12-dimethylbenz (a) anthracene followed by repeated

Cross-resistance to antineoplastic agents in a human small-cell lung-cancer subline resistant to okadaic Acid.

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We report on a human small cell lung cancer subline (H69/OA100) resistant to okadaic acid, an inhibitor of protein phosphatases. H69/OA100 showed cross-resistance to cis-diamminedichloroplatinum(II) (CDDP), adriamycin, and vinca alkaloids. Intracellular retention of adriamycin and CDDP in H69/OA100

Profiles and levels of fatty acid esters of okadaic acid group toxins and pectenotoxins during toxin depuration. Part I: brown crab (Cancer pagurus).

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In 2002, two outbreaks of diarrhetic shellfish poisoning (DSP) occurred in Norway, which was later confirmed to be caused by the consumption of brown crab (Cancer pagurus) contaminated predominantly by esters of okadaic acid (OA) after feeding on toxic blue mussels (Mytilus edulis). In addition to

Inhibition of apoptosis in human tumour cells by okadaic acid.

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Gamma-radiation, tetrandrine, bistratene A, and cisplatin were all found to induce pronounced morphological changes characteristic of apoptosis and extensive DNA fragmentation in the human BM13674 cell line 8 h after treatment. Apoptosis induced in BM13674 cells by these diverse agents was markedly

The marine toxin okadaic acid induces alterations in the expression level of cancer-related genes in human neuronal cells.

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Okadaic acid (OA) is one of the most common and highly distributed marine toxins. It can be accumulated in several molluscs and other marine organisms and cause acute gastrointestinal symptoms after oral consumption by humans, called diarrheic shellfish poisoning. However other toxic effects beyond

Effects of the tumour promoter okadaic acid on intracellular protein phosphorylation and metabolism.

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Okadaic acid is a polyether derivative of 38-carbon fatty acid, and is implicated as the causative agent of diarrhetic shellfish poisoning. It is a potent tumour promoter that is not an activator of protein kinase C, but is a powerful inhibitor of protein phosphatases-1 and -2A (PP1 and PP2A) in
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