phosphatase/hipoksi

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Hypoxia-mediated regulation of Cdc25A phosphatase by p21 and miR-21.

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Hypoxia is a common feature of solid tumors and represents a critical factor in their progression and responsiveness to chemotherapy and radiotherapy. We now report that hypoxic exposure of colon cancer cells decreased the protein levels of the cell cycle-controlling phosphatase Cdc25A. Hypoxia

Pattern-specific sustained activation of tyrosine hydroxylase by intermittent hypoxia: role of reactive oxygen species-dependent downregulation of protein phosphatase 2A and upregulation of protein kinases.

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We investigated the role of protein phosphatases (PP) and protein kinases in tyrosine hydroxylase (TH) activation by two patterns of intermittent hypoxia (IH) in rat brainstem. Rats exposed to either IH(15s) (15 s, 5% O(2); 5 min, 21%O(2)) or IH(90s) (90 s each of 10% O(2) & 21%O(2)) for 10 days

Hypoxia followed by re-oxygenation induces oxidation of tyrosine phosphatases.

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Hypoxia and hypoxia/reoxygenation (H/R) are components of tissue ischemia and reperfusion implicated in myocardial infarction, organ transplantation, and tumor perfusion. H/R enhances production of reactive oxygen species (ROS). Candidate molecular targets of ROS are the catalytic site cysteine of

Dual-specificity phosphatase 26 (DUSP26) stimulates Aβ42 generation by promoting amyloid precursor protein axonal transport during hypoxia.

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Amyloid beta peptide (Aβ) is a pathological hallmark of Alzheimer's disease (AD) and is generated through the sequential cleavage of amyloid precursor protein (APP) by β- and γ-secretases. Hypoxia is a known risk factor for AD and stimulates Aβ generation by γ-secretase; however, the underlying

Okadaic acid-sensitive protein phosphatases constrain phrenic long-term facilitation after sustained hypoxia.

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Phrenic long-term facilitation (pLTF) is a serotonin-dependent form of pattern-sensitive respiratory plasticity induced by intermittent hypoxia (IH), but not sustained hypoxia (SH). The mechanism(s) underlying pLTF pattern sensitivity are unknown. SH and IH may differentially regulate

Mitogen-activated protein kinase phosphatase-1 (MKP-1) expression is induced by low oxygen conditions found in solid tumor microenvironments. A candidate MKP for the inactivation of hypoxia-inducible stress-activated protein kinase/c-Jun N-terminal protein kinase activity.

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Pathophysiological hypoxia is an important modulator of gene expression in solid tumors and other pathologic conditions. We observed that transcriptional activation of the c-jun proto-oncogene in hypoxic tumor cells correlates with phosphorylation of the ATF2 transcription factor. This finding

Increased myofibrillar protein phosphatase-1 activity impairs rat aortic smooth muscle activation after hypoxia.

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We hypothesized that increased myofibrillar type 1 protein phosphatase (PP1) catalytic activity contributes to impaired aortic smooth muscle contraction after hypoxia. Our results show that inhibition of PP1 activity with microcystin-LR (50 nmol/l) or okadaic acid (100 nmol/l) increased

Connexin43 phosphorylation state and intercellular communication in cultured astrocytes following hypoxia and protein phosphatase inhibition.

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The effects of hypoxia and phosphatase inhibitors on connexin43 (Cx43) phosphorylation state, gap junctional intercellular communication (GJIC) and immunolabelling with anti-Cx43 antibodies were investigated in cultured astrocytes. Astrocytes contained predominantly phosphorylated forms of Cx43 and

[Acid phosphatase activity and the state of lysosomal membranes in a primary culture of cardiomyocytes of newborn rats during hypoxia].

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Acid phosphatase activity, ATP and cyclic nucleotide levels were studied in primary cardiomyocyte cultures of newborn rats under hypoxic conditions. It was shown that incubation of cardiac cells in Eagle's medium supplemented with 10% calf serum during hypoxia (5% O2, 5% CO2, 90% N2) caused an hour

[Serum acid phosphatase activity in rats with hypoxia of different etiologies].

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Experiments on male rats have shown that the acid phosphatase activity increases in all the types of hypoxia (circulatory-hemic, hemic and hypoxic), in blood serum. An increase in the activity of this enzyme distinctly correlates with hypoxia gravity. A supposition is advanced that the blood enzyme

Effects of Src Kinase Inhibition on Expression of Protein Tyrosine Phosphatase 1B after Brain Hypoxia in a Piglet Animal Model.

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BACKGROUND Protein tyrosine phosphatases (PTPs) in conjunction with protein tyrosine kinases (PTKs) regulate cellular processes by posttranslational modifications of signal transduction proteins. PTP nonreceptor type 1B (PTP-1B) is an enzyme of the PTP family. We have previously shown that hypoxia

Effect of hypoxia on protein tyrosine phosphatase activity and expression of protein tyrosine phosphatases PTP-1B, PTP-SH1 and PTP-SH2 in the cerebral cortex of guinea pig fetus.

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The present study tested the hypothesis that the hypoxia in utero results in decreased protein tyrosine phosphatase (PTP) activity in cytosolic and membrane fractions and increased expression of PTPs (PTP-1B, PTP-SH1 and PTP-SH2) in the cytosol and the membrane fraction of the cerebral cortex of

The tyrosine phosphatase SHP-1 regulates hypoxia inducible factor-1α (HIF-1α) protein levels in endothelial cells under hypoxia.

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BACKGROUND The tyrosine phosphatase SHP-1 negatively influences endothelial function, such as VEGF signaling and reactive oxygen species (ROS) formation, and has been shown to influence angiogenesis during tissue ischemia. In ischemic tissues, hypoxia induced angiogenesis is crucial for restoring

Protein kinase and phosphatase responses to anoxia in crayfish, Orconectes virilis: purification and characterization of cAMP-dependent protein kinase.

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The freshwater crayfish, Orconectes virilis, shows good anoxia tolerance, enduring 20 h in N(2)-bubbled water at 15 degrees C. Metabolic responses to anoxia by tolerant species often include reversible phosphorylation control over selected enzymes. To analyze the role of serine/threonine kinases and

Regulation of protein phosphatase 1gamma activity in hypoxia through increased interaction with NIPP1: implications for cellular metabolism.

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Eukaryotic cells sense decreased oxygen levels and respond by altering their metabolic strategy to sustain non-respiratory ATP production through glycolysis, and thus promote cell survival in a hypoxic environment. Protein phosphatase 1 (PP1) has been recently implicated in the governance of the

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