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threonine/hypoxia

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OBJECTIVE To explore the effects of Panax Quinquefolium Saponin (PQS) on phosphatidylinositol 3-kinase/serine threonine kinase (PI3K/Akt) pathway of neonatal rat myocardial cells subjected to hypoxia. METHODS Neonatal rat myocardial cells were cultured in vitro. After the myocardial cell injury was

Transcriptional regulation of serine/threonine kinase-15 (STK15) expression by hypoxia and HIF-1.

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The serine/threonine kinase-15 (STK15) acts as a cell cycle regulator being overexpressed in various tumors. One mechanism that could contribute to overexpression of STK15 is tumor hypoxia where hypoxia-inducible factor-1 (HIF-1) is a major regulator of transcription. Therefore, we analyzed whether

Targeting oncogenic serine/threonine-protein kinase BRAF in cancer cells inhibits angiogenesis and abrogates hypoxia.

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Carcinomas are comprised of transformed epithelial cells that are supported in their growth by a dedicated neovasculature. How the genetic milieu of the epithelial compartment influences tumor angiogenesis is largely unexplored. Drugs targeted to mutant cancer genes may act not only on tumor cells

Transcriptome sequencing of the naked mole rat (Heterocephalus glaber) and identification of hypoxia tolerance genes.

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The naked mole rat (NMR; Heterocephalus glaber) is a small rodent species found in regions of Kenya, Ethiopia and Somalia. It has a high tolerance for hypoxia and is thus considered one of the most important natural models for studying hypoxia tolerance mechanisms. The various mechanisms underlying
1. Hypoxia-induced cardiomyocyte apoptosis contributes significantly to cardiac dysfunction following trauma, shock and burn injury. There is evidence that heat shock protein (HSP) 90 is anti-apoptotic in cardiomyocytes subjected to a variety of apoptotic stimuli. Because HSP90 acts as an upstream

Nuclear Parkin Activates the ERRα Transcriptional Program and Drives Widespread Changes in Gene Expression Following Hypoxia

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Parkin is an E3 ubiquitin ligase well-known for facilitating clearance of damaged mitochondria by ubiquitinating proteins on the outer mitochondrial membrane. However, knowledge of Parkin's functions beyond mitophagy is still limited. Here, we demonstrate that Parkin has functions in the nucleus and

Role of Rho kinases in PKG-mediated relaxation of pulmonary arteries of fetal lambs exposed to chronic high altitude hypoxia.

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An increase in Rho kinase (ROCK) activity is implicated in chronic hypoxia-induced pulmonary hypertension. In the present study, we determined the role of ROCKs in cGMP-dependent protein kinase (PKG)-mediated pulmonary vasodilation of fetal lambs exposed to chronic hypoxia. Fourth generation
Protein kinase C (PKC) and mitogen-activated protein (MAP) kinase are protein-serine/threonine kinases which are important regulators of diverse cellular processes including metabolism, proliferation and differentiation. This study shows that both hypoxia and X irradiation of serum-deprived Chinese

Transient hypoxia differentially decreases GRK2 protein levels in CHO cells stably expressing the m1 mAChR.

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G protein-coupled kinase 2 (GRK2) has a key role in regulating signaling activities of a variety of G protein-coupled receptors (GPCRs). Several recent studies have directly implicated GRK2 phosphorylation in desensitization of GPCRs. In addition, binding by G(betagamma) or phosphorylation by PKC or

5-Aza-2'-deoxycytidine increases hypoxia tolerance-dependent autophagy in mouse neuronal cells by initiating the TSC1/mTOR pathway.

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tractText>Our previous study found that 5-Aza-2'-deoxycytidine (5-Aza-CdR) can repress the expression and activity of protein serine/threonine phosphatase-1γ (PP1γ) in mouse hippocampus. It is well known that PP1γ regulates cell metabolism, which is related to hypoxia/ischaemia tolerance. It has

Regulation of mammalian target of rapamycin complex 1 (mTORC1) by hypoxia: causes and consequences.

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Integration of cellular and extracellular signals maintains tissue homeostasis under conditions of normal proliferation and stress. A central player in regulating responses to stress is the serine/threonine kinase mammalian target of rapamycin (mTOR). In many cancers, mTOR complex 1 (mTORC1)
Hypoxia promotes cancer progression, and metastasis. The major protein expressed in hypoxic solid cancer is hypoxia-inducible factor 1 (HIF1). We show that enhanced phosphorylation of a conventional protein kinase C isoform, PKCα, at threonine 638 (T(638)) by hypoxia-mimetic cobalt chloride induces

Hypoxia inhibits the SDF-1-dependent migration of human leukemic cell line HL-60 via blocking of Akt activation.

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Hypoxia is known to regulate the expression of genes involved in the migration of various cell types. Although many studies have shown that hypoxia increases cell migration, it still remains unclear whether hypoxia could modulate the stromal cell derived factor-1 (SDF-1)-dependent migration of
Oxygen is an environmental/developmental signal that regulates cellular energetics, growth, and differentiation processes. Despite its central role in nearly all higher life processes, the molecular mechanisms for sensing oxygen levels and the pathways involved in transducing this information are

ILKAP Binding to and Dephosphorylating HIF-1α is Essential for Apoptosis Induced by Severe Hypoxia.

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OBJECTIVE Integrin-linked kinase-associated phosphatase (ILKAP), a serine/threonine phosphatase that belongs to the protein phosphatase 2C family, has a role in cell survival and apoptosis. Hypoxia-inducible factor 1α (HIF-1α) is the key transcription factor in the response to oxygen deficiency in
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