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Regulation of proliferation-survival decisions during tumor cell hypoxia.

Regulation of proliferation-survival decisions during tumor cell hypoxia.

http://www.wikidata.org/entity/Q39583941

about

Hypoxia and cell cycle regulation of the von Hippel-Lindau tumor suppressor Quantitative profiling of chromatome dynamics reveals a novel role for HP1BP3 in hypoxia-induced oncogenesis Hypoxia-inducible factor-1alpha mRNA contains an internal ribosome entry site that allows efficient translation during normoxia and hypoxia Ca2+-activated K+ channels in human melanoma cells are up-regulated by hypoxia involving hypoxia-inducible factor-1alpha and the von Hippel-Lindau protein Molecular responses to hypoxia in tumor cells Transcriptional repression of human cad gene by hypoxia inducible factor-1alpha Hypoxia-inducible transcription factor-1alpha promotes hypoxia-induced A549 apoptosis via a mechanism that involves the glycolysis pathway Cellular and molecular mechanisms underlying oxygen-dependent radiosensitivity Phosphoinositide 3-kinase accelerates necrotic cell death during hypoxia GLUT-1 reduces hypoxia-induced apoptosis and JNK pathway activation Differential roles of hypoxia-inducible factor 1alpha (HIF-1alpha) and HIF-2alpha in hypoxic gene regulation Redox regulation of p53 during hypoxia.IGF-I activates PKB and prevents anoxic apoptosis in Achilles tendon cells.Transcription factor HIF-1 is a necessary mediator of the pasteur effect in mammalian cells.Reactive oxygen intermediates regulate cellular response to apoptotic stimuli: an hypothesis.Hypoxic tumor microenvironment and cancer cell differentiation.p53 and cancer therapy: a double-edged sword.Hypoxia and regulation of cancer cell stemness.Multiple functions of hypoxia-regulated miR-210 in cancer.Apoptosis and cancer drug targeting.Adaptation to oxygen deprivation in cultures of human pluripotent stem cells, endothelial progenitor cells, and umbilical vein endothelial cells Endoplasmic reticulum stress accelerates p53 degradation by the cooperative actions of Hdm2 and glycogen synthase kinase 3beta.Adaptation to hypoxia and acidosis in carcinogenesis and tumor progression Bcl-2 family members and functional electron transport chain regulate oxygen deprivation-induced cell death.Mechanisms of apoptosis in central nervous system tumors: application to theory.Armoring CRAds with p21/Waf-1 shRNAs: the next generation of oncolytic adenoviruses.The Aqueous Soluble Polyphenolic Fraction of Psidium guajava Leaves Exhibits Potent Anti-Angiogenesis and Anti-Migration Actions on DU145 Cells.Hypoxia-induced energy stress regulates mRNA translation and cell growth.Diagnostic, prognostic and therapeutic implications of carbonic anhydrases in cancer.Relationship of hypoxia-inducible factor 1alpha and p21WAF1/CIP1 expression to cell apoptosis and clinical outcome in patients with gastric cancer.How to overcome (and exploit) tumor hypoxia for targeted gene therapy.Expression of hypoxia-inducible carbonic anhydrases in brain tumors.ACLY and ACC1 Regulate Hypoxia-Induced Apoptosis by Modulating ETV4 via α-ketoglutarate.Nanoparticles for Targeting Intratumoral Hypoxia: Exploiting a Potential Weakness of Glioblastoma.Hypoxia activates tumor suppressor p53 by inducing ATR-Chk1 kinase cascade-mediated phosphorylation and consequent 14-3-3γ inactivation of MDMX protein.Angiotensin-(1-7) Suppresses Hepatocellular Carcinoma Growth and Angiogenesis via Complex Interactions of Angiotensin II Type 1 Receptor, Angiotensin II Type 2 Receptor and Mas Receptor.Influence of transarterial chemoembolization on angiogenesis and expression of vascular endothelial growth factor and basic fibroblast growth factor in rat with Walker-256 transplanted hepatoma: an experimental study.High-uptake areas on positron emission tomography with the hypoxic radiotracer (18)F-FRP170 in glioblastomas include regions retaining proliferative activity under hypoxia Function of carbonic anhydrase IX in glioblastoma multiforme.Influence of a three-dimensional, microarray environment on human cell culture in drug screening systems.

P2860

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P2860

Regulation of proliferation-survival decisions during tumor cell hypoxia.

http://www.wikidata.org/entity/Q39583941

description

1998 nî lūn-bûn

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1998年の論文

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1998年論文

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1998年論文

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1998年論文

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1998年論文

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1998年論文

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1998年论文

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1998年论文

@zh

1998年论文

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name

Regulation of proliferation-survival decisions during tumor cell hypoxia.

@en

Regulation of proliferation-survival decisions during tumor cell hypoxia.

@nl

type

label

Regulation of proliferation-survival decisions during tumor cell hypoxia.

@en

Regulation of proliferation-survival decisions during tumor cell hypoxia.

@nl

prefLabel

Regulation of proliferation-survival decisions during tumor cell hypoxia.

@en

Regulation of proliferation-survival decisions during tumor cell hypoxia.

@nl

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Molecular and Cellular Biology

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Regulation of proliferation-survival decisions during tumor cell hypoxia.

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A Wells

http://www.w3.org/2001/XMLSchema#string

C Schmaltz

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D E Fisher

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P2860

Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis

Induction of apoptosis in fibroblasts by c-myc protein

Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages

Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours

Cleavage of poly(ADP-ribose) polymerase by a proteinase with properties like ICE

Bcl-2 functions in an antioxidant pathway to prevent apoptosis

Apoptosis induced in Jurkat cells by several agents is preceded by intracellular acidification

Cell acidification in apoptosis: granulocyte colony-stimulating factor delays programmed cell death in neutrophils by up-regulating the vacuolar H(+)-ATPase.

Abrogation of oncogene-associated apoptosis allows transformation of p53-deficient cells.

Kinetic and physical studies of cell death induced by chemotherapeutic agents or hyperthermia.

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