Loss of pVHL is sufficient to cause HIF dysregulation in primary cells but does not promote tumor growth - Wikidata - awgldk - TriplyDB

Loss of pVHL is sufficient to cause HIF dysregulation in primary cells but does not promote tumor growth

Loss of pVHL is sufficient to cause HIF dysregulation in primary cells but does not promote tumor growth

http://www.wikidata.org/entity/Q33998089

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Identification of novel VHL target genes and relationship to hypoxic response pathways Inhibition of HIF2alpha is sufficient to suppress pVHL-defective tumor growth Hypoxia-inducible factor-dependent degeneration, failure, and malignant transformation of the heart in the absence of the von Hippel-Lindau protein pVHL function is essential for endothelial extracellular matrix deposition.Developmentally arrested structures preceding cerebellar tumors in von Hippel-Lindau disease A central role for hypoxic signaling in cartilage, bone, and hematopoiesis.HIF-1alpha induces cell cycle arrest by functionally counteracting Myc.Decreased growth of Vhl-/- fibrosarcomas is associated with elevated levels of cyclin kinase inhibitors p21 and p27.Angiogenesis inhibitors: current strategies and future prospects.Induction of SENP1 in endothelial cells contributes to hypoxia-driven VEGF expression and angiogenesis.Metastatic paraganglioma.Differential regulation of the transcriptional activities of hypoxia-inducible factor 1 alpha (HIF-1alpha) and HIF-2alpha in stem cells Deletion of the von Hippel-Lindau gene causes sympathoadrenal cell death and impairs chemoreceptor-mediated adaptation to hypoxia.Multiple factors affecting cellular redox status and energy metabolism modulate hypoxia-inducible factor prolyl hydroxylase activity in vivo and in vitro.Scientific and clinical opportunities for modeling blood disorders with embryonic stem cells Hypoxia-inducible factors and hypoxic cell death in tumour physiology.Von Hippel-Lindau disease (VHL): a need for a murine model with retinal hemangioblastoma The VHL tumor suppressor in development and disease: functional studies in mice by conditional gene targeting.VHL: oxygen sensing and vasculogenesis.Role and mechanism of hypoxia-inducible factor-1 in cell growth and apoptosis of breast cancer cell line MDA-MB-231 Salternamide A Suppresses Hypoxia-Induced Accumulation of HIF-1α and Induces Apoptosis in Human Colorectal Cancer Cells.The von Hippel-Lindau tumor suppressor protein and Egl-9-Type proline hydroxylases regulate the large subunit of RNA polymerase II in response to oxidative stress.MicroRNA-101 targets von Hippel-Lindau tumor suppressor (VHL) to induce HIF1α mediated apoptosis and cell cycle arrest in normoxia condition.Estrogen receptor α is a novel target of the Von Hippel-Lindau protein and is responsible for the proliferation of VHL-deficient cells under hypoxic conditions.Functional evaluation of the apoptosome in renal cell carcinoma.Transcription association of VHL and SDH mutations link hypoxia and oxidoreductase signals in pheochromocytomas.Hypoxia-inducible factors: central regulators of the tumor phenotype.Current understanding of the molecular mechanisms of kidney cancer: a primer for urologists.Hypoxia inducible factor-1alpha inactivation unveils a link between tumor cell metabolism and hypoxia-induced cell death.The ubiquitin ligase Siah2 regulates tumorigenesis and metastasis by HIF-dependent and -independent pathways.MiR675-5p Acts on HIF-1α to Sustain Hypoxic Responses: A New Therapeutic Strategy for Glioma The VHL tumor suppressor and HIF: insights from genetic studies in mice The role of hypoxia-inducible factors in tumorigenesis.Biology of hypoxia-inducible factor-2alpha in development and disease Loss of VHL promotes progerin expression, leading to impaired p14/ARF function and suppression of p53 activity.VHL Type 2B gene mutation moderates HIF dosage in vitro and in vivo.Pleiotropic effects of the trichloroethylene-associated P81S VHL mutation on metabolism, apoptosis, and ATM-mediated DNA damage response.HIF2alpha cooperates with RAS to promote lung tumorigenesis in mice pVHL-mediated transcriptional repression of c-Myc by recruitment of histone deacetylases.Regulation of KLF4 turnover reveals an unexpected tissue-specific role of pVHL in tumorigenesis.

P2860

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P2860

Loss of pVHL is sufficient to cause HIF dysregulation in primary cells but does not promote tumor growth

http://www.wikidata.org/entity/Q33998089

description

2003 nî lūn-bûn

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2003 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2003 թվականի հունվարին հրատարակված գիտական հոդված

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2003年の論文

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2003年論文

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2003年論文

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2003年論文

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2003年论文

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Loss of pVHL is sufficient to ...... does not promote tumor growth

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Loss of pVHL is sufficient to ...... does not promote tumor growth

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Andrew M Arsham

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

Brian Keith

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Fiona A Mack

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James Gnarra

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M Celeste Simon

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W Kimryn Rathmell

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P2860

The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis

The Hallmarks of Cancer

HIFalpha targeted for VHL-mediated destruction by proline hydroxylation: implications for O2 sensing

C. elegans EGL-9 and mammalian homologs define a family of dioxygenases that regulate HIF by prolyl hydroxylation

A conserved family of prolyl-4-hydroxylases that modify HIF

Regulation of hypoxia-inducible mRNAs by the von Hippel-Lindau tumor suppressor protein requires binding to complexes containing elongins B/C and Cul2

Redox-regulated recruitment of the transcriptional coactivators CREB-binding protein and SRC-1 to hypoxia-inducible factor 1alpha

The von Hippel-Lindau tumor-suppressor gene product forms a stable complex with human CUL-2, a member of the Cdc53 family of proteins

Mechanism of regulation of the hypoxia-inducible factor-1 alpha by the von Hippel-Lindau tumor suppressor protein

Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation

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1

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12559177

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4120823

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