Accumulation of Krebs cycle intermediates and over-expression of HIF1alpha in tumours which result from germline FH and SDH mutations. - Wikidata - awgldk - TriplyDB

Accumulation of Krebs cycle intermediates and over-expression of HIF1alpha in tumours which result from germline FH and SDH mutations.

Accumulation of Krebs cycle intermediates and over-expression of HIF1alpha in tumours which result from germline FH and SDH mutations.

http://www.wikidata.org/entity/Q46575022

about

Fumarase: a mitochondrial metabolic enzyme and a cytosolic/nuclear component of the DNA damage response The FH mutation database: an online database of fumarate hydratase mutations involved in the MCUL (HLRCC) tumor syndrome and congenital fumarase deficiency Structural and mechanistic studies on the inhibition of the hypoxia-inducible transcription factor hydroxylases by tricarboxylic acid cycle intermediates UBE2QL1 is disrupted by a constitutional translocation associated with renal tumor predisposition and is a novel candidate renal tumor suppressor gene Inactivation of the FLCN tumor suppressor gene induces TFE3 transcriptional activity by increasing its nuclear localization Metabolism of kidney cancer: from the lab to clinical practice Applications of metabolomics in cancer research Regulation of human metabolism by hypoxia-inducible factor State of the science: an update on renal cell carcinoma Oncometabolite 2-hydroxyglutarate is a competitive inhibitor of α-ketoglutarate-dependent dioxygenases Cell-permeating alpha-ketoglutarate derivatives alleviate pseudohypoxia in succinate dehydrogenase-deficient cells Metabolic, autophagic, and mitophagic activities in cancer initiation and progression Hypoxia-Inducible Histone Lysine Demethylases: Impact on the Aging Process and Age-Related Diseases Breast Cancer Metabolism and Mitochondrial Activity: The Possibility of Chemoprevention with Metformin Cancer Metabolism and Drug Resistance Decoding Warburg's hypothesis: tumor-related mutations in the mitochondrial respiratory chain Succinate Dehydrogenase Loss in Familial Paraganglioma: Biochemistry, Genetics, and Epigenetics Ascorbate as a co-factor for fe- and 2-oxoglutarate dependent dioxygenases: physiological activity in tumor growth and progression Cancer metabolism: key players in metabolic reprogramming Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles' heel?Physiological consequences of complex II inhibition for aging, disease, and the mKATP channel Targeted therapeutic strategies for the management of renal cell carcinoma Pancreatic cancer early detection: expanding higher-risk group with clinical and metabolomics parameters Protein lysine acylation and cysteine succination by intermediates of energy metabolism IDH mutations in tumorigenesis and their potential role as novel therapeutic targets.Oncometabolites: Unconventional triggers of oncogenic signalling cascades Changing perspective on oncometabolites: from metabolic signature of cancer to tumorigenic and immunosuppressive agents The ever-expanding role of HIF in tumour and stromal biology Regulation of succinate-ubiquinone reductase and fumarate reductase activities in human complex II by phosphorylation of its flavoprotein subunit Inhibition of 2-oxoglutarate dependent oxygenases Redox regulation of mitochondrial function Hypoxia-inducible factor-1alpha regulates beta cell function in mouse and human islets The role of PHD2 mutations in the pathogenesis of erythrocytosis.Role of mitochondrial dysfunction in cancer progression The role of angiogenic factors in fibroid pathogenesis: potential implications for future therapy Risk-oriented approach to hereditary adrenal pheochromocytoma.Mitochondrial reactive oxygen species production in excitable cells: modulators of mitochondrial and cell function.Warburg effect's manifestation in aggressive pheochromocytomas and paragangliomas: insights from a mouse cell model applied to human tumor tissue.Birt-Hogg-Dubé: tumour suppressor function and signalling dynamics central to folliculin.Somatic pairing of chromosome 19 in renal oncocytoma is associated with deregulated EGLN2-mediated [corrected] oxygen-sensing response.

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P2860

Accumulation of Krebs cycle intermediates and over-expression of HIF1alpha in tumours which result from germline FH and SDH mutations.

http://www.wikidata.org/entity/Q46575022

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Alam NA

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Barclay E

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Barwell J

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Brière JJ

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P2860

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

Mutations in the fumarate hydratase gene cause hereditary leiomyomatosis and renal cell cancer in families in North America

Architecture of succinate dehydrogenase and reactive oxygen species generation

On the Origin of Cancer Cells

A role for mitochondrial enzymes in inherited neoplasia and beyond

Distinct clinical features of paraganglioma syndromes associated with SDHB and SDHD gene mutations

Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-alpha prolyl hydroxylase

The R22X mutation of the SDHD gene in hereditary paraganglioma abolishes the enzymatic activity of complex II in the mitochondrial respiratory chain and activates the hypoxia pathway

Gene mutations in the succinate dehydrogenase subunit SDHB cause susceptibility to familial pheochromocytoma and to familial paraganglioma

Mutations in SDHD, a mitochondrial complex II gene, in hereditary paraganglioma

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10.1093/HMG/DDI227

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15

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14

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