Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.4.1.2 (glutamate dehydrogenase)
 4,380 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A Neurospora spheroplast assay was used to study the cytotoxicity and mutagenicity of cis platin (cis dichlorodiammine platinum II) in a eukaryote. Mutagenicity was measured by using reversion of several alleles of the am (NH3 assimilatory glutamate dehydrogenase) gene. A mutation (uvs-2) that disables a DNA repair pathway in Neurospora resulted in reduced sensitivity to and elimination of mutability by cis platin. The implications for other eukaryotic systems (including human cells) are discussed.
Carcinogenesis 1984 Aug
PMID:Cytotoxicity and mutagenicity of cis platin assayed in neurospora. 623 55

Glutamate dehydrogenase activity in mitochondrial fraction of the liver and muscle tissue of tumor-bearing rats was studied in the dynamics of Guerin's carcinoma growth and after preliminary low-dose irradiation. At the initial stages of Guerin's carcinoma growth, maximum activity of glutamate dehydrogenase was observed in the liver, while in the muscle tissue, catabolic transformations of amino acids was activated at the logarithmic phase of carcinogenesis and tended to inhibition at the terminal stages. Low-dose irradiation was followed by activation glutamate dehydrogenase in mitochondrial fraction of the liver and inhibition of this enzyme in mitochondrial fraction of the muscle tissue.
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PMID:Effects of low-dose radiation on glutamate dehydrogenase activity in tissues of rats with transplanted Guerin's carcinoma. 2431 38

Glutaminolysis is a crucial factor for tumor metabolism in the carcinogenesis of several tumors but has not been clarified for oral squamous cell carcinoma (OSCC) yet. Expression of glutaminolysis-related solute carrier family 1, member 5 (SLC1A5)/neutral amino acid transporter (ASCT2), glutaminase (GLS), and glutamate dehydrogenase (GLDH) was analyzed in normal oral mucosa (n = 5), oral precursor lesions (simple hyperplasia, n = 11; squamous intraepithelial neoplasia, SIN I-III, n = 35), and OSCC specimen (n = 42) by immunohistochemistry. SLC1A5/ASCT2 and GLS were significantly overexpressed in the carcinogenesis of OSCC compared with normal tissue, while GLDH was weakly detected. Compared with SIN I-III SLC1A5/ASCT2 and GLS expression were significantly increased in OSCC. GLDH expression did not significantly differ from SIN I-III compared with OSCC. This study shows the first evidence of glutaminolysis-related SLC1A5/ASCT2, GLS, and GLDH expression in OSCC. The very weak GLDH expression indicates that glutamine metabolism is rather related to nucleotide or protein/hexosamine biosynthesis or to the function as an antioxidant (glutathione) than to energy production or generation of lactate through entering the tricarboxylic acid cycle. Overcoming glutaminolysis by targeting c-Myc oncogene (e.g. by natural compounds) and thereby cross-activation of mammalian target of rapamycin complex 1 or SLC1A5/ASCT2, GLS inhibitors may be a useful strategy to sensitize cancer cells to common OSCC cancer therapies.
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PMID:Glutaminolysis and carcinogenesis of oral squamous cell carcinoma. 2566 93