Disease relevance of GOT1

• In the present study, marked antitumoural activity of peroral CHS 828 was shown against three different human neuroendocrine tumours, midgut carcinoid (GOT1), pancreatic carcinoid (BON), and medullary thyroid carcinoma (GOT2), transplanted in nude mice [1].
• The membrane pump inhibitor clomipramine had no effect on the uptake of (123)I-MIBG in GOT1 and BON cells, but inhibited the uptake in one out of four primary carcinoid cell cultures and three out of four primary pheochromocytoma cell cultures [2].
• Fusion of ETV6 to GOT1 in a case with myelodysplastic syndrome and t(10;12)(q24;p13) [3].
• Cerebrospinal fluid enzyme levels of creatine kinase (CK), lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT) and angiotensin converting enzyme (ACE) were studied in 40 acute stroke patients comprising 20 lacunar strokes and 20 cortical strokes [4].
• The pretreatment serum GOT (glutamate oxaloacetate transaminase) levels and the pretreatment Karnofsky performance status index were the factors governing the prognosis of the cases with metastatic liver cancer, while toxicity was generally mild [5].

High impact information on GOT1

• Aminooxyacetate, a glutamate-oxaloacetate transaminase inhibitor, specifically inhibited B-cell growth induced by LA, suggesting that this process requires mitochondrial-cytosol transfers [6].
• We have assessed the vitamin B6 status of 40 nonpregnant women of reproductive age, 30 pregnant women, 20 postpartum, not depressed, women and 24 postpartum, depressed women by means of the erythrocyte glutamate-oxaloacetate transaminase activation test (alpha EGOT) [7].
• The complex pattern of the common GOT1 phenotype consists of eight bands with different intensities [8].
• 2. The activities of lactate dehydrogenase, octopine dehydrogenase, phosphoenolpyruvate carboxykinase, cytosolic and mitochondrial glycerol 3-phosphate dehydrogenase and glutamate-oxaloacetate transaminase were measured in order to provide a qualitative indication of the importance of different processes for oxidation of glycolytically formed NADH [9].
• The treatment with 0.005 mmol/100 g rat oxaloacetate was no more effective than saline but when it was combined with the intravenous administration of 0.14 nmol/100 g of recombinant glutamate-oxaloacetate transaminase, recovery was almost complete [10].

Chemical compound and disease context of GOT1

• Hence, this study was launched to evaluate the changes in tumour marker enzymes like lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (SGOT), glutamate pyruvate transaminase (SGPT), alkaline phosphatase, and acid phosphatase in before and after 3 and 6 months tamoxifen treated breast cancer patients [11].
• The massive increase of glutamate-oxaloacetate transaminase and lactate dehydrogenase and the appearance of alkaline phosphatases in a sample of cerebrospinal fluid in which the cytology is normal constitute an easy and reliable test for brain death [12].
• Some important blood parameters for organ toxicity such as sugar, urea, creatinine, serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, albumin, globulin, hemoglobin levels and erythrocyte sedimentation rate remained close to the control values [13].

Biological context of GOT1

• Fluorescence in situ hybridization with the 769E11YAC and BAC 31L5 and 2H23 probes showed the breakpoint to be located proximally to BCL10 and distally to GOT1 genes on chromosomes 1p22 and 10q24, respectively [14].
• We have demonstrated concordant segregation between human LIPA and human chromosome 10 and its enzyme marker glutamate oxaloacetate transaminase-1 (GOT1) in cell hybrid clones [15].
• Confirmation of a de novo duplication, dup(10)(q24 leads to q26), by GOT1 gene dosage studies [16].
• Genetic polymorphism of glutamate oxaloacetate transaminase (GOT1) was demonstrated in human erythrocytes by isoelectric focusing in thin layer polyacrylamide gels and a sensitive and positive detection method [17].
• In this report we present the results of a combined cytogenetic and multicolor spectral karyotype (SKY) analysis of a transplantable human ileal carcinoid (GOT1) [18].

Anatomical context of GOT1

• In the VMAT-expressing NE tumour cell lines GOT1 and BON and in VMAT-expressing primary NE tumour cell cultures (carcinoids, n=4 and pheochromocytomas, n=4), reserpine significantly reduced the uptake of (123)I-MIBG [2].
• Previous investigations in the same pedigree had shown triplex dosage effect of GOT1 on red blood cells of a 10q24 leads to qter trisomic fetus monitored by midtrimester amniocentesis [19].
• Pineapple mitochondria showed very high malate dehydrogenase (MDH), and low malic enzyme (ME) and glutamate-oxaloacetate transaminase (GOT) activities [20].
• Measures were baseline psychotic severity, serum creatine kinase (CK0), lactate dehydrogenase (LDH0), glutamate oxaloacetate transaminase (SGOT0), white blood cell count (WBC0), urine myoglobulin, and the repeated CK (RepCK) measurements taken during recurrent psychotic episodes [21].
• Distribution of lactic dehydrogenase and glutamate oxaloacetate transaminase in buffalo spermatozoa [22].

Associations of GOT1 with chemical compounds

• Serum glutamate-oxaloacetate transaminase (GOT), glutamate-pyruvate transaminase (GPT), leucine amino peptidase (LAP) and bilirubin were measured serially [23].
• Assignment to chromosome 16 of a gene necessary for the expression of human mitochondrial glutamate oxaloacetate transaminase (aspartate aminotransferase) (E.C. 2.6.1.1.) [24].
• Serum levels of hepatic enzyme markers: glutamate pyruvate transaminase (GPT), glutamate oxaloacetate transaminase (GOT), gamma glutamyl transferase (GGT) and alkaline phosphatase (ALP) were determined after oral administration of aloe vera leaves extract and lindane [25].
• High Ethanol primates had significantly higher levels of HDL nonesterified cholesterol than Control and Low Ethanol animals while serum glutamate oxaloacetate transaminase was similar for the three treatments [26].
• Fluorimetric assay of serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase and alpha-hydroxybutyrate dehydrogenase by solution and solid surface fluorescent methods [27].

Other interactions of GOT1

• However, mutation analysis excluded GOT1 as a candidate for the UFS gene [28].
• Thus, the LIPA-GOT1 linkage groups has remained intact during the 80 X 10(6) years of evolution that separates humans and mice [15].
• Cytotoxicity was monitored by measurement of leakage of intracellular enzymes into the culture medium: lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT) [29].
• GOT1 xenografted to nude mice: a unique model for in vivo studies on SSTR-mediated radiation therapy of carcinoid tumors [30].
• Transketolase was used for determining thiamin status, glutathione reductase for determining riboflavin status and glutamate oxaloacetate transaminase for pyridoxine status [31].

Analytical, diagnostic and therapeutic context of GOT1

• There were 13 of 44 (29.6%) abnormal liver function tests (elevations of either glutamate oxaloacetate transaminase (GOT) or glutamate pyruvate transaminase (GPT)) among the high DMF exposure workers, two of 22 (9.1%) abnormal liver function tests among the low DMF exposure workers [32].
• Thin-layer isoelectric focusing in agarose within the pH range of 4.0-6.5 has shown a high resolution of the soluble cytoplasmic glutamate-oxaloacetate transaminase (GOT1) banding pattern [8].
• The possibility of prenatal diagnosis by gene dosage: confirmation of duplication 10q24 to qter from GOT-1 activity in fetal erythrocytes [33].
• No change was observed in hemoglobin, hematocrit, glucose tolerance, plasma lipids, iron, calcium, or serum glutamate-oxaloacetate transaminase after treatment [34].

References