Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the expression and regulation of the rat testis cytosolic aspartate aminotransferase gene. The cytosolic aspartate aminotransferase activity was 5-fold lower in the testis than in the liver and kidney. A 1.9-kilobase mRNA form was detected in the rat testis in contrast to the 2.1- and 1.8-kilobase forms present in other organs. Using Northern blot and S1 mapping analyses, we found that the proximal polyadenylation site was almost exclusively used in the testis as opposed to other organs where the distal site was preferentially used. RNase protection and primer extension analysis showed that transcription was initiated at multiple sites in all organs, but the pattern of those start sites was different in the testis; in particular, a novel transcription start site was specifically detected in this organ (at position -115 from the translation start site). This site was first observed in 29-day-old rats and was maximally utilized in the adult testis. DNase I footprinting using testis nuclear extracts revealed the presence of three sites of DNA-protein interaction in the 250-base pair proximal promoter, a pattern similar to the one found using liver nuclear extracts. However, the proteins bound had different properties as shown by gel retardation experiments. We conclude that the pattern of transcription initiation and the polyadenylation site selection of a housekeeping gene can be tissue-specific.
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PMID:Testis-specific transcription start site in the aspartate aminotransferase housekeeping gene promoter. 817 62

2,4-Dichlorophenoxybutyric acid (2,4-DB) is principally used in the United States as a herbicide on peanuts, soybeans, and alfalfa. In Europe, it is used on cereals, undersown cereals, lucerne (alfalfa), clover, and clover mixtures. A 1-year chronic toxicity study in the dog was performed on 2,4-DB. Doses in the study of 0, 75, 225, and 450 ppm were administered to six animals/sex/group. The top dose was reduced from 675 ppm during week 7 of the study due to body weight loss and decreased food consumption. Four animals/sex/group were euthanized after 52 weeks of treatment and two animals/sex/group were placed on control diet for 4 weeks and euthanized at week 56. Treatment-related findings included reductions in body weight gain and food consumption, and minor increases in inorganic phosphorus, blood urea nitrogen, creatinine, aspartate aminotransferase, and alanine aminotransferase. After the 4-week recovery period, the only parameter that did not return to control levels was the aspartate aminotransferase. Gross pathology evaluation noted distended gallbladders and decreased organ weights were noted in females for the adrenal, spleen, and ovaries. Histologically, the liver and kidney were the target organs. The data from the study support a chronic no observed adverse effect level of 75 ppm (2.39 and 2.15 mg/kg/day for males and females, respectively) for 2,4-DB. There was no indication of any immunotoxic or oncogenic response in the studies. In conclusion, the findings in this study indicate the general low toxicity of 2,4-DB following chronic dietary exposure in the dog.
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PMID:Chronic dietary toxicity study on 2,4-dichlorophenoxybutyric acid in the dog. 992 76

A 1.5-year-old Dalmatian was examined because of vomiting, weight loss, and high serum activities of alanine aminotransferase and aspartate aminotransferase. Abdominal ultrasonography revealed normal appearing hepatic structure with echogenicity, but histologic examination of hepatic biopsy specimens revealed extensive necrosis of hepatocytes involving the centrilobular areas. Macrophages and remaining hepatocytes contained pigments that were positive for copper by rubeanic acid-staining and hepatic copper concentration was high. The dog was treated with crystalloid fluids, antibiotics, and a low copper diet; its condition deteriorated, and the dog was euthanatized. Primary copper storage disease was suspected on the basis of histologic findings and high copper concentration in the liver.
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PMID:Copper associated acute hepatic failure in a dog. 1034 76

A full-length cDNA clone encoding aspartate aminotransferase (AAT) has been identified from a carrot root cDNA library. Degenerate oligo primers were synthesized from the known amino acid sequence of AAT form I from carrot (Daucus carota L. cv Danvers). These primers were utilized in a polymerase chain reaction to amplify a portion of a carrot AAT gene from first strand cDNA synthesized from poly(A)(+) RNA isolated from 5-d-old cell suspension cultures. The resulting 750-bp fragment was cloned, mapped, and sequenced. The cloned fragment, mpAAT1, was used as a probe to identify a full-length cDNA clone in a library constructed from poly(A)(+) RNA isolated from carrot roots. A 1.52-kb full-length clone, AAT7, was isolated and sequenced. AAT7 has 54% nucleotide identity with both the mouse cytoplasmic and mitochondrial AAT genes. The deduced amino acid sequence has 52 and 53% identity with the deduced amino acid sequences of mouse cytoplasmic and mitochondrial AAT genes, respectively. Further analysis of the sequence data suggests that AAT7 encodes a cytoplasmic form of carrot AAT; the evidence includes the (a) absence of a transit or signal sequence, (b) lack of "m-residues," or invariant mitochondrial residues, in the carrot AAT sequence, and (c) high degree of sequence similarity with the amino acid sequence previously obtained for form I of carrot, a cytoplasmic isoenzyme. High- and low-stringency hybridizations to Southern blots of carrot nuclear DNA with AAT7 show that AAT is part of a small multigene family. Northern blot analysis of AAT7 suggests that AAT is expressed throughout cell culture up to 7 d and is highly expressed in roots but not in leaves.
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PMID:Identification and expression of a cDNA clone encoding aspartate aminotransferase in carrot. 1665 71

A 1-year-old female Boer goat was presented with a 1-day history of pigmenturia, anorexia, and shivering. Anemia was not present initially, but progressive hemolytic anemia developed subsequently and was characterized by the finding of Heinz bodies in both intact RBCs and in ghost cells and the presence of atypical fusiform RBCs. Plasma biochemical analysis revealed increased activities of aspartate aminotransferase and gamma-glutamyltransferase, hyperbilirubinemia, and azotemia. Histopathologic examination of a liver biopsy revealed necrosis of individual hepatocytes and intracytoplasmic rhodamine-positive granules, consistent with copper. Copper concentration in ante-mortem hepatic tissue was increased, and a diagnosis of copper toxicosis was made. Despite supportive therapy, the goat continued to decline and was euthanized. Necropsy findings included hepatic necrosis and hemoglobinuric nephrosis. Freshly collected specimens of liver and kidney had markedly increased copper concentrations. The mineral composition of the water, grass hay, and goat chow was evaluated, and toxins and significant mineral imbalances were not found. The underlying cause of the hepatic accumulation and subsequent release of copper remains unclear in this goat. Recently, Boer goats have been recognized as being prone to copper toxicosis and may be more susceptible than other breeds; similar to sheep, Boer goats may experience a hemolytic crisis secondary to copper toxicosis.
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PMID:Copper toxicosis in a Boer goat. 2312 8