Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.99.3 (acyl-CoA dehydrogenase)
 1,425 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pea aphids form a mutualistic association with the endosymbiotic bacterium Buchnera, which is harbored in specialized host cells called bacteriocytes. The adult aphids display dimorphism In which there are winged and wingless morphs. We previously reported that the Buchnera density in bacteriocytes of the winged morph (alate) decreases around final ecdysis, whereas that in the wingless morph (aptera) does not decrease; the decrease in density in alatae is accompanied by activation of the host lysosomal system and by Buchnera degradation. In the present study, we performed a proteomic analysis to clarify the molecular mechanisms underlying the decrease in Buchnera density. By comparing the protein expression profiles of bacteriocytes in alatae and apterae Just after final ecdysis, we identified three and one protein spots that were preferentially expressed in alatae and apterae, respectively. Among the three alate-preferential spots, two were an identical aphid protein, carboxypeptidase vitellogenic-like (CPVL), whereas the other was a mixture of four proteins: gamma-glutamyl hydrolase, acyl-CoA dehydrogenase, aphid short chain acyl-CoA dehydrogenase, and Buchnera S-adenosylmethionine synthetase. The aptera-preferential spot was Buchnera outer membrane protein A. Immunoblot and immunohistochemical analyses using aphid bacteriocytes Just after final ecdysis revealed that expression of aphid CPVL was preferentially upregulated in alatae and was localized around Buchnera cells in the bacterlocytes, suggesting the involvement of CPVL in Buchnera degradation in alatae.
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PMID:Morph-dependent expression and subcellular localization of host serine carboxypeptidase in bacteriocytes of the pea aphid associated with degradation of the endosymbiotic bacterium Buchnera. 1958 1

Hepatocellular carcinoma (HCC) represents a major health problem as it afflicts an increasing number of patients worldwide. Albeit most of the risk factors for HCC are known, this is a deadly syndrome with a life expectancy at the time of diagnosis of less than 1 year. Definition of the molecular principles governing the neoplastic transformation of the liver is an urgent need to facilitate the clinical management of patients, based on innovative methods to detect the disease in its early stages and on more efficient therapies. In the present study, we have combined the analysis of a murine model and human samples of HCC to identify genes differentially expressed early in the process of hepatocarcinogenesis, using a microarray-based approach. Expression of 190 genes was impaired in murine HCC from which 65 were further validated by low-density array real-time polymerase chain reaction (RT-PCR). The expression of the best 45 genes was then investigated in human samples resulting in 18 genes in which expression was significantly modified in HCC. Among them, JUN, methionine adenosyltransferase 1A and 2A, phosphoglucomutase 1, and acyl CoA dehydrogenase short/branched chain indicate defective cell proliferation as well as one carbon pathway, glucose and fatty acid metabolism, both in HCC and cirrhotic liver, a well-known preneoplastic condition. These alterations were further confirmed in public transcriptomic datasets from other authors. In addition, vasodilator-stimulated phosphoprotein, an actin-associated protein involved in cytoskeleton remodeling, was also found to be increased in the liver and serum of cirrhotic and HCC patients. In addition to revealing the impairment of central metabolic pathways for liver homeostasis, further studies may probe the potential value of the reported genes for the early detection of HCC.
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PMID:A signature of six genes highlights defects on cell growth and specific metabolic pathways in murine and human hepatocellular carcinoma. 2156 99