Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.3.14 (ATP synthase)
 7,042 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In our previous study, the age-dependent testis vacuolisation and sperm dysfunction were found in Attractin (Atrn)-deficient mice, Atrn(mg-3J) , which is a null or nearly null allele. To explore the potential mechanism involved in these pathological changes, Attractin knock-down in mouse Sertoli cells TM4 (psiAtrn-TM4) was successfully established by stable RNA interference. The TM4 transfected by psiRNA-hH1 (psiRNA-TM4) was the control group, in which the expression of Atrn was not affected. The proteomic changes among the psiAtrn-TM4, primary cultures of Sertoli cells of Atrn(mg-3J) (mu-Sc) and control cells (psiRNA-TM4) were compared by two-dimensional gel electrophoresis. Fifteen differentially expressed protein spots of those cells were identified by matrix-assisted laser desorption/ionisation time-of-flight mass spectrometry and the NCBI proteins database. Except the decreased expression of superoxide dismutase (SOD), there were several novel proteins associated with Atrn function, including downregulated ATP synthase, peroxiredoxin 2 and upregulated caspase 6, ketohexokinase, etc., in psiAtrn-TM4 and mu-Sc. These data suggest that these differentially expressed proteins may be associated with the function of Atrn in Sertoli cells, thus providing a new clue to interpret the mechanism of testis degeneration in Atrn mutants.
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PMID:New clues to identify proteins correlated with Attractin. 2399 93

3-Monochloro-1,2-propanediol (3-MCPD) is the most toxic chloropropanols compounds in foodstuff which mainly generated during thermal processing. Kidney is one of the primary target organs for 3-MCPD. Using human embryonic kidney cell (HEK293FT) as an in vitro model, we found that 3-MCPD caused concentration-dependent increase in cytoxicity as assessed by dye uptake, lactatedehydrogenase (LDH) leakage and MTT assays. HEK293FT cell treated with 3-MCPD suffered the decrease of mitochondrial membrane potential and the impairment of mitochondrial oxidative phosphorylation system, especially the reduced amount of mRNA expression and protein synthesis of electron transport chain complex II, complex IV, and complex III. More importantly, energy release (ATP synthesis) was significantly inhibited by 3-MCPD resulting from the down regulation expressions of ATP synthase (ATP6 and ATP8), as well as the loss of transmembrane potential required for synthesis of ATP. The decreased ratio of mitochondrial apoptogenic factors Bax/Bcl-2 and the cytochrome-c release from mitochondria to cytosol followed by the activation of apoptotic initiators caspase 9 and apoptotic executioners (caspase 3, caspase 6 and caspase 7) leading to apoptosis. The activation of caspase 8 and caspase 2 implied that there were probably other factors to induce the caspase-dependent apoptosis.
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PMID:3-Monochloro-1,2-propanediol (3-MCPD) induces apoptosis via mitochondrial oxidative phosphorylation system impairment and the caspase cascade pathway. 2773 82