Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P23193 (transcription elongation factor)
 739 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The protective effect of berberine against antioxidant, antilipid peroxidation in serum and liver tissue, and positive transcription elongation factor b (P-TEFb) expression in liver tissue of type 2 diabetic rats was investigated. Overnight fasted rats were intraperitoneally injected 35 mg/kg streptozotocin. Diabetic rats were admitted after 2 weeks and given a high-carbohydrate/high-fat diet to induce hyperlipidemias. From week 16, diabetic rats were treated with 75, 150, 300 mg/kg berberine, 100mg/kg fenofibrate or 4 mg/kg rosiglitazone for another 16 weeks. P-TEFb (composed of cyclin-dependent kinase 9 and cyclin T1) mRNA and protein expression in liver tissue were detected by real time PCR and immunohistochemistry, respectively. Berberine significantly up-regulated the declined cyclin-dependent kinase 9, cyclin T1 mRNA and protein expression in diabetic rat liver. Berberine obviously decreased malondialdehyde level and increased catalase, superoxide dismutase, glutathione peroxidase, and glutathione activities in liver tissue and serum of diabetic rats. These results suggest that the effects of berberine on up-regulation of P-TEFb expression, antioxidant and antilipid peroxidation may be related to its protective potential on diabetes.
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PMID:Protective effect of berberine on antioxidant enzymes and positive transcription elongation factor b expression in diabetic rat liver. 2082 2

The expression of subunits of mitochondrial respiratory complexes and components of the protein synthesis machinery from the nucleolus to the ribosome was analyzed in the mediodorsal thalamus in seven cases of fatal familial insomnia (FFI) compared with age-matched controls. NDUFB8 (complex I subunit), SDHB (complex II subunit), UQCRC2 (complex III subunit), COX2 (complex IV subunit), and ATP50 (complex V subunit) expression levels, as revealed by western blotting, were reduced in FFI. Voltage-dependent anion channel (VDAC) and ATP5H were also reduced due to the marked depopulation of neurons. In contrast, a marked increase in superoxide dismutase 2 (SOD2) was found in reactive astrocytes thus suggesting that astrocytes are key factors in oxidative stress responses. The histone-binding chaperones nucleolin and nucleoplasmin 3, and histone H3 di-methylated K9 were markedly reduced together with a decrease in the expression of protein transcription elongation factor eEF1A. These findings show severe impairment in the expression of crucial components of mitochondrial function and protein synthesis in parallel with neuron loss in mediodorsal thalamus at terminal stages of FFI. Therapeutic measures must be taken long before the appearance of clinical symptoms to prevent the devastating effects of FFI.
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PMID:Fatal familial insomnia: mitochondrial and protein synthesis machinery decline in the mediodorsal thalamus. 2735 67