The differentiating of neurons and other distinct cell types during embryonic development requires the selective activation or repressing of many different sets of genes. Gene expression patterns in neurons are modulated by multiple extracellular and intracellular stimuli. The transcriptional regulation of individual gene is mediated by small DNA sequences such as silencer and enhancer, and the expression pattern can be determined by the integration of the effects of a very large number of these cis-acting elements. These DNA elements either activate or repress promoter activity depending upon the nature of the transcription factors that bind to them. It is possible that there are different regulatory mechanisms of gene expression in the nerve system.

Objective To observe the protective effects of AG on the myocardial ultrastructure of diabetic rats.Methods STZ-induced diabetic male SD rats were divided into two groups: aminoguanidine(AG group,50 mg?kg~(-1) body weight by daily gavage) and diabetes mellitus groups(DM group).Age-matched normal male SD rats served as normal control(NC group).After 10 weeks of treatment the level of blood glucose was measured and the rats were killed.Cardiac muscle were observed by transmission electronic microscope.Results The changes of cardiac ultrastructure had no significant difference between AG-group and NC-group and were better in AG group than in DM group as following:(1) Myofibril arranged tidily with intact regular edge;(2) Mitochodria were big and normomorph with crests arranging densely,some mitochondria gathered locally;(3)Base membrane of blood vessels didn′t thicken with lumen not narrowed;(4) The collagenous fiber in stroma reduced but amorphous material didn′t reduced. Conclusions The ultrastructure pictures of diabetic cardiomyopathy is inhibited or delayed by AG,which suggests that AGEs may play some role in the development of diabetic cardiomyopathy.

OBJECTIVETo clone and identify the gene encoding human ubiquitin binding enzyme 2 and study its expression pattern.

METHODSAccording to the sequence of human EST, which is highly homologous to the mouse ubiquitin binding/conjugating enzyme (E2), primers were synthesized to screen the human fetal brain cDNA library. The gene was analyzed by bioinformatics technique and its expression pattern was studied by using multiple-tissue Northern blot.

RESULTSTwo cDNA clones encoding human ubiquitin conjugating enzyme have been isolated and identified. Both containing the ubiquitin conjugating domain, the 2 cDNA clones are 88% identical in amino acid sequences and splicing isoforms to each other only with an exon excised to form the short sequence. They belong to a highly conserved and widely expressed E2 enzyme family. Northern blot shows that they are expressed exclusively in adult human heart, placenta, and pancreas but no transcripts can be detected in brain, lung, liver, skeletal muscle or kidney.

CONCLUSIONSThe gene encoding human ubiquitin binding enzyme is expressed under temporal control. As a key enzyme in the degradation of proteins, ubiquitin conjugating enzymes play a central role in the expression regulation on the level of post-translation.

Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA, Complementary ; genetics ; Female ; Humans ; Mice ; Molecular Sequence Data ; Myocardium ; metabolism ; Pancreas ; metabolism ; Placenta ; metabolism ; Rats ; Sequence Alignment ; Sequence Analysis, DNA ; Ubiquitin ; genetics ; Ubiquitin-Conjugating Enzymes ; biosynthesis ; chemistry ; genetics