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Articles by S. Jiang
Total Records ( 2 ) for S. Jiang
  Q. Fang , S. Chen , Y. Wang , S. Jiang , R. Zhang , C. Hu , C. Wang , F. Liu , K. Xiang and W. Jia
  Aims  Hepatocyte nuclear factor-1α (HNF-1α) regulates the expression of genes encoding proteins involved in glucose metabolism and insulin secretion. Mutations in the HNF-1α gene cause maturity-onset diabetes of the young Type 3. However, the mechanism leading to this disease has not been completely ascertained. Previously, we found a novel mutation in the regulatory element of the human HNF-1α gene in two Chinese diabetes pedigrees. The nucleotide at position -128 T was substituted by G (nt-128 T[RIGHTWARDS ARROW]G). In this study, we analysed the functional defect of nt-128 T[RIGHTWARDS ARROW]G in HNF-1α transcription activity.

Methods  Luciferase reporter gene assays were carried out to examine the functional characteristics of this mutant. Electrophoretic mobility shift assays and chromatin immunoprecipitation were performed to confirm the binding of nuclear proteins to oligonucleotides.

Results  The variant construct (nt-128 T[RIGHTWARDS ARROW]G) had a 1.65-fold increase in promoter activity compared with that of the wild-type construct in HepG2 cells and a 1.33-fold increase in MIN6 cells, respectively. The variant resided at a FOXA/HNF-3 binding site identified by a series of competitive electrophoretic mobility shift assays and antibody supershift analyses. The assays showed a differential binding affinity in the wild-type and the nt-128 T[RIGHTWARDS ARROW]G mutant fragments by FOXA/HNF-3. Chromatin immunoprecipitation indicated that FOXA/HNF-3 bound to this region in vivo. One nucleotide substitution in the FOXA/HNF-3 site in the human HNF-1α regulatory element caused an increase of HNF-1α transcriptional activity.

Conclusions  Our data suggested that this substitution in the promoter region affects DNA-protein interaction and HNF-1α gene transcription. The mutant may contribute to the development of diabetes in these two nt-128 T[RIGHTWARDS ARROW]G pedigrees of Chinese.

  Qing-hua Zheng , S. Jiang , F. Zhang , T. Peng and C. Chen
  In this study, we propose a low-delay ALM protocol named TapMulti on Tapestry to achieve scalability and low-delay, . In TapMulti protocol, a delivery tree is designed to reduce end-to-end delay and improve stability of multicast system. This low-delay delivery tree is constructed on Tapestry and it can guarantee a tradeoff between delay and network-traffic load of multicast system by constraining width (maximal out-degree of node in the delivery tree) and depth of the delivery tree. Moreover, the efficient and proportional route mechanism of Tapestry is exploited to decrease the control cost to maintain multicast delivery tree. Simulated results indicate that, compared with other existing ALM approaches on Tapestry, TapMulti is of distinct advantages in aspects of end-to-end delay and control cost.
 
 
 
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