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Articles by H Dong
Total Records ( 2 ) for H Dong
  Y Xu , H Lei , H Dong , L Zhang , Q Qin , J Gao , Y Zou and X. Yan

Previous studies found that the forkhead transcription factor 2 (FOXL2) gene mutations are responsible for both types of blepharophimosis–ptosis–epicanthus inversus syndrome (BPES) but have not established any systematic statistic model for the complex and even contradictory results about genotype–phenotype correlations between them. This study is aimed to find possible mutations of FOXL2 gene in a Chinese family with type II BPES by using DNA sequencing and to further clarify genotype–phenotype correlations between FOXL2 mutations and BPES by using a systematic statistical method, namely Multifactor Dimensionality Reduction (MDR). A novel mutation (g.933_965dup) which could result in an expansion of the polyalanine (polyAla) tract was detected in all patients of this family. MDR analysis for intragenic mutations of FOXL2 gene reported in previous BPES studies indicated that the mutations which led to much stronger disturbance of amino acid sequence were responsible for more type I BPES, while other kinds of mutation were responsible for more type II BPES. In conclusion, the present study found a novel FOXL2 gene mutation in a Chinese BPES family and a new general genotype–phenotype correlation tendency between FOXL2 intragenic mutations and BPES, both of which expanded the knowledge about FOXL2 gene and BPES.

  H Dong , K. N Shim , J. M. J Li , C Estrema , T. A Ornelas , F Nguyen , S Liu , S. L Ramamoorthy , S Ho , J. M Carethers and J. Y. C. Chow

We recently reported that transforming growth factor-β (TGF-β) induces an increase in cytosolic Ca2+ ([Ca2+]cyt) in pancreatic cancer cells, but the mechanisms by which TGF-β mediates [Ca2+]cyt homeostasis in these cells are currently unknown. Transient receptor potential (TRP) channels and Na+/Ca2+ exchangers (NCX) are plasma membrane proteins that play prominent roles in controlling [Ca2+]cyt homeostasis in normal mammalian cells, but little is known regarding their roles in the regulation of [Ca2+]cyt in pancreatic cancer cells and pancreatic cancer development. Expression and function of NCX1 and TRPC1 proteins were characterized in BxPc3 pancreatic cancer cells. TGF-β induced both intracellular Ca2+ release and extracellular Ca2+ entry in these cells; however, 2-aminoethoxydiphenyl borate [2-APB; a blocker for both inositol 1,4,5-trisphosphate (IP3) receptor and TRPC], LaCl3 (a selective TRPC blocker), or KB-R7943 (a selective inhibitor for the Ca2+ entry mode of NCX) markedly inhibited the TGF-β-induced increase in [Ca2+]cyt. 2-APB or KB-R7943 treatment was able to dose-dependently reverse membrane translocation of PKC induced by TGF-β. Transfection with small interfering RNA (siRNA) against NCX1 almost completely abolished NCX1 expression in BxPc3 cells and also inhibited PKC serine phosphorylation induced by TGF-β. Knockdown of NCX1 or TRPC1 by specific siRNA transfection reversed TGF-β-induced pancreatic cancer cell motility. Therefore, TGF-β induces Ca2+ entry likely via TRPC1 and NCX1 and raises [Ca2+]cyt in pancreatic cancer cells, which is essential for PKC activation and subsequent tumor cell invasion. Our data suggest that TRPC1 and NCX1 may be among the potential therapeutic targets for pancreatic cancer.

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