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Articles by M Jung
Total Records ( 3 ) for M Jung
  O Kwon , S. J Jeong , S. O Kim , L He , H. G Lee , K. L Jang , H Osada , M Jung , B. Y Kim and J. S. Ahn
 

E-cadherin, as a tumor suppressor, plays an important role for intercellular adhesion involved in metastasis. Although K-Ras is highly expressed in a variety of cancers, the regulation of E-cadherin expression by K-Ras in association with DNA methylation and cell metastasis has not been completely clarified. In this study, E-cadherin expression was repressed in 267B1/K-Ras human epithelial prostate cancer cells stably overexpressing K-Ras, resulting from hypermethylation of E-cadherin promoter as evidenced by methylation-specific polymerase chain reaction (PCR), bisulfite sequencing, real-time reverse transcription–PCR and western blot analysis. The increased level of DNA methyltransferase (DNMT) 3b in 267B1/K-Ras cells was reduced by small interfering RNA-mediated knockdown of k-ras, whereas DNMT1 and DNMT3a did not change regardless of K-Ras or 5-aza-2'-deoxycytidine (5'-AzaC) treatment. Furthermore, binding of DNMT3b to E-cadherin promoter was increased in 267B1/K-Ras cells but was reduced by 5'-AzaC, as revealed by chromatin immunoprecipitation assay, which was in agreement with cell aggregation and invasive mobilization of the cells. Hence, our data suggest that increased binding of DNMT3b to E-cadherin promoter region by K-Ras cause promoter hypermethylation for reduced expression of E-cadherin, leading to the decreased cell aggregation and increased metastasis of human prostate cancer cells overexpressing K-Ras.

  M Jung and K. Lee
 

This article attempts to identify the determinants of total factor productivity (TFP) catch-up by Korean firms compared with that of Japanese firms. The degree of catch-up is measured in terms of the TFP gap between each Korean firm and the industry average of the Japanese firms in each sector. Regressions are then employed to establish the determinants of the TFP gap or catch-up. These determinants are classified into two groups: sectoral- and firm-level variables. Sectoral-level variables, drawn from the sectoral innovation system literature, test the hypothesis that catch-up is more likely to occur in certain sectors than in others. It is found that TFP catch-up by Korean firms is more likely to occur in sectors where technologies are more explicit and easily embodied in imported equipment. This discovery helps explain why the TFP of Korean firms is now close to, or even higher than those of Japanese firms in the electronics sector, and why TFP gaps still remain after some catch-up in the automobile sectors associated with more tacit knowledge regimes. Second, the degree of the sectors’ top firm dominance is positively related to the TFP catch-up, implying that catch-up is more likely to occur in sectors with more monopolistic market structures. It is also shown that firms in a monopolistic market structure should be subjected to the world market discipline to attain better performance in the productivity catch-up. Third, sector-level variables only affect international TFP catch-up, whereas firm-level variables determine intranational catch-up. Important results remain consistent in some robustness tests using different proxies for sectoral variables and catch-up as measured in labor productivity, as well as in the results obtained from using period average variables rather than yearly variables.

  S Infantino , B Benz , T Waldmann , M Jung , R Schneider and M. Reth
 

Signals processed through the B cell antigen receptor (BCR) control both the proliferation and differentiation of B lymphocytes. How these different signaling modes are established at the BCR is poorly understood. We show that a conserved arginine in the tail sequence of the Ig subunit of the BCR is methylated by the protein arginine methyltransferase 1. This modification negatively regulates the calcium and PI-3 kinase pathways of the BCR while promoting signals leading to B cell differentiation. Thus, Ig arginine methylation can play an important role in specifying the outcome of BCR signaling.

 
 
 
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