http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
NF-κB 신호전달과정의 음성적 조절 -배아줄기세포에서의 조절을 포함하여
이충일 ( Choong Il Lee ),심상형 ( Sang Hhyung Sim ),김영은 ( Young Eun Kim ),황유원 ( Yoo Weon Hwang ),하양화 ( Yang Hwa Ha ),한재민 ( Jae Min Han ),김경아 ( Kyeong A Kim ),황보은 ( Eun Hwang Bo ),이영희 ( Young Hee Lee ) 한국조직공학과 재생의학회 2010 조직공학과 재생의학 Vol.7 No.3
NF-κB is a transcriptional factor which is involved in many biological processes including immunity, inflammation, and cell survival. Many investigators studied on the mechanism involved in activation of NF-κB signalling pathway via ubiquitination and degradation of IkB. Recently, termination of NF-κB signaling after activation is regarded as another essential regulating step. In addition to the negative feedback by IkB protein, ubiquitination and degradation of nuclear p65/RelA, a crucial subunit of NF-κB, is considered another mechanism to terminate the NF-κB signaling. COMMD1, PDLIM2, GCN5 and NMRAL1 are recently reported as proteins related with p65/ RelA ubiquitination. Interestingly, ubiquitination and degradation of p65/RelA through viral protein was also found in the process of viral infection to escape from host defence mechanism. In contrast with somatic cells, expression of NF-κB is relatively low in undifferentiated embryonic stem (ES) cells, and activity of NF-κB is down-regulated by Nanog via direct interaction. Furthermore, enforced expression of NF-κB resulted in differentiation suggesting that down regulation of NF-κB contributes to the maintenance of ES cells. Therefore, better understanding on the negative regulation of NF-κB signaling in somatic cells as well as in ES cells might give more insights into therapeutics targeting NF-κB signaling.