NF-κB 신호전달과정의 음성적 조절 -배아줄기세포에서의 조절을 포함하여
의약학 > 의공학
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 )
조직공학과 재생의학 2010년, 제7권 제3호, 269~275페이지(총7페이지)
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    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.
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