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[국내논문] 지질대사 조절에서 SREBP의 역할
SREBP as a Global Regulator for Lipid Metabolism 원문보기

생명과학회지 = Journal of life science, v.28 no.10 = no.222, 2018년, pp.1233 - 1243  

이원화 (한국생명공학연구원 노화제어연구단) ,  서영교 (한국생명공학연구원 노화제어연구단)

초록
AI-Helper 아이콘AI-Helper

SREBPs는 지질의 항상성 및 대사를 조절하는 전사 인자이다. 이들은 내인성 콜레스테롤, 지방산(FA), 트리아실글리세롤(TG) 및 인지질 합성에 필요한 효소의 발현을 정밀하게 조절한다. 3종류의 SREBP 단백질은 2개의 다른 유전자에 의해 암호화 된다. SREBP1 유전자는 SREBP-1a와 SREBP-1c를 만든다. 이는 RNA의 alternative splicing에 의한 대체 프로모터의 이용으로부터 유도된다. SREBP-2는 별도의 유전자에서 유래한다. 또한, SREBPs는 ER 스트레스, 염증, 자가포식세포사멸과 같은 수많은 병인과정에 관여하며, 비만, 이상 지질혈증, 당뇨병 및 비알콜성 지방간 질환 등을 유발하는 것으로 알려져 있다. 유전체의 분석은 SREBPs가 생물학적 신호 전달, 세포 신진 대사, 및 성장을 조절하는 중요한 연결고리임을 보여 주었다. 이 과정에서 SREBP는 PI3K-Akt-mTOR 경로를 통해 활성화 된다고 알려져 있다. 하지만 정확한 분자 메커니즘은 좀더 밝혀져야 한다. 이 리뷰에서는 세포, 기관 및 생물개체 수준의 생리학 및 병태 생리학 영역에서 SREBP의 역할에 대한 포괄적인 이해를 넓혀 줄 것이다.

Abstract AI-Helper 아이콘AI-Helper

Sterol regulatory-element binding proteins (SREBPs) are a family of transcription factors that regulate lipid homeostasis and metabolism by controlling the expression of enzymes required for endogenous cholesterol, fatty acid (FA), triacylglycerol, and phospholipid synthesis. The three SREBPs are en...

주제어

표/그림 (3)

AI 본문요약
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가설 설정

  • TSC1 및 TSC2 이중 knockout (mTORC1 활성화 모델) 마우스 fibroblst에서 mTORC1에 의해 유도 되는 여러 유전자 중에서, SREBP1과 SREBP2는 S6K1에 의해 매개되는 세포 증식을 촉진시킨다[9]. 이러한 사실은 mTORC1-S6K1 상호 작용이 인슐린 저항성 조건 하에서 SREBP 활성화 및 지방간 형성에 중요하다는 가설을 증명하는 것이다. 또한 mTORC1의 만성 활성화는 인슐린 내성을 일으키는 것으로 알려져 있으며[1], 이것은 저용량의 mTOR 억제제인 라파마이신에 의한 인슐린 내성의 개선을 설명한다.
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