[논문]TNF 신호전달에서 RIPK와 MLKL의 기능적 생리적 특성

박영훈; 정미숙; 장세복

doi:10.5352/jls.2016.26.7.868

TNF 신호전달에서 RIPK와 MLKL의 기능적 생리적 특성
Functional and Physiological Characteristic of RIPK and MLKL in TNF Signaling 원문보기

생명과학회지 = Journal of life science, v.26 no.7 = no.195, 2016년, pp.868 - 874

박영훈 (부산대학교 자연과학대학 분자생물학과) , 정미숙 (부산대학교 자연과학대학 분자생물학과) , 장세복 (부산대학교 자연과학대학 분자생물학과)

초록
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수용체 상호작용 단백질 인산화 효소 RIPK1 (Receptor-interacting protein kinases 1)과 RIPK3은 고도로 보존된 인산화 효소 부위를 통하여 세린이나 트레오닌의 하이드록실기를 인산화하는 세린 또는 트레오닌-단백질 인산화 효소 군에 속한다. RIPK군은 염증이나 선천성 면역뿐 만 아니라 세포사멸이나 괴사와 같은 프로그램화된 세포사 멸을 중재하는데 중요한 역할을 담당한다. RIPK1과 다른 TNFR1 관련 단백질들의 상호작용은 TNF 수용체 1(TNFR1)에 사이토카인이 결합할 때 생존 촉진 전사인자 NF-κB의 활성을 조절하는 신호전달복합체 I을 조립하는 것으로 알려져 왔다. 뿐만 아니라, RIPK1과 RIPK3은 프로그램화된 세포괴사를 중재하는 RIP 동형 상호작용 모티브(RHIM)를 통하여 상호작용하고, 이러한 괴사는 세포사멸의 유형과는 다른 형태학적 특징을 가진 돌발적이고 제어되지 않는 세포사멸 유형으로 오랫동안 알려져 왔다. RIPK1과 RIPK3에 존재하는 RHIM의 고도로 보존된 서열들이 이들의 상호작용을 조절하며 이들은 necrosome이라 불리는 세포질 내 아밀로이드 복합체의 조립을 유도 한다. 또한 necrosome은 최근에 하위 신호전달을 조절하는 RIPK3의 기질로 확인된 혼합형 인산화 효소 도메인-유사 단백질(MLKL)을 포함한다. 본 리뷰는 TNF 신호전달에서 RIPK와 MLKL의 기능적, 생리적 특징들에 관한 개요를 제공한다.

Abstract ▼ AI-Helper

Receptor-interacting protein kinase 1 (RIPK1) and RIPK3 are members of the serine or threonine protein kinase superfamily that phosphorylates the hydroxyl group of serine or threonine through the highly conserved kinase region. The RIPK family plays a crucial role not only in inflammation and innate immunity, but also in mediating programmed cell death, such as apoptosis and necroptosis. The interaction between RIPK1 and other TNFR1-related proteins has been shown to assemble a signaling complex I that controls activation of the pro-survival transcription factor NF-κB upon binding of cytokines to TNF receptor 1 (TNFR1). Moreover, RIPK1 and RIPK3 interact through their RIP homotypic interaction motifs (RHIMs) to mediate programmed necrosis, which has long been considered an accidental and uncontrolled cell death form with morphological characteristics differing from those of apoptosis. Highly conserved sequences of RHIM in RIPK1 and RIPK3 were shown to regulate their binary interaction, leading to assembly of a cytosolic amyloid complex termed the “necrosome”. The necrosome also contains mixed lineage kinase domain-like protein (MLKL), which has been found recently to be a substrate of RIPK3 to mediate downstream signaling. This review provides an overview of the functional and physiological characteristics of RIPKs and MLKL in TNF signaling.

주제어

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제안 방법

Although many previous studies have focused on the mechanism of RIPK family members in inflammation and innate immunity, it is clear that these proteins have many functional and physiological characteristics that are derived from their crucial mechanism in programmed cell death signaling. These studies confirm that RIPKs and its related molecules play a pivotal role in the assembly of death complexes, which are identified by nuclear magnetic resonance and X-ray diffraction studies. Furthermore, many of the regulatory mechanisms of RIPK1 in apoptosis are mediated by biquitination of the kinase domain or combination through DD interaction.

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