File:Wnt signaling pathway.png
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Summary
[edit]DescriptionWnt signaling pathway.png |
English: Afther Wnt is synthesized, Wnt is acylated by the porcupine enzyme in the endoplasmic reticulum, resulting in the covalent bonding of palmitoleic acid to a conserved serine residue. It then travels through endosomes to the Golgi apparatus, where it binds to a carrier protein called Wntless, and subsequently, binds to lipoproteins in exosomes before being secreted into the cell's outer membrane.
Once secreted outside the cell, Wnt binds to frizzled receptors present in surrounding cells, particularly stem cells. Wnt binds to the frizzled receptor through palmitoleic acid and to the LRP co-stimulatory receptor on the other side, forming a triple complex. This Wnt-frizzled-LRP complex recruits the intracellular Dishevelled protein (DVL) to the intracellular domain of frizzled receptor and inactivates destruction complexes (Axin, GSK3, APC, CK1) which phoshorylates beta-catenin. Beta-catenin that has not undergone phosphorylation and ubiquitination enters the nucleus in a stable state and binds to the transcription factor TCF1, inducing the expression of genes involved in cell division and proliferation, such as c-Myc and CyclinD. In the absence of Wnt, the frizzled receptor cannot form a complex with the LRP co-stimulatory receptor. Instead, the LRP receptor binds to inhibitory receptors DKK1 and Kremen to maintain an inactive state. At this time, the destruction complex is active and phosphorylates β-catenin. The phosphorylated β-catenin is multi-ubiquitinated by β-TrCP and degraded by the proteolytic complex proteasome. In the nucleus, TCF-1 acts as a transcriptional repressor along with the Groucho co-repressor to suppress gene expression.한국어: 윈트(Wnt)는 소포체에 존재하는 포큐파인(porcupine) 효소에 의해 팔미톨레산(palmitoleic acid)이 달려 성숙한 윈트가 된다. 이후 엔도좀을 타고 골지체로 이동한 윈트는 윈트리스(Wntless)라는 운반 단백질과 결합한 뒤 엑소좀에서 지방단백질과 결합하여 세포 외막으로 분비된다.
세포 바깥으로 분비된 윈트는 주변의 세포(특히 줄기세포)에 존재하는 프리즐드(frizzled) 수용체에 결합한다. 윈트는 팔미톨레산을 통해 프리즐드 수용체와 결합하고 다른 한쪽으로 LRP 공자극수용체와 결합해 삼중복합체(triple complex)를 이루게 된다. 이러한 윈트-프리즐드-LRP 복합체는 세포내 디셰블드를 프리즐드 수용체의 세포내 도메인으로 유도한다. 디셰블드는 파괴 복합체(Axin, GSK3, APC, CK1)를 유도해 불활성화 시켜 베타-카테닌에 대한 인산화 작용을 억제시킨다. 인산화 및 유비키틴화가 일어나지 않은 베타-카테닌은 안정화된 상태로 핵 내부로 들어가 전사인자인 TCF1과 결합해 c-Myc, 사이클린(CyclinD)과 같이 세포 분열 및 증식에 관여하는 유전자의 발현을 유도한다. 윈트가 없는 상태에서 프리즐드 수용체는 LRP 공자극수용체와 복합체를 이루지 못하며, LRP 수용체는 DKK1과 크리멘(Kremen) 억제 수용체와 결합하여 비활성 상태를 유지한다. 이때 세포내에 존재하는 파괴 복합체는 베타-카테닌을 인산화 시키며, 인산화된 베타-카테닌은 베타-TrCP에 의해 다중 유비키틴화 되어 단백질 분해 복합체인 프로티아좀(proteasome)에 의해 분해된다. 핵 내에서 TCF-1은 그루쵸(Groucho) 전자 인자와 함께 전자 억제자로 작용해 유전자의 발현을 억제시킨다. |
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Author | Srgokribb |
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