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COPⅠ 既能作用于小泡运输又能作用于管状运输。

COPI acts in both vesicular and tubular transport.

机构信息

Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Nat Cell Biol. 2011 Jul 3;13(8):996-1003. doi: 10.1038/ncb2273.

Abstract

Intracellular transport occurs through two general types of carrier, either vesicles or tubules. Coat proteins act as the core machinery that initiates vesicle formation, but the counterpart that initiates tubule formation has been unclear. Here, we find that the coat protein I (COPI) complex initially drives the formation of Golgi buds. Subsequently, a set of opposing lipid enzymatic activities determines whether these buds become vesicles or tubules. Lysophosphatidic acid acyltransferase-γ (LPAATγ) promotes COPI vesicle fission for retrograde vesicular transport. In contrast, cytosolic phospholipase A2-α (cPLA2α) inhibits this fission event to induce COPI tubules, which act in anterograde intra-Golgi transport and Golgi ribbon formation. These findings not only advance a molecular understanding of how COPI vesicle fission is achieved, but also provide insight into how COPI acts in intra-Golgi transport and reveal an unexpected mechanistic relationship between vesicular and tubular transport.

摘要

细胞内运输通过两种一般类型的载体进行,即囊泡或小管。外套蛋白作为启动囊泡形成的核心机制发挥作用,但启动小管形成的对应物尚不清楚。在这里,我们发现衣壳蛋白 I(COPI)复合物最初驱动高尔基体芽的形成。随后,一组相反的脂质酶活性决定了这些芽是形成囊泡还是小管。溶血磷脂酸酰基转移酶-γ(LPAATγ)促进 COPI 囊泡分裂,以进行逆行囊泡运输。相比之下,细胞质型磷脂酶 A2-α(cPLA2α)抑制这种分裂事件,从而诱导 COPI 小管形成,其在顺行的高尔基体内部运输和高尔基体带形成中发挥作用。这些发现不仅推进了对 COPI 囊泡分裂如何实现的分子理解,还深入了解了 COPI 在高尔基体内部运输中的作用,并揭示了囊泡运输和管状运输之间意想不到的机制关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d167/3149785/a72329280176/nihms294065f1.jpg

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