Dynamin 2 is required for phagocytosis in macrophages.

Dynamin 2 is required for phagocytosis in macrophages.
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动力蛋白2是巨噬细胞中吞噬作用所必需的。

DOI:
10.1084/jem.190.12.1849
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发表时间:
1999-12-20
影响因子:
15.3
通讯作者:
Aderem, A
Aderem, A
中科院分区:
医学1区
文献类型:
--
作者:
Gold, E S;Underhill, D M;Morrissette, N S;Guo, J;McNiven, M A;Aderem, A

文献摘要

被引文献

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细胞通过内吞作用内化可溶性配体,并通过基于肌动蛋白的吞噬作用内化大颗粒。GTP酶的动力蛋白家族介导内吞囊泡从质膜的断裂。我们在这里报告,发动蛋白2,一种普遍表达的发动蛋白亚型,在巨噬细胞的吞噬作用中发挥作用。发动蛋白2富集在早期吞噬体上,并且发动蛋白2的显性负突变体的表达在颗粒周围的膜延伸阶段显著抑制颗粒内化。这种吞噬作用的停滞类似于磷酸肌醇3-激酶(PI 3 K)抑制剂的抑制,PI 3 K的抑制可防止发动蛋白募集到颗粒结合部位。虽然突变发动蛋白在巨噬细胞中的表达抑制了颗粒的内化,但它对颗粒结合引起的炎症介质的产生没有影响。
Cells internalize soluble ligands through endocytosis and large particles through actin-based phagocytosis. The dynamin family of GTPases mediates the scission of endocytic vesicles from the plasma membrane. We report here that dynamin 2, a ubiquitously expressed dynamin isoform, has a role in phagocytosis in macrophages. Dynamin 2 is enriched on early phagosomes, and expression of a dominant-negative mutant of dynamin 2 significantly inhibits particle internalization at the stage of membrane extension around the particle. This arrest in phagocytosis resembles that seen with inhibitors of phosphoinositide 3-kinase (PI3K), and inhibition of PI3K prevents the recruitment of dynamin to the site of particle binding. Although expression of mutant dynamin in macrophages inhibited particle internalization, it had no effect on the production of inflammatory mediators elicited by particle binding.