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  4. Regulation of Clathrin-Mediated Endocytosis
 
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Regulation of Clathrin-Mediated Endocytosis

Journal
Annual review of biochemistry
Journal Volume
87
Journal Issue
1
Pages
871
Date Issued
2018-06-20
Author(s)
Mettlen, Marcel
PING-HUNG CHEN  
Srinivasan, Saipraveen
Danuser, Gaudenz
Schmid, Sandra L
DOI
10.1146/annurev-biochem-062917-012644
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/627778
URL
https://api.elsevier.com/content/abstract/scopus_id/85046409140
Abstract
Clathrin-mediated endocytosis (CME) is the major endocytic pathway in mammalian cells. It is responsible for the uptake of transmembrane receptors and transporters, for remodeling plasma membrane composition in response to environmental changes, and for regulating cell surface signaling. CME occurs via the assembly and maturation of clathrin-coated pits that concentrate cargo as they invaginate and pinch off to form clathrin-coated vesicles. In addition to the major coat proteins, clathrin triskelia and adaptor protein complexes, CME requires a myriad of endocytic accessory proteins and phosphatidylinositol lipids. CME is regulated at multiple steps-initiation, cargo selection, maturation, and fission-and is monitored by an endocytic checkpoint that induces disassembly of defective pits. Regulation occurs via posttranslational modifications, allosteric conformational changes, and isoform and splice-variant differences among components of the CME machinery, including the GTPase dynamin. This review summarizes recent findings on the regulation of CME and the evolution of this complex process.
Subjects
AP2; adaptor protein-2; dynamin; endocytic accessory proteins; endocytic checkpoint; evolution; signaling
SDGs

[SDGs]SDG14

Publisher
ANNUAL REVIEWS
Type
review

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