Regulation of Clathrin-Mediated Endocytosis

Marcel Mettlen, Ping Hung Chen, Saipraveen Srinivasan, Gaudenz Danuser, Sandra L. Schmid

Research output: Contribution to journalReview articlepeer-review

320 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)871-896
Number of pages26
JournalAnnual review of biochemistry
StatePublished - Jun 20 2018


  • AP2
  • adaptor protein-2
  • dynamin
  • endocytic accessory proteins
  • endocytic checkpoint
  • evolution
  • signaling

ASJC Scopus subject areas

  • Biochemistry


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