Clathrin-independent carrier
Clathrin-independent carriers (CLICs) are prevalent tubulovesicular membranes responsible for non-clathrin mediated endocytic events. They appear to endocytose material into GPI-anchored protein-enriched early endosomal compartment (GEECs). Collectively, CLICs and GEECs comprise the Cdc42-mediated CLIC/GEEC endocytic pathway, which is regulated by GRAF1.[1][2][3]
Each of RhoA, Arf6, or Cdc42 has the capacity to modulate one of the three distinct clathrin-independent endocytic (CIE) pathways. Within the CIE pathway controlled by Cdc42, CLICs serve as the primary carriers facilitating uptake. The CLIC pathway encompasses scission of the plasma membrane (PM) independent of dynamin, dependence on Arf1 activity, enrichment in GPI-anchored proteins, increased susceptibility to cholesterol depletion, and substantial participation in the internalization of cholera toxin B subunit (CTxB) and fluid. CLICs merge with early endosomes after they undergo maturation into the GEEC along with the attachment of Rab5 and EEA-1.
References[edit]
- ^ Lundmark, R.; Doherty, G.J.; Howes, M.T.; et al. (November 2008). "The GTPase-Activating Protein GRAF1 Regulates the CLIC/GEEC Endocytic Pathway". Current Biology. 18 (22): 1802–8. doi:10.1016/j.cub.2008.10.044. PMC 2726289. PMID 19036340.
- ^ Rossatti, P.; Ziegler, L.; Schregle, R; et al. (November 2019). "Cdc42 Couples T Cell Receptor Endocytosis to GRAF1-Mediated Tubular Invaginations of the Plasma Membrane". Cells. 8 (11): 1388. doi:10.3390/cells8111388. PMC 6912536. PMID 31690048.
- ^ Elkin, S.R.; Lakoduk, A.M.; Schmid, S.L. (May 2016). "Endocytic pathways and endosomal trafficking: a primer". Wiener Medizinische Wochenschrift. 166 (7–8): 196–204. doi:10.1007/s10354-016-0432-7. PMC 4873410. PMID 26861668.
 | This protein-related article is a stub. You can help Wikipedia by expanding it. |