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
- ^ 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. Bibcode: 2008CBio...18.1802L. 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. |
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
- ^ 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. Bibcode: 2008CBio...18.1802L. 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.
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