Molecular mechanisms of clathrin-independent endocytosis

Hansen, Carsten Gram; Nichols, Benjamin J.

doi:10.1242/jcs.033951

Cited by 252 publications

(217 citation statements)

References 124 publications

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“…Further analysis revealed that centers of clathrin-coated and caveolar vesicles were ~130 nm apart ( Figure 3C). (2) By using transmission electron microscopy, we observed morphologically characteristic clathrin-coated pits and caveolae (the flaskshaped membrane invagination) at the plasma membrane as previously described [30,31]. The partially fused caveolar and clathrin-coated vesicles were also observed ( Figure 3D).…”

Section: Fusion Of Clathrin-coated Vesicles and Caveolar Vesicles Undsupporting

confidence: 74%

Internalization of the TGF-β type I receptor into caveolin-1 and EEA1 double-positive early endosomes

Yan

et al. 2015

Cell Res

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Endocytosis and intracellular sorting of transforming growth factor-β (TGF-β) receptors play an important regulatory role in TGF-β signaling. Two major endocytic pathways, clathrin-and caveolae-mediated endocytosis, have been reported to independently mediate the internalization of TGF-β receptors. In this study, we demonstrate that the clathrin-and caveolae-mediated endocytic pathways can converge during TGF-β receptor endocytic trafficking. By tracking the intracellular dynamics of fluorescently-labeled TGF-β type I receptor (TβRI), we found that after mediating TβRI internalization, certain clathrin-coated vesicles and caveolar vesicles are fused underneath the plasma membrane, forming a novel type of caveolin-1 and clathrin double-positive vesicles. Under the regulation of Rab5, the fused vesicles are targeted to early endosomes and thus deliver the internalized TβRI to the caveolin-1 and EEA1 double-positive early endosomes (caveolin-1-positive early endosomes). We further showed that the caveolin-1-positive early endosomes are positive for Smad3/SARA, Rab11 and Smad7/Smurf2, and may act as a multifunctional device for TGF-β signaling and TGF-β receptor recycling and degradation. Therefore, these findings uncover a novel scenario of endocytosis, the direct fusion of clathrin-coated and caveolae vesicles during TGF-β receptor endocytic trafficking, which leads to the formation of the multifunctional sorting device, caveolin-1-positive early endosomes, for TGF-β receptors.

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Section: Fusion Of Clathrin-coated Vesicles and Caveolar Vesicles Undsupporting

confidence: 74%

Internalization of the TGF-β type I receptor into caveolin-1 and EEA1 double-positive early endosomes

Yan

et al. 2015

Cell Res

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“…28 Endocytic pathways have been mainly classified as clathrin-dependent or -independent, 28 the later can be further classified as dynamin-dependent orindependent pathway. Dynamin is a large GTPase directly involved in pinching off endocytic vesicles from the plasma membrane.…”

Section: Discussionmentioning

confidence: 99%

Macrophage endocytosis of high-mobility group box 1 triggers pyroptosis

et al. 2014

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Macrophages can be activated and regulated by high-mobility group box 1 (HMGB1), a highly conserved nuclear protein.Inflammatory functions of HMGB1 are mediated by binding to cell surface receptors, including the receptor for advanced glycation end products (RAGE), Toll-like receptor (TLR)2, TLR4, and TLR9. Pyroptosis is a caspase-1-dependent programmed cell death, which features rapid plasma membrane rupture, DNA fragmentation, and release of proinflammatory intracellular contents. Pyroptosis can be triggered by various stimuli, however, the mechanism underlying pyroptosis remains unclear. In this study, we identify a novel pathway of HMGB1-induced macrophage pyroptosis. We demonstrate that HMGB1, acting through RAGE and dynamin-dependent signaling, initiates HMGB1endocytosis, which in turn induces cell pyroptosis. The endocytosis of HMGB1 triggers a cascade of molecular events, including cathepsin B release from ruptured lysosomes followed by pyroptosome formation and caspase-1 activation. We further confirm that HMGB1-induced macrophage pyroptosis also occurs in vivo during endotoxemia, suggesting a pathophysiological significance for this form of pyroptosis in the development of inflammation. These findings shed light on the regulatory role of ligand-receptor internalization in directing cell fate, which may have an important role in the progress of inflammation following infection and injury.

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“…Many NCE pathways have been reported, including caveolar-type endocytosis, CLIC/GEEC-type endocytosis, the putative flotillin-associated endocytic structures, phagocytosis, macropinocytosis, dorsal ruffles (or waves), and entosis [62,63]. Caveolar-type endocytosis is the best studied NCE.…”

Section: Clathrin-dependent and Clathrin-independent Endocytic Pathwaysmentioning

confidence: 99%

“…Clathrinindependent endocytosis itself has been further dissected into seemingly distinct pathways, based on the reliance of these pathways on certain proteins and lipids, their differential drug sensitivities and their abilities to internalize particular cargos [134]. Many NCE pathways have been reported including caveolar-type endocytosis, CLIC/GEEC-type endocytosis, the putative flotillin-associated endocytic structures, phagocytosis, macropinocytosis, dorsal ruffles (or waves), and entosis [62,63]. New evidence suggests that EGF-induced EGFR endocytosis may also be mediated by NCE.…”

Section: Endocytosis Of Egfrmentioning

confidence: 99%

Mutual Regulation of Receptor-Mediated Cell Signalling and Endocytosis: EGF Receptor System as an Example

Wang¹

2012

Molecular Regulation of Endocytosis

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Molecular mechanisms of clathrin-independent endocytosis

Cited by 252 publications

References 124 publications

Internalization of the TGF-β type I receptor into caveolin-1 and EEA1 double-positive early endosomes

Internalization of the TGF-β type I receptor into caveolin-1 and EEA1 double-positive early endosomes

Macrophage endocytosis of high-mobility group box 1 triggers pyroptosis

Mutual Regulation of Receptor-Mediated Cell Signalling and Endocytosis: EGF Receptor System as an Example

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