late endosomes

late endosomes

membrane-bound compartments located near the Golgi apparatus with an internal pH of 5.5. Ligands or material delivered from early endosomes are readied for delivery to lysosomes.
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BACE1 is mostly presented within late endosomes at the presynaptic terminals of patient brains, and it increases synaptic Ap levels (28).
The biogenesis and release of exosomes can be roughly divided into two steps: the formation of multivesicular bodies (MVBs) and their fusion with the plasma membrane [Figure 1].[25] The endocytic vesicles mature to early endosomes and then the late endosomes by inward budding of the plasma membrane.[26] The late endosomes turn into MVBs by accumulating the intraluminal vesicles (ILVs) which consist of endosomal sorting complex required for transport, proteins, lipids, and RNAs.[23] Thereafter, the MVBs fuse with the plasma membrane and release the ILVs, which are called exosomes.[13] MVs are released by the outward budding of the plasma membrane or from the endosomal compartments.[27] ABs are released after cells undergo apoptosis.{Figure 1}
For the maturation to be effective, the autophagosome must be fused with early or late endosomes forming a structure called amphisome (33,34).
NP-C is a rare disorder of intracellular transport of endocytosed cholesterol with sequestration of unesterified cholesterol in lysosomes and late endosomes. Most of its patients (95%) have mutations in the NPC1 gene (8).
STARD3 protein is anchored to late endosomes and together with ER-anchored vesicle-associated membrane protein-associated proteins A and B STARD3 contributes to formation of MCSs between endosomes and ER.
Inhibition of autophagy has been shown to decrease the amount of cytosolic proteins in late endosomes, which are components of the MVB which can be targeted for degradation or released as exosomes.
Some studies found that the nanoparticles positioned in the late endosomes or secondary lysosomes of the cytoplasm [23, 24].
The giant organelles in beige and Chediak-Higashi fibroblasts are derived from late endosomes and mature lysosomes.
The formation of isolation membranes by trans-Golgi/endosomal fusion is also supported by studies showing a requirement for Rab9, which is a GTPase essential for the trafficking of proteins from late endosomes to trans-Golgi membranes.
In both Muller and RPE cells, a portion of ocriplasmin foci was found to colocalize with Rab7 positive late endosomes, which are committed to become lysosomes.
In the first pathway, apolipoprotein A-I (apoA-I) binds ABCA1 at the cell surface, where lipids are picked up by apoA-I and then internalized and targeted to late endosomes. In the second, apoA-I forms complexes with phospholipids and cholesterol at the cell surface in a process that is promoted by ABCA1 activity.

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