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Autophagy (or autophagocytosis; from the Greek αὐτόφαγος, autóphagos, meaning "self-devouring" [1] and κύτος, kýtos, meaning "hollow") [2] is the natural, conserved degradation of the cell that removes unnecessary or dysfunctional components through a lysosome-dependent regulated mechanism. [3]
Therefore, to modulate the activity of this autophagic pathway, the cell stringently regulates the levels of the CMA receptor at the lysosomal membrane by controlling the degradation rates of LAMP-2A monomers in lysosomes and by de novo synthesis of LAMP-2A molecules.
A lysosome (/ ˈ l aɪ s ə ˌ s oʊ m /) is a single membrane-bound organelle found in many animal cells. [1] [2] They are spherical vesicles that contain hydrolytic enzymes that digest many kinds of biomolecules. A lysosome has a specific composition, of both its membrane proteins and its lumenal proteins.
Through autophagy viral particles are delivered into the lysosome degradation pathway and interrogate with a specific type of pattern recognition receptor to initiate type I interferon (IFN-I) expression and viral clearance. Interestingly, ATG5-ATG12/ATG16L1 complex negatively regulates RIG-I-like receptor pathway and IFN-I expression. A mouse ...
Microautophagy is one of the three common forms of autophagic pathway, but unlike macroautophagy and chaperone-mediated autophagy, it is mediated—in mammals by lysosomal action or in plants and fungi by vacuolar action—by direct engulfment of the cytoplasmic cargo.
However the significance of this localization is not known. Mature yeast autophagosomes fuse directly with vacuoles or lysosomes and do not form amphisomes as in mammals. [8] In yeast autophagosome maturation, there are also other known players as Atg1, Atg13 and Atg17. Atg1 is a kinase upregulated upon induction of autophagy.
After finishing vesicle expansion, the autophagosome is ready for fusion with the lysosome and Atg8 can either be released from the membrane for recycling (see below) or gets degraded in the autolysosome if left uncleaved. ATG8 is also required for a different autophagy-related process called the cytoplasm-to-vacuole targeting (Cvt) pathway. [14]
Pharmacological inhibition of AKT/PKB activates TFEB, promotes lysosome biogenesis and autophagy, and ameliorates neuropathology in mouse models of Juvenile Batten disease and Sanfilippo syndrome type B. [26] [27] TFEB is activated in Trex1-deficient cells via inhibition of mTORC1 activity, resulting in an expanded lysosomal compartment. [28]