Lysosome biogenesis and lysosomal membrane proteins: trafficking meets function
By P. Saftig, Judith Klumperman. Nature reviews. Molecular cell biology, 2009
1,646 citations recorded by the source corpus.
Subfields: Cell Biology, Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/837c92f1481a43c9a368a7f36296a02e7c3aa1d8
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Citations in the corpus
- Lysosomes as a therapeutic target (2019, background): “Catabolism is the main function of conventional lysosomes, and several other lysosome related organelles (LROs), such as mel anosomes, the late endosomal major histocompatibility complex class II (MHCII) compartment (MIIC), lytic granules from neutrophils, eosinophils, basophils, mast cells, CD8 + T”
- PARP-1 cleavage fragments: signatures of cell-death proteases in neurodegeneration (2010, background): “Lysosomes were initially described as participants in catabolic autophagic cell death when exhausted or damaged organelles were digested and secreted into the cytoplasm [117].”
- Handbook of ion channels (2015, background): “Alternatively, they can also be transported first to the PM and then to LELs via endocytosis (40).”
- Towards a systems understanding of MHC class I and MHC class II antigen presentation (2011, background): “How maturation signals by lipopolysaccharide control these pathways is unclear, but they may show some resemblance to the induced secretion of other lysosome-related organelles, such as cytolytic granules, melanosomes and Weibel–Palade bodie”
- Cysteine cathepsins: From structure, function and regulation to new frontiers (2011, background): “After the removal of the signal peptide, the propeptide assists in the proper folding of the enzyme and targeting to the endosomes/ lysosomes using a specific mannose-6-phosphate receptor (M6PR) pathway, simultaneously acting as an inhibitor to prevent any inappropriate proteolytic activity of the z”
- Endosome maturation (2011, background): “These include the following (Mellman, 1996; Zerial and McBride, 2001; Maxfield and McGraw, 2004; Piper and Katzmann, 2007; Luzio et al, 2007b; van Meel and Klumperman, 2008; Woodman and Futter, 2008; Saftig and Klumperman, 2009; Jovic et al, 2010; Von Bartheld and Altick, 2011).”
- Lysosomal Physiology (2015, background): “Additionally, retrograde trafficking recycles the mannose-6-P receptor, which is required for TGN-to-LEL delivery of hydrolases (5).”
- A lysosome-to-nucleus signalling mechanism senses and regulates the lysosome via mTOR and TFEB (2012, background): “adaptive response of the lysosome (Luzio et al, 2007; Ballabio and Gieselmann, 2009; Saftig and Klumperman, 2009).”
- The cell biology of disease: lysosomal storage disorders: the cellular impact of lysosomal dysfunction. (2012, neutral): “In comparison to endosomes and autophagosomes, lysosomes are smaller in size, are highly enriched in particular transmembrane proteins and hydrolytic enzymes (including proteases, glycosidases, nucleases, phosphatases, and lipases), have a higher buoyant density, an electrondense appearance by trans”
- The Nutrient-Responsive Transcription Factor TFE3, Promotes Autophagy, Lysosomal Biogenesis, and Clearance of Cellular Debris (2014, background): “In addition to their role in biomolecular degradation and recycling, lysosomes are also critical for several cellular and physiological functions including cholesterol homeostasis, down-regulation of surface receptors, inactivation of pathogenic organisms, antigen presentation, repair of the plasma ”
- Lysosomal membrane permeabilization and cell death (2018, background): “and the targeting of lysosomal proteins to the lysosome.(9) In the transGolgi network, newly synthesized lysosomal hydrolases are bound by mannose-6-phosphate receptors (MPRs) and delivered first to endosomes, in which MPRs are dissociated in the low endosomal pH environment.”