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Journal articles on the topic 'Lysosomale Degradation'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

Parkinson-Lawrence, Emma J., Tetyana Shandala, Mark Prodoehl, Revecca Plew, Glenn N. Borlace, and Doug A. Brooks. "Lysosomal Storage Disease: Revealing Lysosomal Function and Physiology." Physiology 25, no. 2 (2010): 102–15. http://dx.doi.org/10.1152/physiol.00041.2009.

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The discovery over five decades ago of the lysosome, as a degradative organelle and its dysfunction in lysosomal storage disorder patients, was both insightful and simple in concept. Here, we review some of the history and pathophysiology of lysosomal storage disorders to show how they have impacted on our knowledge of lysosomal biology. Although a significant amount of information has been accrued on the molecular genetics and biochemistry of lysosomal storage disorders, we still do not fully understand the mechanistic link between the storage material and disease pathogenesis. However, the a

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2

Lakatos, Lőrincz, Szabó, et al. "Sec20 is Required for Autophagic and Endocytic Degradation Independent of Golgi-ER Retrograde Transport." Cells 8, no. 8 (2019): 768. http://dx.doi.org/10.3390/cells8080768.

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Endocytosis and autophagy are evolutionarily conserved degradative processes in all eukaryotes. Both pathways converge to the lysosome where cargo is degraded. Improper lysosomal degradation is observed in many human pathologies, so its regulatory mechanisms are important to understand. Sec20/BNIP1 (BCL2/adenovirus E1B 19 kDa protein-interacting protein 1) is a BH3 (Bcl-2 homology 3) domain-containing SNARE (soluble N-ethylmaleimide-sensitive factor-attachment protein receptors) protein that has been suggested to promote Golgi-ER retrograde transport, mitochondrial fission, apoptosis and mitop

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3

Zunke, Friederike. "The function of lysosomes and their role in Parkinson’s disease." Neuroforum 26, no. 1 (2020): 43–51. http://dx.doi.org/10.1515/nf-2019-0035.

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AbstractLysosomes are cellular organelles that are important for the degradation and recycling of various biomolecules. Specialized lysosomal membrane proteins, as well as soluble enzymes, are important for the efficient turn-over of lysosomal substrates. A deficiency in the degradative capacity of lysosomes leads to severe pathologies referred to as lysosomal storage disorders. There is increasing evidence for the importance of lysosomal function in neurodegenerative disorders, including Parkinson’s disease. One reason for this might be the vulnerability of neuronal cells. Since neurons do no

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Majumder, Priyanka, and Oishee Chakrabarti. "ESCRTs and associated proteins in lysosomal fusion with endosomes and autophagosomes." Biochemistry and Cell Biology 94, no. 5 (2016): 443–50. http://dx.doi.org/10.1139/bcb-2016-0099.

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Endolysosomal and autophagosomal degradation pathways are highly connected at various levels, sharing multiple molecular effectors that modulate them individually or simultaneously. These two lysosomal degradative pathways are primarily involved in the disposal of cargo internalized from the cell surface or long-lived proteins or aggregates and aged organelles present in the cytosol. Both of these pathways involve a number of carefully regulated vesicular fusion events that are dependent on ESCRT proteins. The ESCRT proteins especially ESCRT-I and III participate in the regulation of fusion ev

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5

Zhong, Xi Zoë, Yuanjie Zou, Xue Sun, et al. "Inhibition of Transient Receptor Potential Channel Mucolipin-1 (TRPML1) by Lysosomal Adenosine Involved in Severe Combined Immunodeficiency Diseases." Journal of Biological Chemistry 292, no. 8 (2017): 3445–55. http://dx.doi.org/10.1074/jbc.m116.743963.

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Impaired adenosine homeostasis has been associated with numerous human diseases. Lysosomes are referred to as the cellular recycling centers that generate adenosine by breaking down nucleic acids or ATP. Recent studies have suggested that lysosomal adenosine overload causes lysosome defects that phenocopy patients with mutations in transient receptor potential channel mucolipin-1 (TRPML1), a lysosomal Ca2+ channel, suggesting that lysosomal adenosine overload may impair TRPML1 and then lead to subsequent lysosomal dysfunction. In this study, we demonstrate that lysosomal adenosine is elevated

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6

Gullapalli, Anuradha, Breann L. Wolfe, Courtney T. Griffin, Terry Magnuson, and JoAnn Trejo. "An Essential Role for SNX1 in Lysosomal Sorting of Protease-activated Receptor-1: Evidence for Retromer-, Hrs-, and Tsg101-independent Functions of Sorting Nexins." Molecular Biology of the Cell 17, no. 3 (2006): 1228–38. http://dx.doi.org/10.1091/mbc.e05-09-0899.

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Sorting nexin 1 (SNX1) and SNX2 are the mammalian homologues of the yeast Vps5p retromer component that functions in endosome-to-Golgi trafficking. SNX1 is also implicated in endosome-to-lysosome sorting of cell surface receptors, although its requirement in this process remains to be determined. To assess SNX1 function in endocytic sorting of protease-activated receptor-1 (PAR1), we used siRNA to deplete HeLa cells of endogenous SNX1 protein. PAR1, a G-protein-coupled receptor, is proteolytically activated by thrombin, internalized, sorted predominantly to lysosomes, and efficiently degraded.

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Li, Guangbi, Jason Kidd, and Pin-Lan Li. "Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases." International Journal of Molecular Sciences 21, no. 5 (2020): 1559. http://dx.doi.org/10.3390/ijms21051559.

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Podocytes are visceral epithelial cells covering the outer surface of glomerular capillaries in the kidney. Blood is filtered through the slit diaphragm of podocytes to form urine. The functional and structural integrity of podocytes is essential for the normal function of the kidney. As a membrane-bound organelle, lysosomes are responsible for the degradation of molecules via hydrolytic enzymes. In addition to its degradative properties, recent studies have revealed that lysosomes may serve as a platform mediating cellular signaling in different types of cells. In the last decade, increasing

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8

Blumenreich, Shani, Or B. Barav, Bethan J. Jenkins, and Anthony H. Futerman. "Lysosomal Storage Disorders Shed Light on Lysosomal Dysfunction in Parkinson’s Disease." International Journal of Molecular Sciences 21, no. 14 (2020): 4966. http://dx.doi.org/10.3390/ijms21144966.

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The lysosome is a central player in the cell, acting as a clearing house for macromolecular degradation, but also plays a critical role in a variety of additional metabolic and regulatory processes. The lysosome has recently attracted the attention of neurobiologists and neurologists since a number of neurological diseases involve a lysosomal component. Among these is Parkinson’s disease (PD). While heterozygous and homozygous mutations in GBA1 are the highest genetic risk factor for PD, studies performed over the past decade have suggested that lysosomal loss of function is likely involved in

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9

Recla, Sabine, Andreas Hahn, and Christian Apitz. "Pulmonary arterial hypertension associated with impaired lysosomal endothelin-1 degradation." Cardiology in the Young 25, no. 4 (2014): 773–76. http://dx.doi.org/10.1017/s1047951114000997.

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AbstractWe report on a boy with severe pulmonary arterial hypertension associated with mucolipidosis, a rare lysosomal storage disorder. During diagnostic catheterisation, we found increased endothelin-1 levels, but normal big endothelin-1-levels (the precursor form of endothelin-1), which suggests impaired degradation of endothelin-1 rather than increased synthesis. As endothelin-1 degradation takes place in the lysosome, it appears likely that lysosomal dysfunction caused by the underlying disease contributes to the development of pulmonary arterial hypertension in this patient.

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10

Kavčič, Nežka, Katarina Pegan, and Boris Turk. "Lysosomes in programmed cell death pathways: from initiators to amplifiers." Biological Chemistry 398, no. 3 (2017): 289–301. http://dx.doi.org/10.1515/hsz-2016-0252.

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Abstract Lysosome is the central organelle for intracellular degradation of biological macromolecules and organelles. The material destined for degradation enters the lysosomes primarily via endocytosis, autophagy and phagocytosis, and is degraded through the concerted action of more than 50 lysosomal hydrolases. However, lysosomes are also linked with numerous other processes, including cell death, inflammasome activation and immune response, as well as with lysosomal secretion and cholesterol recycling. Among them programmed cell death pathways including apoptosis have received major attenti

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11

De Leo, Ester, Mohamed A. Elmonem, Sante Princiero Berlingerio, et al. "Cell-Based Phenotypic Drug Screening Identifies Luteolin as Candidate Therapeutic for Nephropathic Cystinosis." Journal of the American Society of Nephrology 31, no. 7 (2020): 1522–37. http://dx.doi.org/10.1681/asn.2019090956.

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BackgroundMutations in the gene that encodes the lysosomal cystine transporter cystinosin cause the lysosomal storage disease cystinosis. Defective cystine transport leads to intralysosomal accumulation and crystallization of cystine. The most severe phenotype, nephropathic cystinosis, manifests during the first months of life, as renal Fanconi syndrome. The cystine-depleting agent cysteamine significantly delays symptoms, but it cannot prevent progression to ESKD and does not treat Fanconi syndrome. This suggests the involvement of pathways in nephropathic cystinosis that are unrelated to lys

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12

Li, Yuan, Baohui Chen, Wei Zou, et al. "The lysosomal membrane protein SCAV-3 maintains lysosome integrity and adult longevity." Journal of Cell Biology 215, no. 2 (2016): 167–85. http://dx.doi.org/10.1083/jcb.201602090.

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Lysosomes degrade macromolecules and recycle metabolites as well as being involved in diverse processes that regulate cellular homeostasis. The lysosome is limited by a single phospholipid bilayer that forms a barrier to separate the potent luminal hydrolases from other cellular constituents, thus protecting the latter from unwanted degradation. The mechanisms that maintain lysosomal membrane integrity remain unknown. Here, we identified SCAV-3, the Caenorhabditis elegans homologue of human LIMP-2, as a key regulator of lysosome integrity, motility, and dynamics. Loss of scav-3 caused rupture

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13

Li, Guangbi, Dandan Huang, Jinni Hong, Owais M. Bhat, Xinxu Yuan, and Pin-Lan Li. "Control of lysosomal TRPML1 channel activity and exosome release by acid ceramidase in mouse podocytes." American Journal of Physiology-Cell Physiology 317, no. 3 (2019): C481—C491. http://dx.doi.org/10.1152/ajpcell.00150.2019.

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The transient receptor potential mucolipin 1 (TRPML1) channel has been reported to mediate lysosomal Ca2+ release that is involved in Ca2+-dependent lysosome trafficking and autophagic flux. However, this regulatory mechanism of lysosomal TRPML1 channel activity in podocytes remains poorly understood. In the present study, we tested whether the TRPML1 channel in podocytes mediates lysosome trafficking, which is essential for multivesicular body (MVB) degradation by lysosomes. We first demonstrated the abundant expression of TRPML1 channel in podocytes. By GCaMP3 Ca2+ imaging, we characterized

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Bandyopadhyay, Urmi, Susmita Kaushik, Lyuba Varticovski, and Ana Maria Cuervo. "The Chaperone-Mediated Autophagy Receptor Organizes in Dynamic Protein Complexes at the Lysosomal Membrane." Molecular and Cellular Biology 28, no. 18 (2008): 5747–63. http://dx.doi.org/10.1128/mcb.02070-07.

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ABSTRACT Chaperone-mediated autophagy (CMA) is a selective type of autophagy by which specific cytosolic proteins are sent to lysosomes for degradation. Substrate proteins bind to the lysosomal membrane through the lysosome-associated membrane protein type 2A (LAMP-2A), one of the three splice variants of the lamp2 gene, and this binding is limiting for their degradation via CMA. However, the mechanisms of substrate binding and uptake remain unknown. We report here that LAMP-2A organizes at the lysosomal membrane into protein complexes of different sizes. The assembly and disassembly of these

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15

Lockwood, T. D. "Distinction between major chloroquine-inhibitable and adrenergic-responsive pathways of protein degradation and their relation to tissue ATP content in the Langendorff isolated perfused rat heart." Biochemical Journal 251, no. 2 (1988): 341–46. http://dx.doi.org/10.1042/bj2510341.

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In the Langendorff isolated perfused rat heart, 36% of total basal protein degradation was inhibited by the lysosomal inhibitor chloroquine (30 microM), after elimination of rapid turnover proteins during a 3 h preliminary degradation period. Prior inhibition of degradation with chloroquine was additive to the 30% inhibition caused by simultaneous infusion of 50-200 nM-isoprenaline. This additivity suggests that the adrenergic-controlled process is independent of the lysosomal degradative pathway. After discontinuation of drug infusions, the isoprenaline-inhibited degradation rate returned to

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Mashima, Ryuichi, Torayuki Okuyama, and Mari Ohira. "Biomarkers for Lysosomal Storage Disorders with an Emphasis on Mass Spectrometry." International Journal of Molecular Sciences 21, no. 8 (2020): 2704. http://dx.doi.org/10.3390/ijms21082704.

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Lysosomal storage disorders (LSDs) are characterized by an accumulation of various substances, such as sphingolipids, mucopolysaccharides, and oligosaccharides. The LSD enzymes responsible for the catabolism are active at acidic pH in the lysosomal compartment. In addition to the classically established lysosomal degradation biochemistry, recent data have suggested that lysosome plays a key role in the autophagy where the fusion of autophagosome and lysosome facilitates the degradation of amino acids. A failure in the lysosomal function leads to a variety of manifestations, including neurovisc

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Kim, Ji Young, Eun Jung Lee, Yuri Ahn та ін. "Cathepsin L, a Target of Hypoxia-Inducible Factor-1-α, Is Involved in Melanosome Degradation in Melanocytes". International Journal of Molecular Sciences 22, № 16 (2021): 8596. http://dx.doi.org/10.3390/ijms22168596.

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Hypoxic conditions induce the activation of hypoxia-inducible factor-1α (HIF-1α) to restore the supply of oxygen to tissues and cells. Activated HIF-1α translocates into the nucleus and binds to hypoxia response elements to promote the transcription of target genes. Cathepsin L (CTSL) is a lysosomal protease that degrades cellular proteins via the endolysosomal pathway. In this study, we attempted to determine if CTSL is a hypoxia responsive target gene of HIF-1α, and decipher its role in melanocytes in association with the autophagic pathway. The results of our luciferase reporter assay showe

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Coleman, Jack, Yuejun Xiang, Praveen Pande, Dee Shen, Divina Gatica, and Wayne F. Patton. "A Live-Cell Fluorescence Microplate Assay Suitable for Monitoring Vacuolation Arising from Drug or Toxic Agent Treatment." Journal of Biomolecular Screening 15, no. 4 (2010): 398–405. http://dx.doi.org/10.1177/1087057110364242.

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Lysosomes are membrane-bound subcellular organelles involved in the degradation of macromolecules and pathogens in diverse processes, including endocytosis, phagocytosis, and autophagy. A red fluorescent probe was developed that is selectively sequestered in acidic organelles. U20S cells pretreated with 64 µM chloroquine for as little as 5 h show a dramatic increase in lysosome-like vesicle number and volume. The probe can be employed for highlighting lysosome-like organelles under conditions wherein cells produce vacuoles that contain most of the degradative enzymes of the lysosome but are no

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Ebner, Michael, Philipp Alexander Koch, and Volker Haucke. "Phosphoinositides in the control of lysosome function and homeostasis." Biochemical Society Transactions 47, no. 4 (2019): 1173–85. http://dx.doi.org/10.1042/bst20190158.

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Abstract Lysosomes are the main degradative compartments of mammalian cells and serve as platforms for cellular nutrient signaling and sterol transport. The diverse functions of lysosomes and their adaptation to extracellular and intracellular cues are tightly linked to the spatiotemporally controlled synthesis, turnover and interconversion of lysosomal phosphoinositides, minor phospholipids that define membrane identity and couple membrane dynamics to cell signaling. How precisely lysosomal phosphoinositides act and which effector proteins within the lysosome membrane or at the lysosomal surf

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Kopitz, J., A. Arnold, T. Meissner, and M. Cantz. "Protein catabolism in fibroblasts cultured from patients with mucolipidosis II and other lysosomal disorders." Biochemical Journal 295, no. 2 (1993): 577–80. http://dx.doi.org/10.1042/bj2950577.

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Protein catabolism in fibroblasts cultured from the skin of normal individuals and of patients with mucolipidosis II (I-cell disease) and several other lysosomal storage diseases was examined by metabolic labelling with [3H]leucine and following the fate of radioactive proteins in pulse-chase experiments. In mucolipidosis II cells, overall protein degradative rates were found to be distinctly lower than in normal control cells. To distinguish lysosomal from non-lysosomal degradation, labelling experiments were carried out in the presence and absence of 10 mM NH4Cl, an inhibitor of lysosomal fu

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Zhang, Ming, Li Chen, Shicong Wang, and Tuanlao Wang. "Rab7: roles in membrane trafficking and disease." Bioscience Reports 29, no. 3 (2009): 193–209. http://dx.doi.org/10.1042/bsr20090032.

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The endocytosis pathway controls multiple cellular and physiological events. The lysosome is the destination of newly synthesized lysosomal hydrolytic enzymes. Internalized molecules or particles are delivered to the lysosome for degradation through sequential transport along the endocytic pathway. The endocytic pathway is also emerging as a signalling platform, in addition to the well-known role of the plasma membrane for signalling. Rab7 is a late endosome-/lysosome-associated small GTPase, perhaps the only lysosomal Rab protein identified to date. Rab7 plays critical roles in the endocytic

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Gallon, Matthew, and Peter J. Cullen. "Retromer and sorting nexins in endosomal sorting." Biochemical Society Transactions 43, no. 1 (2015): 33–47. http://dx.doi.org/10.1042/bst20140290.

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The evolutionarily conserved endosomal retromer complex rescues transmembrane proteins from the lysosomal degradative pathway and facilitates their recycling to other cellular compartments. Retromer functions in conjunction with numerous associated proteins, including select members of the sorting nexin (SNX) family. In the present article, we review the molecular architecture and cellular roles of retromer and its various functional partners. The endosomal network is a crucial hub in the trafficking of proteins through the cellular endomembrane system. Transmembrane proteins, here termed carg

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Buratta, Sandra, Brunella Tancini, Krizia Sagini, et al. "Lysosomal Exocytosis, Exosome Release and Secretory Autophagy: The Autophagic- and Endo-Lysosomal Systems Go Extracellular." International Journal of Molecular Sciences 21, no. 7 (2020): 2576. http://dx.doi.org/10.3390/ijms21072576.

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Beyond the consolidated role in degrading and recycling cellular waste, the autophagic- and endo-lysosomal systems play a crucial role in extracellular release pathways. Lysosomal exocytosis is a process leading to the secretion of lysosomal content upon lysosome fusion with plasma membrane and is an important mechanism of cellular clearance, necessary to maintain cell fitness. Exosomes are a class of extracellular vesicles originating from the inward budding of the membrane of late endosomes, which may not fuse with lysosomes but be released extracellularly upon exocytosis. In addition to gar

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Domagala, Antoni, Klaudyna Fidyt, Malgorzata Bobrowicz, Joanna Stachura, Kacper Szczygiel, and Malgorzata Firczuk. "Typical and Atypical Inducers of Lysosomal Cell Death: A Promising Anticancer Strategy." International Journal of Molecular Sciences 19, no. 8 (2018): 2256. http://dx.doi.org/10.3390/ijms19082256.

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Lysosomes are conservative organelles with an indispensable role in cellular degradation and the recycling of macromolecules. However, in light of recent findings, it has emerged that the role of lysosomes in cancer cells extends far beyond cellular catabolism and includes a variety of cellular pathways, such as proliferation, metastatic potential, and drug resistance. It has been well described that malignant transformation leads to alterations in lysosomal structure and function, which, paradoxically, renders cancer cells more sensitive to lysosomal destabilization. Furthermore, lysosomes ar

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Zhang, Weichao, Xi Yang, Liang Chen, et al. "A conserved ubiquitin- and ESCRT-dependent pathway internalizes human lysosomal membrane proteins for degradation." PLOS Biology 19, no. 7 (2021): e3001361. http://dx.doi.org/10.1371/journal.pbio.3001361.

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The lysosome is an essential organelle to recycle cellular materials and maintain nutrient homeostasis, but the mechanism to down-regulate its membrane proteins is poorly understood. In this study, we performed a cycloheximide (CHX) chase assay to measure the half-lives of approximately 30 human lysosomal membrane proteins (LMPs) and identified RNF152 and LAPTM4A as short-lived membrane proteins. The degradation of both proteins is ubiquitin dependent. RNF152 is a transmembrane E3 ligase that ubiquitinates itself, whereas LAPTM4A uses its carboxyl-terminal PY motifs to recruit NEDD4-1 for ubiq

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Jeong, Seokmin, Jun-Kyu Byun, Sung Cho, et al. "Transcription Factor Eb Is Required for Macropinocytosis-Mediated Growth Recovery of Nutrient-Deprived Kras-Mutant Cells." Nutrients 10, no. 11 (2018): 1638. http://dx.doi.org/10.3390/nu10111638.

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Macropinocytosis is a regulated form of endocytosis that mediates the nonselective uptake of nutrients to support growth under nutrient-deprived conditions. KRAS-mutant cancer cells upregulate macropinocytosis to import extracellular proteins, which subsequently undergo proteolytic degradation in the lysosome. Although transcription factor EB (TFEB) is a master regulator of lysosomal biogenesis and function, its role in the degradation of extracellular protein from macropinocytosis in KRAS-mutant cells has not previously been elucidated. In this study, we investigated the role of TFEB in the r

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Tooze, Sharon A. "Molecules and membranes: Emerging details shed light on mammalian autophagy." Biochemist 34, no. 2 (2012): 4–7. http://dx.doi.org/10.1042/bio03402004.

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Autophagy, which literally means ‘self eating’, is a highly conserved intracellular degradative process mediated by lysosomal enzymes. Autophagy was identified using electron microscopy in the 1950s by cell biologists studying the lysosome and it was recognized as a lysosomal degradative pathway (for a review of the original publications, see Tooze et al.1) Recently, a number of key findings have elucidated the pivotal role played by autophagy in tissue homoeostasis and human disease, such as cancer, neurodegeneration, infection, immunity and aging2. Autophagy is also tightly linked to neonata

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Serrano-Puebla, Ana, and Patricia Boya. "Lysosomal membrane permeabilization as a cell death mechanism in cancer cells." Biochemical Society Transactions 46, no. 2 (2018): 207–15. http://dx.doi.org/10.1042/bst20170130.

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Lysosomes are acidic organelles that contain hydrolytic enzymes that mediate the intracellular degradation of macromolecules. Damage of these organelles often results in lysosomal membrane permeabilization (LMP) and the release into the cytoplasm of the soluble lysosomal contents, which include proteolytic enzymes of the cathepsin family. This, in turn, activates several intracellular cascades that promote a type of regulated cell death, called lysosome-dependent cell death (LDCD). LDCD can be inhibited by pharmacological or genetic blockade of cathepsin activity, or by protecting the lysosoma

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Tanaka, Yoshinori, Nobuyuki Tanaka, Yasushi Saeki, et al. "c-Cbl-Dependent Monoubiquitination and Lysosomal Degradation of gp130." Molecular and Cellular Biology 28, no. 15 (2008): 4805–18. http://dx.doi.org/10.1128/mcb.01784-07.

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ABSTRACT Interleukin 6 (IL-6), a pleiotropic cytokine, functions in cells through its interaction with its receptor complex, which consists of two ligand-binding α subunits and two signal-transducing subunits known as gp130. There is a wealth of studies on signals mediated by gp130, but its downregulation is less well understood. Here we found that IL-6 stimulation induced lysosome-dependent degradation of gp130, which correlated with an increase in the K63-linked polyubiquitination of gp130. The stimulation-dependent ubiquitination of gp130 was mediated by c-Cbl, an E3 ligase, which was recru

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Kelly, Catriona, Paul Canning, Paul J. Buchanan, et al. "Toll-like receptor 4 is not targeted to the lysosome in cystic fibrosis airway epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 5 (2013): L371—L382. http://dx.doi.org/10.1152/ajplung.00372.2011.

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The innate immune response to bacterial infection is mediated through Toll-like receptors (TLRs), which trigger tightly regulated signaling cascades through transcription factors including NF-κB. LPS activation of TLR4 triggers internalization of the receptor-ligand complex which is directed toward lysosomal degradation or endocytic recycling. Cystic fibrosis (CF) patients display a robust and uncontrolled inflammatory response to bacterial infection, suggesting a defect in regulation. This study examined the intracellular trafficking of TLR4 in CF and non-CF airway epithelial cells following

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Saftig, Paul, Bernd Schröder, and Judith Blanz. "Lysosomal membrane proteins: life between acid and neutral conditions." Biochemical Society Transactions 38, no. 6 (2010): 1420–23. http://dx.doi.org/10.1042/bst0381420.

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Whereas we have a profound understanding about the function and biogenesis of the protein constituents in the lumen of the lysosomal compartment, much less is known about the functions of proteins of the lysosomal membrane. Proteomic analyses of the lysosomal membrane suggest that, apart from the well-known lysosomal membrane proteins, additional and less abundant membrane proteins are present. The identification of disease-causing genes and the in-depth analysis of knockout mice leading to mutated or absent membrane proteins of the lysosomal membrane have demonstrated the essential role of th

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Steinberg, Benjamin E., Kassidy K. Huynh, Alexandre Brodovitch, et al. "A cation counterflux supports lysosomal acidification." Journal of Cell Biology 189, no. 7 (2010): 1171–86. http://dx.doi.org/10.1083/jcb.200911083.

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The profound luminal acidification essential for the degradative function of lysosomes requires a counter-ion flux to dissipate an opposing voltage that would prohibit proton accumulation. It has generally been assumed that a parallel anion influx is the main or only counter-ion transport that enables acidification. Indeed, defective anion conductance has been suggested as the mechanism underlying attenuated lysosome acidification in cells deficient in CFTR or ClC-7. To assess the individual contribution of counter-ions to acidification, we devised means of reversibly and separately permeabili

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Singh, Rajesh K., Abigail S. Haka, Arky Asmal, et al. "TLR4 (Toll-Like Receptor 4)-Dependent Signaling Drives Extracellular Catabolism of LDL (Low-Density Lipoprotein) Aggregates." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 1 (2020): 86–102. http://dx.doi.org/10.1161/atvbaha.119.313200.

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Objective: Aggregation and modification of LDLs (low-density lipoproteins) promote their retention and accumulation in the arteries. This is a critical initiating factor during atherosclerosis. Macrophage catabolism of agLDL (aggregated LDL) occurs using a specialized extracellular, hydrolytic compartment, the lysosomal synapse. Compartment formation by local actin polymerization and delivery of lysosomal contents by exocytosis promotes acidification of the compartment and degradation of agLDL. Internalization of metabolites, such as cholesterol, promotes foam cell formation, a process that dr

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Mullin, Kylie A., Bernardo J. Foth, Steven C. Ilgoutz, et al. "Regulated Degradation of an Endoplasmic Reticulum Membrane Protein in a Tubular Lysosome in Leishmania mexicana." Molecular Biology of the Cell 12, no. 8 (2001): 2364–77. http://dx.doi.org/10.1091/mbc.12.8.2364.

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The cell surface of the human parasite Leishmania mexicana is coated with glycosylphosphatidylinositol (GPI)-anchored macromolecules and free GPI glycolipids. We have investigated the intracellular trafficking of green fluorescent protein- and hemagglutinin-tagged forms of dolichol-phosphate-mannose synthase (DPMS), a key enzyme in GPI biosynthesis in L. mexicana promastigotes. These functionally active chimeras are found in the same subcompartment of the endoplasmic reticulum (ER) as endogenous DPMS but are degraded as logarithmically growing promastigotes reach stationary phase, coincident w

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Yang, Yujie, and William K. Chan. "Glycogen Synthase Kinase 3 Beta Regulates the Human Aryl Hydrocarbon Receptor Cellular Content and Activity." International Journal of Molecular Sciences 22, no. 11 (2021): 6097. http://dx.doi.org/10.3390/ijms22116097.

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The aryl hydrocarbon receptor (AHR) is a cytosolic receptor which is involved in diverse cellular events in humans. The most well-characterized function of AHR is its ability to upregulate gene transcription after exposure to its ligands, such as environmental toxicants, dietary antioxidants, drugs, and endogenous ligands. The cellular content of AHR is partly controlled by its degradation via the ubiquitin–proteasome system and the lysosome-dependent autophagy. We used human cervical cancer (HeLa) cells to investigate how AHR undergoes protein degradation and how its activity is modulated. Si

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Høyvik, H., P. B. Gordon, T. O. Berg, P. E. Strømhaug, and P. O. Seglen. "Inhibition of autophagic-lysosomal delivery and autophagic lactolysis by asparagine." Journal of Cell Biology 113, no. 6 (1991): 1305–12. http://dx.doi.org/10.1083/jcb.113.6.1305.

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Overall autophagy was measured in isolated hepatocytes as the sequestration and lysosomal hydrolysis of electroinjected [14C]lactose, using HPLC to separate the degradation product [14C]glucose from undegraded lactose. In addition, the sequestration step was measured separately as the transfer from cytosol to sedimentable cell structures of electroinjected [3H]raffinose or endogenous lactate dehydrogenase (LDH; in the presence of leupeptin to inhibit lysosomal proteolysis). Inhibitor effects at postsequestrational steps could be detected as the accumulation of autophaged lactose (which otherwi

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Stark, Michal, Tomás F. D. Silva, Guy Levin, Miguel Machuqueiro, and Yehuda G. Assaraf. "The Lysosomotropic Activity of Hydrophobic Weak Base Drugs is Mediated via Their Intercalation into the Lysosomal Membrane." Cells 9, no. 5 (2020): 1082. http://dx.doi.org/10.3390/cells9051082.

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Lipophilic weak base therapeutic agents, termed lysosomotropic drugs (LDs), undergo marked sequestration and concentration within lysosomes, hence altering lysosomal functions. This lysosomal drug entrapment has been described as luminal drug compartmentalization. Consistent with our recent finding that LDs inflict a pH-dependent membrane fluidization, we herein demonstrate that LDs undergo intercalation and concentration within lysosomal membranes. The latter was revealed experimentally and computationally by (a) confocal microscopy of fluorescent compounds and drugs within lysosomal membrane

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Zhang, Yanlin, Xueqin Cao, Wawa Zhu, et al. "Resveratrol Enhances Autophagic Flux and Promotes Ox-LDL Degradation in HUVECs via Upregulation of SIRT1." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/7589813.

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Oxidized low-density lipoprotein- (Ox-LDL-) induced autophagy dysfunction in human vascular endothelial cells contributes to the development of atherosclerosis (AS). Resveratrol (RSV) protects against Ox-LDL-induced endothelium injury. The objective of this study was to determine the mechanisms underlying Ox-LDL-induced autophagy dysfunction and RSV-mediated protection in human umbilical vein endothelial cells (HUVECs). The results showed that Ox-LDL suppressed the expression of sirtuin 1 (SIRT1) and increased LC3-II and sequestosome 1 (p62) protein levels without altering p62 mRNA levels in H

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Dikic, I. "Mechanisms controlling EGF receptor endocytosis and degradation." Biochemical Society Transactions 31, no. 6 (2003): 1178–81. http://dx.doi.org/10.1042/bst0311178.

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Activated EGF (epidermal growth factor) receptors are removed from the cell surface via endocytosis and subsequent degradation in the lysosome. This ultimately attenuates EGF receptor signals and diminishes the level of cell activation. The mechanisms underlying the EGF receptor down-regulation are beginning to be elucidated at the molecular level. Recent reports have indicated that receptor monoubiquitination and networks of protein–protein interactions control distinct steps in EGF receptor internalization, endosomal trafficking and sorting for lysosomal degradation. The emerging importance

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RADISKY, Derek C., and Jerry KAPLAN. "Iron in cytosolic ferritin can be recycled through lysosomal degradation in human fibroblasts." Biochemical Journal 336, no. 1 (1998): 201–5. http://dx.doi.org/10.1042/bj3360201.

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Examination of the mechanism of intracellular iron recovery from lysosomally-degraded ferritin in vivo has been complicated by the continuous flux of cellular iron through ferritin molecules. Here we incubated human fibroblasts with cationic ferritin, a derivative of horse spleen ferritin, as a technique for delivering immunologically distinct ferritin molecules directly to lysosomes. Using this method, we found increased endogenous ferritin levels after the cellular degradation of cationic ferritin, demonstrating that cells can utilize lysosomal ferritin to produce increased cytosolic ferriti

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Wang, Ruoxi, Jieqiong Tan, Tingting Chen, et al. "ATP13A2 facilitates HDAC6 recruitment to lysosome to promote autophagosome–lysosome fusion." Journal of Cell Biology 218, no. 1 (2018): 267–84. http://dx.doi.org/10.1083/jcb.201804165.

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Mutations in ATP13A2 cause Kufor-Rakeb syndrome, an autosomal recessive form of juvenile-onset atypical Parkinson’s disease (PD). Recent work tied ATP13A2 to autophagy and other cellular features of neurodegeneration, but how ATP13A2 governs numerous cellular functions in PD pathogenesis is not understood. In this study, the ATP13A2-deficient mouse developed into aging-dependent phenotypes resembling those of autophagy impairment. ATP13A2 deficiency impaired autophagosome–lysosome fusion in cultured cells and in in vitro reconstitution assays. In ATP13A2-deficient cells or Drosophila melanogas

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Lawrence, B. P., and W. J. Brown. "Inhibition of protein synthesis separates autophagic sequestration from the delivery of lysosomal enzymes." Journal of Cell Science 105, no. 2 (1993): 473–80. http://dx.doi.org/10.1242/jcs.105.2.473.

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To investigate the role of newly synthesized proteins during autophagic sequestration and degradation, the effects of protein synthesis inhibition on autophagic vacuole (AV) formation and degradation were analyzed. The inhibition of protein synthesis was found to separate autophagic sequestration from the delivery of lysosomal enzymes to (AVs). Pretreatment with cycloheximide for &gt; or = 3 h caused a drastic inhibition of autophagy-induced degradation. Surprisingly, morphological analyses showed that the inhibition of protein synthesis for up to 12 h did not block the formation of nascen

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Cuervo, A. M., E. Knecht, S. R. Terlecky, and J. F. Dice. "Activation of a selective pathway of lysosomal proteolysis in rat liver by prolonged starvation." American Journal of Physiology-Cell Physiology 269, no. 5 (1995): C1200—C1208. http://dx.doi.org/10.1152/ajpcell.1995.269.5.c1200.

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Lysosomal uptake and degradation of polypeptides such as glyceraldehyde-3-phosphate dehydrogenase (GAPDH), ribonuclease A (RNase A), and RNase S-peptide (residues 1-20 of RNase A) are progressively activated in rat liver by starvation before isolation of lysosomes. This pathway of proteolysis is selective, since it is stimulated by the heat shock cognate protein of 73 kDa (HSC73) and ATP-MgCl2, and lysosomal uptake of RNase A could be competed by GAPDH but not by ovalbumin. A portion of intracellular HSC73 is associated with certain lysosomes, and the amount of lysosomal HSC73 increases by 5-

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Rodríguez, Ana, Paul Webster, Javier Ortego, and Norma W. Andrews. "Lysosomes Behave as Ca2+-regulated Exocytic Vesicles in Fibroblasts and Epithelial Cells." Journal of Cell Biology 137, no. 1 (1997): 93–104. http://dx.doi.org/10.1083/jcb.137.1.93.

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Lysosomes are considered to be a terminal degradative compartment of the endocytic pathway, into which transport is mostly unidirectional. However, specialized secretory vesicles regulated by Ca2+, such as neutrophil azurophil granules, mast cell–specific granules, and cytotoxic lymphocyte lytic granules, share characteristics with lysosomes that may reflect a common biogenesis. In addition, the involvement of Ca2+ transients in the invasion mechanism of the parasite Trypanosoma cruzi, which occurs by fusion of lysosomes with the plasma membrane, suggested that lysosome exocytosis might be a g

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Kuentzel, Katharina B., Ivan Bradić, Alena Akhmetshina, et al. "Defective Lysosomal Lipolysis Causes Prenatal Lipid Accumulation and Exacerbates Immediately after Birth." International Journal of Molecular Sciences 22, no. 19 (2021): 10416. http://dx.doi.org/10.3390/ijms221910416.

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Cholesterol and fatty acids are essential lipids that are critical for membrane biosynthesis and fetal organ development. Cholesteryl esters (CE) are degraded by hormone-sensitive lipase (HSL) in the cytosol and by lysosomal acid lipase (LAL) in the lysosome. Impaired LAL or HSL activity causes rare pathologies in humans, with HSL deficiency presenting less severe clinical manifestations. The infantile form of LAL deficiency, a lysosomal lipid storage disorder, leads to premature death. However, the importance of defective lysosomal CE degradation and its consequences during early life are inc

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Gowrishankar, Swetha, and Shawn M. Ferguson. "Lysosomes relax in the cellular suburbs." Journal of Cell Biology 212, no. 6 (2016): 617–19. http://dx.doi.org/10.1083/jcb.201602082.

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Lysosomes support cellular homeostasis by degrading macromolecules and recycling nutrients. In this issue, Johnson et al. (2016. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201507112) reveal a heterogeneity in lysosomal pH and degradative ability that correlates with lysosome subcellular localization, raising questions about the functional implications and mechanisms underlying these observations.

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Vats, Somya, and Ravi Manjithaya. "A reversible autophagy inhibitor blocks autophagosome–lysosome fusion by preventing Stx17 loading onto autophagosomes." Molecular Biology of the Cell 30, no. 17 (2019): 2283–95. http://dx.doi.org/10.1091/mbc.e18-08-0482.

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Autophagy is an evolutionarily conserved intracellular lysosomal degradation pathway. It is a multistep process involving de novo formation of double membrane autophagosomes that capture cytosolic constituents (cargo) and eventually fuse with lysosomes wherein the cargo gets degraded and resulting simpler biomolecules get recycled. In addition to their autophagy function, several of the autophagy-related proteins work at the interface of other vesicular trafficking pathways. Hence, development of specific autophagy modulators that do not perturb general endo-lysosomal traffic possesses unique

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Burlando, Bruno, Barbara Marchi, Isabella Panfoli, and Aldo Viarengo. "Essential role of Ca2+-dependent phospholipase A2in estradiol-induced lysosome activation." American Journal of Physiology-Cell Physiology 283, no. 5 (2002): C1461—C1468. http://dx.doi.org/10.1152/ajpcell.00429.2001.

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The mechanism of lysosome activation by 17β-estradiol has been studied in mussel blood cells. Cell treatment with estradiol induced a sustained increase of cytosolic free Ca2+that was completely prevented by preincubating the cells with the Ca2+chelator BAPTA-AM. Estradiol treatment was also followed by destabilization of the lysosomal membranes, as detected in terms of the lysosomes' increased permeability to neutral red. The effect of estradiol on lysosomes was almost completely prevented by preincubation with the inhibitor of cytosolic Ca2+-dependent PLA2(cPLA2), arachidonyl trifluoromethyl

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Villamil Giraldo, Ana M., Hanna Appelqvist, Thomas Ederth, and Karin Öllinger. "Lysosomotropic agents: impact on lysosomal membrane permeabilization and cell death." Biochemical Society Transactions 42, no. 5 (2014): 1460–64. http://dx.doi.org/10.1042/bst20140145.

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Lysosomes are acidic organelles essential for degradation, signalling and cell homoeostasis. In addition, they play a key role in cell death. Permeabilization of the lysosomal membrane and release of hydrolytic enzymes to the cytosol accompanies apoptosis signalling in several systems. The regulatory mechanism of lysosomal stability is, however, poorly understood. Lipophilic or amphiphilic compounds with a basic moiety will become protonated and trapped within lysosomes, and such lysosomotropic behaviour is also found in many pharmacological drugs. The natural sphingolipid sphingosine exhibits

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Rome, L. H., and D. F. Hill. "Lysosomal degradation of glycoproteins and glycosaminoglycans. Efflux and recycling of sulphate and N-acetylhexosamines." Biochemical Journal 235, no. 3 (1986): 707–13. http://dx.doi.org/10.1042/bj2350707.

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Lysosomal degradation of the carbohydrate portion of glycoproteins and glycosaminoglycans produces monosaccharides and sulphate, which must efflux from the lysosomes before re-entering biosynthetic pathways. We examined the degradation of glycoproteins and glycosaminoglycans by lysosomes isolated from cultured human diploid fibroblasts. Cells were grown for 24 h in medium containing [3H]glucosamine and [35S]sulphate. When lysosomes are isolated from these cells, they contain label primarily in macromolecules (glycoproteins and glycosaminoglycans). Glycoprotein degradation by isolated lysosomes

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