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Artykuły w czasopismach na temat „Lysosome - related organelles”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Dell'Angelica, Esteban C., Chris Mullins, Steve Caplan, and Juan S. Bonifacino. "Lysosome‐related organelles." FASEB Journal 14, no. 10 (2000): 1265–78. http://dx.doi.org/10.1096/fasebj.14.10.1265.

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DELL'ANGELICA, E. C. "Lysosome-related organelles." FASEB Journal 14, no. 10 (2000): 1265–78. http://dx.doi.org/10.1096/fj.14.10.1265.

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Hermann, Greg J., Lena K. Schroeder, Caroline A. Hieb, et al. "Genetic Analysis of Lysosomal Trafficking inCaenorhabditis elegans." Molecular Biology of the Cell 16, no. 7 (2005): 3273–88. http://dx.doi.org/10.1091/mbc.e05-01-0060.

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The intestinal cells of Caenorhabditis elegans embryos contain prominent, birefringent gut granules that we show are lysosome-related organelles. Gut granules are labeled by lysosomal markers, and their formation is disrupted in embryos depleted of AP-3 subunits, VPS-16, and VPS-41. We define a class of gut granule loss (glo) mutants that are defective in gut granule biogenesis. We show that the glo-1 gene encodes a predicted Rab GTPase that localizes to lysosome-related gut granules in the intestine and that glo-4 encodes a possible GLO-1 guanine nucleotide exchange factor. These and other gl

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4

Cutler, D. F. "Introduction: lysosome-related organelles." Seminars in Cell & Developmental Biology 13, no. 4 (2002): 261–62. http://dx.doi.org/10.1016/s108495210200054x.

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Santo, Manuela, and Ivan Conte. "Emerging Lysosomal Functions for Photoreceptor Cell Homeostasis and Survival." Cells 11, no. 1 (2021): 60. http://dx.doi.org/10.3390/cells11010060.

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Lysosomes are membrane-bound cell organelles that respond to nutrient changes and are implicated in cell homeostasis and clearance mechanisms, allowing effective adaptation to specific cellular needs. The relevance of the lysosome has been elucidated in a number of different contexts. Of these, the retina represents an interesting scenario to appreciate the various functions of this organelle in both physiological and pathological conditions. Growing evidence suggests a role for lysosome-related mechanisms in retinal degeneration. Abnormal lysosomal activation or inhibition has dramatic conseq

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Watts, Colin. "Lysosomes and lysosome‐related organelles in immune responses." FEBS Open Bio 12, no. 4 (2022): 678–93. http://dx.doi.org/10.1002/2211-5463.13388.

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Luzio, J. P., Y. Hackmann, N. M. G. Dieckmann, and G. M. Griffiths. "The Biogenesis of Lysosomes and Lysosome-Related Organelles." Cold Spring Harbor Perspectives in Biology 6, no. 9 (2014): a016840. http://dx.doi.org/10.1101/cshperspect.a016840.

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Biswas, Suprakash, Tanoy Dutta, Akshay Silswal, Rohit Bhowal, Deepak Chopra, and Apurba L. Koner. "Strategic engineering of alkyl spacer length for a pH-tolerant lysosome marker and dual organelle localization." Chemical Science 12, no. 28 (2021): 9630–44. http://dx.doi.org/10.1039/d1sc00542a.

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A series naphthalimide-based fluorophores were designed by alkyl spacer length engineering to discover a pH-tolerant lysosomal marker. This approach also allows to probe lysosome-related organelles in C. elegans and communication between organelles.

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Newell-Litwa, Karen, Gloria Salazar, Yoland Smith, and Victor Faundez. "Roles of BLOC-1 and Adaptor Protein-3 Complexes in Cargo Sorting to Synaptic Vesicles." Molecular Biology of the Cell 20, no. 5 (2009): 1441–53. http://dx.doi.org/10.1091/mbc.e08-05-0456.

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Neuronal lysosomes and their biogenesis mechanisms are primarily thought to clear metabolites and proteins whose abnormal accumulation leads to neurodegenerative disease pathology. However, it remains unknown whether lysosomal sorting mechanisms regulate the levels of membrane proteins within synaptic vesicles. Using high-resolution deconvolution microscopy, we identified early endosomal compartments where both selected synaptic vesicle and lysosomal membrane proteins coexist with the adaptor protein complex 3 (AP-3) in neuronal cells. From these early endosomes, both synaptic vesicle membrane

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Morgan, Anthony J. "Ca2+ dialogue between acidic vesicles and ER." Biochemical Society Transactions 44, no. 2 (2016): 546–53. http://dx.doi.org/10.1042/bst20150290.

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Extracellular stimuli evoke the synthesis of intracellular second messengers, several of which couple to the release of Ca2+ from Ca2+-storing organelles via activation of cognate organellar Ca2+-channel complexes. The archetype is the inositol 1,4,5-trisphosphate (IP3) and IP3 receptor (IP3R) on the endoplasmic reticulum (ER). A less understood, parallel Ca2+ signalling cascade is that involving the messenger nicotinic acid adenine dinucleotide phosphate (NAADP) that couples to Ca2+ release from acidic Ca2+ stores [e.g. endo-lysosomes, secretory vesicles, lysosome-related organelles (LROs)].

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Polev, Konstantin, Diana V. Kolygina, Kristiana Kandere-Grzybowska, and Bartosz A. Grzybowski. "Large-Scale, Wavelet-Based Analysis of Lysosomal Trajectories and Co-Movements of Lysosomes with Nanoparticle Cargos." Cells 11, no. 2 (2022): 270. http://dx.doi.org/10.3390/cells11020270.

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Lysosomes—that is, acidic organelles known for degradation/recycling—move through the cytoplasm alternating between bursts of active transport and short, diffusive motions or even pauses. While their mobility is essential for lysosomes’ fusogenic and non-fusogenic interactions with target organelles, their movements have not been characterized in adequate detail. Here, large-scale statistical analysis of lysosomal movement trajectories reveals that lysosome trajectories in all examined cell types—both cancer and noncancerous ones—are superdiffusive and characterized by heavy-tailed distributio

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12

Figon, Florent, Ilse Hurbain, Xavier Heiligenstein, et al. "Catabolism of lysosome-related organelles in color-changing spiders supports intracellular turnover of pigments." Proceedings of the National Academy of Sciences 118, no. 35 (2021): e2103020118. http://dx.doi.org/10.1073/pnas.2103020118.

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Pigment organelles of vertebrates belong to the lysosome-related organelle (LRO) family, of which melanin-producing melanosomes are the prototypes. While their anabolism has been extensively unraveled through the study of melanosomes in skin melanocytes, their catabolism remains poorly known. Here, we tap into the unique ability of crab spiders to reversibly change body coloration to examine the catabolism of their pigment organelles. By combining ultrastructural and metal analyses on high-pressure frozen integuments, we first assess whether pigment organelles of crab spiders belong to the LRO

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Marks, Michael S., Harry FG Heijnen, and Graça Raposo. "Lysosome-related organelles: unusual compartments become mainstream." Current Opinion in Cell Biology 25, no. 4 (2013): 495–505. http://dx.doi.org/10.1016/j.ceb.2013.04.008.

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Lee, Dongun, and Jeong Hee Hong. "Niemann-Pick Disease Type C (NPDC) by Mutation of NPC1 and NPC2: Aberrant Lysosomal Cholesterol Trafficking and Oxidative Stress." Antioxidants 12, no. 12 (2023): 2021. http://dx.doi.org/10.3390/antiox12122021.

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Cholesterol trafficking is initiated by the endocytic pathway and transported from endo/lysosomes to other intracellular organelles. Deficiencies in cholesterol-sensing and binding proteins NPC1 and NPC2 induce accumulation in lysosomes and the malfunction of trafficking to other organelles. Each organelle possesses regulatory factors to induce cholesterol trafficking. The mutation of NPC1 and NPC2 genes induces Niemann-Pick disease type C (NPDC), which is a hereditary disease and causes progressive neurodegeneration, developmental disability, hypotonia, and ataxia. Oxidative stress induces da

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15

Raposo, Graça, Danielle Tenza, Diane M. Murphy, Joanne F. Berson, and Michael S. Marks. "Distinct Protein Sorting and Localization to Premelanosomes, Melanosomes, and Lysosomes in Pigmented Melanocytic Cells✪." Journal of Cell Biology 152, no. 4 (2001): 809–24. http://dx.doi.org/10.1083/jcb.152.4.809.

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Melanosomes and premelanosomes are lysosome-related organelles with a unique structure and cohort of resident proteins. We have positioned these organelles relative to endosomes and lysosomes in pigmented melanoma cells and melanocytes. Melanosome resident proteins Pmel17 and TRP1 localized to separate vesicular structures that were distinct from those enriched in lysosomal proteins. In immunogold-labeled ultrathin cryosections, Pmel17 was most enriched along the intralumenal striations of premelanosomes. Increased pigmentation was accompanied by a decrease in Pmel17 and by an increase in TRP1

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16

Li, Chenghao, Zhuo Zheng, and Meishan Jin. "The Significance of Lysosome in the Diagnosis and Subclassification of Alzheimer’s Disease." Science of Advanced Materials 15, no. 2 (2023): 233–42. http://dx.doi.org/10.1166/sam.2023.4441.

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Lysosomes are the main degradation organelles in eukaryotic cells, and their dysfunction is closely related to Alzheimer’s disease (AD). Our goal is to identify the lysosomal molecular subtype of AD and explore the mechanisms. By differential analysis, 50 differentially expressed lysosomal genes in AD were identified. R-package “ROCR” was used to calculate ROC curves and AUC values for lysosomal genes. “ConsensusClusterPlus” was used for consistent clustering of the AD data set. The contents of 28 kinds of immune cells in AD samples were calculated using the R-package “GSVA”. The R package “li

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17

Gwynn, Babette, Steven L. Ciciotte, Susan J. Hunter, et al. "Defects in the cappuccino (cno) gene on mouse chromosome 5 and human 4p cause Hermansky-Pudlak syndrome by an AP-3–independent mechanism." Blood 96, no. 13 (2000): 4227–35. http://dx.doi.org/10.1182/blood.v96.13.4227.

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Abstract Defects in a triad of organelles (melanosomes, platelet granules, and lysosomes) result in albinism, prolonged bleeding, and lysosome abnormalities in Hermansky-Pudlak syndrome (HPS). Defects in HPS1, a protein of unknown function, and in components of the AP-3 complex cause some, but not all, cases of HPS in humans. There have been 15 inherited models of HPS described in the mouse, underscoring its marked genetic heterogeneity. Here we characterize a new spontaneous mutation in the mouse, cappuccino (cno), that maps to mouse chromosome 5 in a region conserved with human 4p15-p16. Mel

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Gwynn, Babette, Steven L. Ciciotte, Susan J. Hunter, et al. "Defects in the cappuccino (cno) gene on mouse chromosome 5 and human 4p cause Hermansky-Pudlak syndrome by an AP-3–independent mechanism." Blood 96, no. 13 (2000): 4227–35. http://dx.doi.org/10.1182/blood.v96.13.4227.h8004227_4227_4235.

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Defects in a triad of organelles (melanosomes, platelet granules, and lysosomes) result in albinism, prolonged bleeding, and lysosome abnormalities in Hermansky-Pudlak syndrome (HPS). Defects in HPS1, a protein of unknown function, and in components of the AP-3 complex cause some, but not all, cases of HPS in humans. There have been 15 inherited models of HPS described in the mouse, underscoring its marked genetic heterogeneity. Here we characterize a new spontaneous mutation in the mouse, cappuccino (cno), that maps to mouse chromosome 5 in a region conserved with human 4p15-p16. Melanosomes

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19

Baust, Thorsten, Mihaela Anitei, Cornelia Czupalla, et al. "Protein Networks Supporting AP-3 Function in Targeting Lysosomal Membrane Proteins." Molecular Biology of the Cell 19, no. 5 (2008): 1942–51. http://dx.doi.org/10.1091/mbc.e08-02-0110.

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The AP-3 adaptor complex targets selected transmembrane proteins to lysosomes and lysosome-related organelles. We reconstituted its preferred interaction with liposomes containing the ADP ribosylation factor (ARF)-1 guanosine triphosphatase (GTPase), specific cargo tails, and phosphatidylinositol-3 phosphate, and then we performed a proteomic screen to identify new proteins supporting its sorting function. We identified ≈30 proteins belonging to three networks regulating either AP-3 coat assembly or septin polymerization or Rab7-dependent lysosomal transport. RNA interference shows that, among

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Di Pietro, Santiago M., Juan M. Falcón-Pérez, Danièle Tenza, et al. "BLOC-1 Interacts with BLOC-2 and the AP-3 Complex to Facilitate Protein Trafficking on Endosomes." Molecular Biology of the Cell 17, no. 9 (2006): 4027–38. http://dx.doi.org/10.1091/mbc.e06-05-0379.

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The adaptor protein (AP)-3 complex is a component of the cellular machinery that controls protein sorting from endosomes to lysosomes and specialized related organelles such as melanosomes. Mutations in an AP-3 subunit underlie a form of Hermansky-Pudlak syndrome (HPS), a disorder characterized by abnormalities in lysosome-related organelles. HPS in humans can also be caused by mutations in genes encoding subunits of three complexes of unclear function, named biogenesis of lysosome-related organelles complex (BLOC)-1, -2, and -3. Here, we report that BLOC-1 interacts physically and functionall

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21

Chintala, Sreenivasulu, Jian Tan, Rashi Gautam, et al. "The Slc35d3 gene, encoding an orphan nucleotide sugar transporter, regulates platelet-dense granules." Blood 109, no. 4 (2006): 1533–40. http://dx.doi.org/10.1182/blood-2006-08-040196.

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Abstract Platelet dense granules are lysosome-related organelles which contain high concentrations of several biologically important low-molecular-weight molecules. These include calcium, serotonin, adenine nucleotides, pyrophosphate, and polyphosphate, which are necessary for normal blood hemostasis. The synthesis of dense granules and other lysosome-related organelles is defective in inherited diseases such as Hermansky-Pudlak syndrome (HPS) and Chediak-Higashi syndrome (CHS). HPS and CHS mutations in 8 human and at least 16 murine genes have been identified. Previous studies produced contra

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Akbar, Mohammed A., Sanchali Ray, and Helmut Krämer. "The SM Protein Car/Vps33A Regulates SNARE-mediated Trafficking to Lysosomes and Lysosome-related Organelles." Molecular Biology of the Cell 20, no. 6 (2009): 1705–14. http://dx.doi.org/10.1091/mbc.e08-03-0282.

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The SM proteins Vps33A and Vps33B are believed to act in membrane fusions in endosomal pathways, but their specific roles are controversial. In Drosophila, Vps33A is the product of the carnation (car) gene. We generated a null allele of car to test its requirement for trafficking to different organelles. Complete loss of car function is lethal during larval development. Eye-specific loss of Car causes late, light-independent degeneration of photoreceptor cells. Earlier in these cells, two distinct phenotypes were detected. In young adults, autophagosomes amassed indicating that their fusion wi

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Szabo, Mate, Bence Cs. Szabo, Kitti Kurtan, et al. "Look Beyond Plasma Membrane Biophysics: Revealing Considerable Variability of the Dipole Potential Between Plasma and Organelle Membranes of Living Cells." International Journal of Molecular Sciences 26, no. 3 (2025): 889. https://doi.org/10.3390/ijms26030889.

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Due to the lack of measurement techniques suitable for examining compartments of intact, living cells, membrane biophysics is almost exclusively investigated in the plasma membrane despite the fact that its alterations in intracellular organelles may also contribute to disease pathogenesis. Here, we employ a novel, easy-to-use, confocal microscopy-based approach utilizing F66, an environment-sensitive fluorophore in combination with fluorescent organelle markers and quantitative image analysis to determine the magnitude of the molecular order-related dipole potential in the plasma membrane and

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Shiflett, Shelly L., Jerry Kaplan, and Diane McVey WARD. "Chediak-Higashi Syndrome: A Rare Disorder of Lysosomes and Lysosome Related Organelles." Pigment Cell Research 15, no. 4 (2002): 251–57. http://dx.doi.org/10.1034/j.1600-0749.2002.02038.x.

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Blaby-Haas, Crysten E., and Sabeeha S. Merchant. "Lysosome-related Organelles as Mediators of Metal Homeostasis." Journal of Biological Chemistry 289, no. 41 (2014): 28129–36. http://dx.doi.org/10.1074/jbc.r114.592618.

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Metcalf, Daniel, and Adrian M. Isaacs. "The role of ESCRT proteins in fusion events involving lysosomes, endosomes and autophagosomes." Biochemical Society Transactions 38, no. 6 (2010): 1469–73. http://dx.doi.org/10.1042/bst0381469.

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ESCRT (endosomal sorting complex required for transport) proteins were originally identified for their role in delivering endocytosed proteins to the intraluminal vesicles of late-endosomal structures termed multivesicular bodies. Multivesicular bodies then fuse with lysosomes, leading to degradation of the internalized proteins. Four ESCRT complexes interact to concentrate cargo on the endosomal membrane, induce membrane curvature to form an intraluminal bud and finally pinch off the bud through a membrane-scission event to produce the intraluminal vesicle. Recent work suggests that ESCRT pro

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Osanai, Kazuhiro. "Rab38 Mutation and the Lung Phenotype." International Journal of Molecular Sciences 19, no. 8 (2018): 2203. http://dx.doi.org/10.3390/ijms19082203.

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Rab38 is highly expressed in alveolar type II cells, melanocytes, and platelets. These cells are specifically-differentiated cells and contain characteristic intracellular organelles called lysosome-related organelles, i.e., lamellar bodies in alveolar type II cells, melanosomes in melanocytes, and dense granules in platelets. There are Rab38-mutant rodents, i.e., chocolate mice and Ruby rats. While chocolate mice only show oculocutaneous albinism, Ruby rats show oculocutaneous albinism and prolonged bleeding time and, hence, are a rat model of Hermansky-Pudlak syndrome (HPS). Most patients wi

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Raposo, Graça, Benoit Fevrier, Willem Stoorvogel, and Michael S. Marks. "Lysosome-Related Organelles: a View from Immunity and Pigmentation." Cell Structure and Function 27, no. 6 (2002): 443–56. http://dx.doi.org/10.1247/csf.27.443.

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Raposo, Graça, Michael S. Marks, and Daniel F. Cutler. "Lysosome-related organelles: driving post-Golgi compartments into specialisation." Current Opinion in Cell Biology 19, no. 4 (2007): 394–401. http://dx.doi.org/10.1016/j.ceb.2007.05.001.

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Sant’Anna, Celso, Fabiola Parussini, Daniela Lourenço, Wanderley Souza, Juan Jose Cazzulo, and Narcisa Leal Cunha-e-Silva. "All Trypanosoma cruzi developmental forms present lysosome-related organelles." Histochemistry and Cell Biology 130, no. 6 (2008): 1187–98. http://dx.doi.org/10.1007/s00418-008-0486-8.

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Scorza, Simona Ida, Serena Milano, Ilenia Saponara, et al. "TRPML1-Induced Lysosomal Ca2+ Signals Activate AQP2 Translocation and Water Flux in Renal Collecting Duct Cells." International Journal of Molecular Sciences 24, no. 2 (2023): 1647. http://dx.doi.org/10.3390/ijms24021647.

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Lysosomes are acidic Ca2+ storage organelles that actively generate local Ca2+ signaling events to regulate a plethora of cell functions. Here, we characterized lysosomal Ca2+ signals in mouse renal collecting duct (CD) cells and we assessed their putative role in aquaporin 2 (AQP2)-dependent water reabsorption. Bafilomycin A1 and ML-SA1 triggered similar Ca2+ oscillations, in the absence of extracellular Ca2+, by alkalizing the acidic lysosomal pH or activating the lysosomal cation channel mucolipin 1 (TRPML1), respectively. TRPML1-dependent Ca2+ signals were blocked either pharmacologically

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Schroeder, Lena K., Susan Kremer, Maxwell J. Kramer, et al. "Function of the Caenorhabditis elegans ABC Transporter PGP-2 in the Biogenesis of a Lysosome-related Fat Storage Organelle." Molecular Biology of the Cell 18, no. 3 (2007): 995–1008. http://dx.doi.org/10.1091/mbc.e06-08-0685.

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Caenorhabditis elegans gut granules are intestine specific lysosome-related organelles with birefringent and autofluorescent contents. We identified pgp-2, which encodes an ABC transporter, in screens for genes required for the proper formation of gut granules. pgp-2(−) embryos mislocalize birefringent material into the intestinal lumen and are lacking in acidified intestinal V-ATPase–containing compartments. Adults without pgp-2(+) function similarly lack organelles with gut granule characteristics. These cellular phenotypes indicate that pgp-2(−) animals are defective in gut granule biogenes

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Sedwick, Caitlin. "Graça Raposo: Melanosomes, more than skin deep." Journal of Cell Biology 197, no. 5 (2012): 572–73. http://dx.doi.org/10.1083/jcb.1975pi.

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Badadani, Mallikarjun. "Autophagy Mechanism, Regulation, Functions, and Disorders." ISRN Cell Biology 2012 (September 6, 2012): 1–11. http://dx.doi.org/10.5402/2012/927064.

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Autophagy is a self-digesting mechanism responsible for removal of damaged organelles, malformed proteins during biosynthesis, and nonfunctional long-lived proteins by lysosome. Autophagy has been divided into three general types depending on the mechanism by which intracellular materials are delivered into lysosome for degradation that is, microautophagy, chaperone-mediated autophagy (CMA), and macroautophagy. In microautophagy cytoplasm material is sequestered through direct invagination to the lysosomal membrane. Whereas in CMA proteins flagged with pentapeptide motif (KFERQ) were selective

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Ji, Xiaojie, Lihong Zhao, Ankita Umapathy, et al. "Deficiency in Lyst function leads to accumulation of secreted proteases and reduced retinal adhesion." PLOS ONE 17, no. 3 (2022): e0254469. http://dx.doi.org/10.1371/journal.pone.0254469.

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Chediak–Higashi syndrome, caused by mutations in the Lysosome Trafficking Regulator (Lyst) gene, is a recessive hypopigmentation disorder characterized by albinism, neuropathies, neurodegeneration, and defective immune responses, with enlargement of lysosomes and lysosome-related organelles. Although recent studies have suggested that Lyst mutations impair the regulation of sizes of lysosome and lysosome-related organelle, the underlying pathogenic mechanism of Chediak–Higashi syndrome is still unclear. Here we show striking evidence that deficiency in LYST protein function leads to accumulati

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de Figueiredo, Paul, Kelsey Wells, Kai He, et al. "-Brucella induction of RIDD activity promotes intracellular parasitism by subverting BLOS1-controlled immune defense." Journal of Immunology 204, no. 1_Supplement (2020): 67.38. http://dx.doi.org/10.4049/jimmunol.204.supp.67.38.

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Abstract The intracellular bacterial pathogen and biothreat agent Brucella is the causative agent of brucellosis, a global zoonotic disease that is associated with acute and chronic symptoms in humans and animals. The mechanisms by which the pathogen colonizes host cells remain obscure. Here, we demonstrate that infection activates the regulated IRE1-dependent decay (RIDD) of mRNA encoding BLOS1 (biogenesis of lysosome-related organelles 1 subunit 1), a protein that promotes endosome-lysosome fusion. RIDD-deficient host cells as well as mice harboring a RIDD-incompetent variant of IRE1a displa

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Berson, Joanne F., Alexander C. Theos, Dawn C. Harper, Danielle Tenza, Graça Raposo, and Michael S. Marks. "Proprotein convertase cleavage liberates a fibrillogenic fragment of a resident glycoprotein to initiate melanosome biogenesis." Journal of Cell Biology 161, no. 3 (2003): 521–33. http://dx.doi.org/10.1083/jcb.200302072.

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Lysosome-related organelles are cell type–specific intracellular compartments with distinct morphologies and functions. The molecular mechanisms governing the formation of their unique structural features are not known. Melanosomes and their precursors are lysosome-related organelles that are characterized morphologically by intralumenal fibrous striations upon which melanins are polymerized. The integral membrane protein Pmel17 is a component of the fibrils and can nucleate their formation in the absence of other pigment cell–specific proteins. Here, we show that formation of intralumenal fib

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Delahaye, Jared L., Olivia K. Foster, Annalise Vine, et al. "Caenorhabditis elegansHOPS and CCZ-1 mediate trafficking to lysosome-related organelles independently of RAB-7 and SAND-1." Molecular Biology of the Cell 25, no. 7 (2014): 1073–96. http://dx.doi.org/10.1091/mbc.e13-09-0521.

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As early endosomes mature, the SAND-1/CCZ-1 complex acts as a guanine nucleotide exchange factor (GEF) for RAB-7 to promote the activity of its effector, HOPS, which facilitates late endosome–lysosome fusion and the consumption of AP-3–containing vesicles. We show that CCZ-1 and the HOPS complex are essential for the biogenesis of gut granules, cell type–specific, lysosome-related organelles (LROs) that coexist with conventional lysosomes in Caenorhabditis elegans intestinal cells. The HOPS subunit VPS-18 promotes the trafficking of gut granule proteins away from lysosomes and functions downst

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Tang, Tuoxian, Boshuo Jian, and Zhenjiang Liu. "Transmembrane Protein 175, a Lysosomal Ion Channel Related to Parkinson’s Disease." Biomolecules 13, no. 5 (2023): 802. http://dx.doi.org/10.3390/biom13050802.

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Lysosomes are membrane-bound organelles with an acidic lumen and are traditionally characterized as a recycling center in cells. Lysosomal ion channels are integral membrane proteins that form pores in lysosomal membranes and allow the influx and efflux of essential ions. Transmembrane protein 175 (TMEM175) is a unique lysosomal potassium channel that shares little sequence similarity with other potassium channels. It is found in bacteria, archaea, and animals. The prokaryotic TMEM175 consists of one six-transmembrane domain that adopts a tetrameric architecture, while the mammalian TMEM175 is

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Sorokina, Elena M., Sheldon I. Feinstein, Suiping Zhou та Aron B. Fisher. "Intracellular targeting of peroxiredoxin 6 to lysosomal organelles requires MAPK activity and binding to 14-3-3ε". American Journal of Physiology-Cell Physiology 300, № 6 (2011): C1430—C1441. http://dx.doi.org/10.1152/ajpcell.00285.2010.

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Peroxiredoxin 6 (Prdx6), a bifunctional protein with GSH peroxidase and lysosomal-type phospholipase A2 activities, has been localized to both cytosolic and acidic compartments (lamellar bodies and lysosomes) in lung alveolar epithelium. We postulate that Prdx6 subcellular localization affects the balance between the two activities. Immunostaining localized Prdx6 to lysosome-related organelles in the MLE12 and A549 alveolar epithelial cell lines. Inhibition of trafficking by brefeldin A indicated processing of the protein through the vesicular pathway. Trafficking of Prdx6 was decreased by inh

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Ellis, Kathryn, Jennifer Bagwell, and Michel Bagnat. "Notochord vacuoles are lysosome-related organelles that function in axis and spine morphogenesis." Journal of Cell Biology 200, no. 5 (2013): 667–79. http://dx.doi.org/10.1083/jcb.201212095.

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The notochord plays critical structural and signaling roles during vertebrate development. At the center of the vertebrate notochord is a large fluid-filled organelle, the notochord vacuole. Although these highly conserved intracellular structures have been described for decades, little is known about the molecular mechanisms involved in their biogenesis and maintenance. Here we show that zebrafish notochord vacuoles are specialized lysosome-related organelles whose formation and maintenance requires late endosomal trafficking regulated by the vacuole-specific Rab32a and H+-ATPase–dependent ac

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Yoon, Jihee, Min-Ju Oh, Ji-Young Ahn, Simranjeet Singh Sekhon, Yang-Hoon Kim, and Jiho Min. "Lysosome-related organelles extracts from egg-white for hypermelanosis reduction." Molecular & Cellular Toxicology 12, no. 2 (2016): 177–84. http://dx.doi.org/10.1007/s13273-016-0022-1.

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Delevoye, Cédric, Michael S. Marks, and Graça Raposo. "Lysosome-related organelles as functional adaptations of the endolysosomal system." Current Opinion in Cell Biology 59 (August 2019): 147–58. http://dx.doi.org/10.1016/j.ceb.2019.05.003.

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Li, Wei, Michael E. Rusiniak, Sreenivasulu Chintala, Rashi Gautam, Edward K. Novak, and Richard T. Swank. "Murine Hermansky-Pudlak syndrome genes: regulators of lysosome-related organelles." BioEssays 26, no. 6 (2004): 616–28. http://dx.doi.org/10.1002/bies.20042.

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Ma, Xiaowen, Sharon Manley, Hui Qian, et al. "Mitochondria-lysosome-related organelles mediate mitochondrial clearance during cellular dedifferentiation." Cell Reports 42, no. 10 (2023): 113291. http://dx.doi.org/10.1016/j.celrep.2023.113291.

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Seranova, Elena, Kyle J. Connolly, Malgorzata Zatyka, et al. "Dysregulation of autophagy as a common mechanism in lysosomal storage diseases." Essays in Biochemistry 61, no. 6 (2017): 733–49. http://dx.doi.org/10.1042/ebc20170055.

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The lysosome plays a pivotal role between catabolic and anabolic processes as the nexus for signalling pathways responsive to a variety of factors, such as growth, nutrient availability, energetic status and cellular stressors. Lysosomes are also the terminal degradative organelles for autophagy through which macromolecules and damaged cellular components and organelles are degraded. Autophagy acts as a cellular homeostatic pathway that is essential for organismal physiology. Decline in autophagy during ageing or in many diseases, including late-onset forms of neurodegeneration is considered a

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Triolo, Matthew, and David A. Hood. "Manifestations of Age on Autophagy, Mitophagy and Lysosomes in Skeletal Muscle." Cells 10, no. 5 (2021): 1054. http://dx.doi.org/10.3390/cells10051054.

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Sarcopenia is the loss of both muscle mass and function with age. Although the molecular underpinnings of sarcopenia are not fully understood, numerous pathways are implicated, including autophagy, in which defective cargo is selectively identified and degraded at the lysosome. The specific tagging and degradation of mitochondria is termed mitophagy, a process important for the maintenance of an organelle pool that functions efficiently in energy production and with relatively low reactive oxygen species production. Emerging data, yet insufficient, have implicated various steps in this pathway

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Ullate-Agote, Asier, Ingrid Burgelin, Adrien Debry, et al. "Genome mapping of aLYSTmutation in corn snakes indicates that vertebrate chromatophore vesicles are lysosome-related organelles." Proceedings of the National Academy of Sciences 117, no. 42 (2020): 26307–17. http://dx.doi.org/10.1073/pnas.2003724117.

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Reptiles exhibit a spectacular diversity of skin colors and patterns brought about by the interactions among three chromatophore types: black melanophores with melanin-packed melanosomes, red and yellow xanthophores with pteridine- and/or carotenoid-containing vesicles, and iridophores filled with light-reflecting platelets generating structural colors. Whereas the melanosome, the only color-producing endosome in mammals and birds, has been documented as a lysosome-related organelle, the maturation paths of xanthosomes and iridosomes are unknown. Here, we first use 10x Genomics linked-reads an

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Monastyrska, Iryna, Congcong He, Jiefei Geng, Adam D. Hoppe, Zhijian Li, and Daniel J. Klionsky. "Arp2 Links Autophagic Machinery with the Actin Cytoskeleton." Molecular Biology of the Cell 19, no. 5 (2008): 1962–75. http://dx.doi.org/10.1091/mbc.e07-09-0892.

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Macroautophagy involves lysosomal/vacuolar elimination of long-lived proteins and entire organelles from the cytosol. The process begins with formation of a double-membrane vesicle that sequesters bulk cytoplasm, or a specific cargo destined for lysosomal/vacuolar delivery. The completed vesicle fuses with the lysosome/vacuole limiting membrane, releasing its content into the organelle lumen for subsequent degradation and recycling of the resulting macromolecules. A majority of the autophagy-related (Atg) proteins are required at the step of vesicle formation. The integral membrane protein Atg

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Kretzschmar, Doris, Burkhard Poeck, Helmut Roth та ін. "Defective Pigment Granule Biogenesis and Aberrant Behavior Caused by Mutations in the Drosophila AP-3β Adaptin Gene ruby". Genetics 155, № 1 (2000): 213–23. http://dx.doi.org/10.1093/genetics/155.1.213.

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Abstract Lysosomal protein trafficking is a fundamental process conserved from yeast to humans. This conservation extends to lysosome-like organelles such as mammalian melanosomes and insect eye pigment granules. Recently, eye and coat color mutations in mouse (mocha and pearl) and Drosophila (garnet and carmine) were shown to affect subunits of the heterotetrameric adaptor protein complex AP-3 involved in vesicle trafficking. Here we demonstrate that the Drosophila eye color mutant ruby is defective in the AP-3β subunit gene. ruby expression was found in retinal pigment and photoreceptor cell

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