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Artikel ; Online: Post-Translational Modifications of ATG4B in the Regulation of Autophagy.

Park, Na Yeon / Jo, Doo Sin / Cho, Dong-Hyung

2022 Band 11, Heft 8

Abstract: Autophagy plays a key role in eliminating and recycling cellular components in response to stress, including starvation. Dysregulation of autophagy is observed in various diseases, including neurodegenerative diseases, cancer, and diabetes. Autophagy is ... ...

Abstract	Autophagy plays a key role in eliminating and recycling cellular components in response to stress, including starvation. Dysregulation of autophagy is observed in various diseases, including neurodegenerative diseases, cancer, and diabetes. Autophagy is tightly regulated by autophagy-related (ATG) proteins. Autophagy-related 4 (ATG4) is the sole cysteine protease, and four homologs (ATG4A-D) have been identified in mammals. These proteins have two domains: catalytic and short fingers. ATG4 facilitates autophagy by promoting autophagosome maturation through reversible lipidation and delipidation of seven autophagy-related 8 (ATG8) homologs, including microtubule-associated protein 1-light chain 3 (LC3) and GABA type A receptor-associated protein (GABARAP). Each ATG4 homolog shows a preference for a specific ATG8 homolog. Post-translational modifications of ATG4, including phosphorylation/dephosphorylation,
Mesh-Begriff(e)	Animals ; Autophagy/physiology ; Autophagy-Related Protein 8 Family/metabolism ; Autophagy-Related Proteins/metabolism ; Mammals/metabolism ; Microtubule-Associated Proteins/metabolism ; Peptide Hydrolases/metabolism ; Protein Processing, Post-Translational
Chemische Substanzen	Autophagy-Related Protein 8 Family ; Autophagy-Related Proteins ; Microtubule-Associated Proteins ; Peptide Hydrolases (EC 3.4.-)
Sprache	Englisch
Erscheinungsdatum	2022-04-13
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11081330
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Peroxisomal dysfunction in neurodegenerative diseases.

Jo, Doo Sin / Cho, Dong-Hyung

Archives of pharmacal research

2019 Band 42, Heft 5, Seite(n) 393–406

Abstract: Peroxisomes and their (patho-)physiological importance in heath and disease have attracted increasing interest during last few decades. Together with mitochondria, peroxisomes comprise key metabolic platforms for oxidation of various fatty acids and ... ...

Abstract	Peroxisomes and their (patho-)physiological importance in heath and disease have attracted increasing interest during last few decades. Together with mitochondria, peroxisomes comprise key metabolic platforms for oxidation of various fatty acids and redox regulation. In addition, peroxisomes contribute to bile acid, cholesterol, and plasmalogen biosynthesis. The importance of functional peroxisomes for cellular metabolism is demonstrated by the marked brain and systemic organ abnormalities occuring in peroxisome biogenesis disorders and peroxisomal enzyme deficiencies. Current evidences indicate that peroxisomal function is declined with aging, with peroxisomal dysfunction being linked to early onset of multiple age-related diseases including neurodegenerative diseases. Herein, we review recent progress toward understanding the physiological roles and pathological implications of peroxisomal dysfunctions, focusing on neurodegenerative disease.
Mesh-Begriff(e)	Aging/physiology ; Animals ; Brain/cytology ; Brain/metabolism ; Brain/pathology ; Disease Models, Animal ; Humans ; Lipid Metabolism/physiology ; Neurodegenerative Diseases/etiology ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Oxidation-Reduction ; Peroxisomal Disorders/etiology ; Peroxisomal Disorders/metabolism ; Peroxisomal Disorders/pathology ; Peroxisomes/enzymology ; Peroxisomes/metabolism ; Peroxisomes/pathology ; Reactive Oxygen Species/metabolism
Chemische Substanzen	Reactive Oxygen Species
Sprache	Englisch
Erscheinungsdatum	2019-02-09
Erscheinungsland	Korea (South)
Dokumenttyp	Journal Article ; Review
ZDB-ID	447623-2
ISSN	1976-3786 ; 0253-6269
ISSN (online)	1976-3786
ISSN	0253-6269
DOI	10.1007/s12272-019-01131-2
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Peroxisome quality control and dysregulated lipid metabolism in neurodegenerative diseases.

Jo, Doo Sin / Park, Na Yeon / Cho, Dong-Hyung

Experimental & molecular medicine

2020 Band 52, Heft 9, Seite(n) 1486–1495

Abstract: In recent decades, the role of the peroxisome in physiology and disease conditions has become increasingly important. Together with the mitochondria and other cellular organelles, peroxisomes support key metabolic platforms for the oxidation of various ... ...

Abstract	In recent decades, the role of the peroxisome in physiology and disease conditions has become increasingly important. Together with the mitochondria and other cellular organelles, peroxisomes support key metabolic platforms for the oxidation of various fatty acids and regulate redox conditions. In addition, peroxisomes contribute to the biosynthesis of essential lipid molecules, such as bile acid, cholesterol, docosahexaenoic acid, and plasmalogen. Therefore, the quality control mechanisms that regulate peroxisome biogenesis and degradation are important for cellular homeostasis. Current evidence indicates that peroxisomal function is often reduced or dysregulated in various human disease conditions, such as neurodegenerative diseases. Here, we review the recent progress that has been made toward understanding the quality control systems that regulate peroxisomes and their pathological implications.
Mesh-Begriff(e)	Animals ; Biomarkers ; Disease Susceptibility ; Endoplasmic Reticulum/metabolism ; Homeostasis ; Humans ; Lipid Metabolism ; Metabolic Networks and Pathways ; Neurodegenerative Diseases/etiology ; Neurodegenerative Diseases/metabolism ; Oxidation-Reduction ; Peroxisomes/metabolism ; Protein Processing, Post-Translational
Chemische Substanzen	Biomarkers
Sprache	Englisch
Erscheinungsdatum	2020-09-11
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/s12276-020-00503-9
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Peroxisomal dysfunction in neurodegenerative diseases

Jo, Doo Sin / Cho, Dong-Hyung

Archives of pharmacal research. 2019 May, v. 42, no. 5

2019

Abstract	Peroxisomes and their (patho-)physiological importance in heath and disease have attracted increasing interest during last few decades. Together with mitochondria, peroxisomes comprise key metabolic platforms for oxidation of various fatty acids and redox regulation. In addition, peroxisomes contribute to bile acid, cholesterol, and plasmalogen biosynthesis. The importance of functional peroxisomes for cellular metabolism is demonstrated by the marked brain and systemic organ abnormalities occuring in peroxisome biogenesis disorders and peroxisomal enzyme deficiencies. Current evidences indicate that peroxisomal function is declined with aging, with peroxisomal dysfunction being linked to early onset of multiple age-related diseases including neurodegenerative diseases. Herein, we review recent progress toward understanding the physiological roles and pathological implications of peroxisomal dysfunctions, focusing on neurodegenerative disease.
Schlagwörter	bile acids ; biogenesis ; biosynthesis ; brain ; cholesterol ; enzyme deficiencies ; fatty acids ; mitochondria ; neurodegenerative diseases ; oxidation ; peroxisomes
Sprache	Englisch
Erscheinungsverlauf	2019-05
Umfang	p. 393-406.
Erscheinungsort	Pharmaceutical Society of Korea
Dokumenttyp	Artikel
Anmerkung	Review
ZDB-ID	447623-2
ISSN	1976-3786 ; 0253-6269
ISSN (online)	1976-3786
ISSN	0253-6269
DOI	10.1007/s12272-019-01131-2
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: Inhibition of VHL by VH298 Accelerates Pexophagy by Activation of HIF-1α in HeLa Cells.

Kim, Yong Hwan / Park, Na Yeon / Jo, Doo Sin / Bae, Ji-Eun / Kim, Joon Bum / Park, Kyuhee / Jeong, Kwiwan / Kim, Pansoo / Yeom, Eunbyul / Cho, Dong-Hyung

Molecules (Basel, Switzerland)

2024 Band 29, Heft 2

Abstract: Autophagy is a pivotal biological process responsible for maintaining the homeostasis of intracellular organelles. Yet the molecular intricacies of peroxisomal autophagy (pexophagy) remain largely elusive. From a ubiquitin-related chemical library for ... ...

Abstract	Autophagy is a pivotal biological process responsible for maintaining the homeostasis of intracellular organelles. Yet the molecular intricacies of peroxisomal autophagy (pexophagy) remain largely elusive. From a ubiquitin-related chemical library for screening, we identified several inhibitors of the Von Hippel-Lindau (VHL) E3 ligase, including VH298, thereby serving as potent inducers of pexophagy. In this study, we observed that VH298 stimulates peroxisomal degradation by ATG5 dependently and escalates the ubiquitination of the peroxisomal membrane protein ABCD3. Interestingly, the ablation of NBR1 is similar to the curtailed peroxisomal degradation in VH298-treated cells. We also found that the pexophagy induced by VH298 is impeded upon the suppression of gene expression by the translation inhibitor cycloheximide. Beyond VHL inhibition, we discovered that roxadustat, a direct inhibitor of HIF-α prolyl hydroxylase, is also a potent inducer of pexophagy. Furthermore, we found that VH298-mediated pexophagy is blocked by silencing
Mesh-Begriff(e)	Humans ; Macroautophagy ; HeLa Cells ; Autophagy ; Homeostasis ; Von Hippel-Lindau Tumor Suppressor Protein/genetics ; Cyclopropanes ; Pyrrolidines ; Thiazoles
Chemische Substanzen	VH298 ; VHL protein, human (EC 6.3.2.-) ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; Cyclopropanes ; Pyrrolidines ; Thiazoles
Sprache	Englisch
Erscheinungsdatum	2024-01-18
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules29020482
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: PEX13 prevents pexophagy by regulating ubiquitinated PEX5 and peroxisomal ROS.

Demers, Nicholas D / Riccio, Victoria / Jo, Doo Sin / Bhandari, Sushil / Law, Kelsey B / Liao, Weifang / Kim, Choy / McQuibban, G Angus / Choe, Seong-Kyu / Cho, Dong-Hyung / Kim, Peter K

Autophagy

2023 Band 19, Heft 6, Seite(n) 1781–1802

Abstract: Peroxisomes are rapidly degraded during amino acid and oxygen deprivation by a type of selective autophagy called pexophagy. However, how damaged peroxisomes are detected and removed from the cell is poorly understood. Recent studies suggest that the ... ...

Abstract	Peroxisomes are rapidly degraded during amino acid and oxygen deprivation by a type of selective autophagy called pexophagy. However, how damaged peroxisomes are detected and removed from the cell is poorly understood. Recent studies suggest that the peroxisomal matrix protein import machinery may serve double duty as a quality control machinery, where they are directly involved in activating pexophagy. Here, we explored whether any matrix import factors are required to prevent pexophagy, such that their loss designates peroxisomes for degradation. Using gene editing and quantitative fluorescence microscopy on culture cells and a zebrafish model system, we found that PEX13, a component of the peroxisomal matrix import system, is required to prevent the degradation of otherwise healthy peroxisomes. The loss of PEX13 caused an accumulation of ubiquitinated PEX5 on peroxisomes and an increase in peroxisome-dependent reactive oxygen species that coalesce to induce pexophagy. We also found that PEX13 protein level is downregulated to aid in the induction of pexophagy during amino acid starvation. Together, our study points to PEX13 as a novel pexophagy regulator that is modulated to maintain peroxisome homeostasis.
Mesh-Begriff(e)	Animals ; Humans ; Mice ; Macroautophagy ; Autophagy/physiology ; Reactive Oxygen Species/metabolism ; Leucine/metabolism ; Lysine/metabolism ; Actins/metabolism ; Zebrafish/metabolism ; Fibroblasts/metabolism ; Ubiquitin/metabolism ; Peroxisomes/metabolism ; Amino Acids/metabolism ; Oxygen/metabolism ; Sirolimus ; Membrane Proteins/metabolism
Chemische Substanzen	Reactive Oxygen Species ; Leucine (GMW67QNF9C) ; Lysine (K3Z4F929H6) ; Actins ; Ubiquitin ; Amino Acids ; Oxygen (S88TT14065) ; Sirolimus (W36ZG6FT64) ; PEX13 protein, human ; Membrane Proteins
Sprache	Englisch
Erscheinungsdatum	2023-01-01
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2022.2160566
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Tetraarsenic oxide affects non-coding RNA transcriptome through deregulating polycomb complexes in MCF7 cells.

Jeong, Jaehyeon / Hamza, Muhammed Taofiq / Kang, Keunsoo / Jo, Doo Sin / Bae, Ill Ju / Kim, Deukyeong / Cho, Dong-Hyung / Bunch, Heeyoun

Advances in biological regulation

2021 Band 80, Seite(n) 100809

Abstract: Non-coding RNAs (ncRNAs) play important and diverse roles in mammalian cell biology and pathology. Although the functions of an increasing number of ncRNAs have been identified, the mechanisms underlying ncRNA gene expression remain elusive and are ... ...

Abstract	Non-coding RNAs (ncRNAs) play important and diverse roles in mammalian cell biology and pathology. Although the functions of an increasing number of ncRNAs have been identified, the mechanisms underlying ncRNA gene expression remain elusive and are incompletely understood. Here, we investigated ncRNA gene expression in Michigan cancer foundation 7 (MCF7), a malignant breast cancer cell line, on treatment of tetraarsenic oxide (TAO), a potential anti-cancer drug. Our genomic analyses found that TAO up- or down-regulated ncRNA genes genome-wide. A subset of identified ncRNAs with critical biological and clinical functions were validated by real-time quantitative polymerase chain reaction. Intriguingly, these TAO-regulated genes included CDKN2B-AS, HOXA11-AS, SHH, and DUSP5 that are known to interact with or be targeted by polycomb repressive complexes (PRCs). In addition, the PRC subunits were enriched in these TAO-regulated ncRNA genes and TAO treatment deregulated the expression of PRC subunits. Strikingly, TAO decreased the cellular and gene-specific levels of EZH2 expression and H3K27me3. In particular, TAO reduced EZH2 and H3K27me3 and increased transcription at MALAT1 gene. Inhibiting the catalytic activity of EZH2 using GSK343 increased representative TAO-inducible ncRNA genes. Together, our findings suggest that the expression of a subset of ncRNA genes is regulated by PRC2 and that TAO could be a potent epigenetic regulator through PRCs to modulate the ncRNA gene expression in MCF7 cells.
Mesh-Begriff(e)	Antineoplastic Agents/pharmacology ; Arsenic Trioxide/pharmacology ; Autophagy/drug effects ; Autophagy/genetics ; Cell Cycle/drug effects ; Cell Cycle/genetics ; Computational Biology/methods ; DNA Repair/drug effects ; Enhancer of Zeste Homolog 2 Protein/genetics ; Enhancer of Zeste Homolog 2 Protein/metabolism ; Exocytosis/drug effects ; Gene Expression Regulation, Neoplastic ; Gene Ontology ; Genome, Human ; HEK293 Cells ; Histones/genetics ; Histones/metabolism ; Humans ; MCF-7 Cells ; Molecular Sequence Annotation ; Polycomb-Group Proteins/classification ; Polycomb-Group Proteins/genetics ; Polycomb-Group Proteins/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; RNA, Untranslated/classification ; RNA, Untranslated/genetics ; RNA, Untranslated/metabolism ; Transcriptome
Chemische Substanzen	Antineoplastic Agents ; Histones ; MALAT1 long non-coding RNA, human ; Polycomb-Group Proteins ; RNA, Long Noncoding ; RNA, Untranslated ; EZH2 protein, human (EC 2.1.1.43) ; Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43) ; Arsenic Trioxide (S7V92P67HO)
Sprache	Englisch
Erscheinungsdatum	2021-04-14
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2667413-0
ISSN	2212-4934 ; 2212-4926
ISSN (online)	2212-4934
ISSN	2212-4926
DOI	10.1016/j.jbior.2021.100809
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Chemical mimetics of the N-degron pathway alleviate systemic inflammation by activating mitophagy and immunometabolic remodeling.

Silwal, Prashanta / Kim, Young Jae / Lee, Yoon Jee / Kim, In Soo / Jeon, Sang Min / Roh, Taylor / Kim, Jin Kyung / Lee, Min Joung / Heo, Jun Young / Jo, Doo Sin / Lee, Sang-Hee / Cho, Dong-Hyung / Kim, Jin Man / Kwon, Yong Tae / Jo, Eun-Kyeong

Experimental & molecular medicine

2023 Band 55, Heft 2, Seite(n) 333–346

Abstract: The Arg/N-degron pathway, which is involved in the degradation of proteins bearing an N-terminal signal peptide, is connected to p62/SQSTM1-mediated autophagy. However, the impact of the molecular link between the N-degron and autophagy pathways is ... ...

Abstract	The Arg/N-degron pathway, which is involved in the degradation of proteins bearing an N-terminal signal peptide, is connected to p62/SQSTM1-mediated autophagy. However, the impact of the molecular link between the N-degron and autophagy pathways is largely unknown in the context of systemic inflammation. Here, we show that chemical mimetics of the N-degron Nt-Arg pathway (p62 ligands) decreased mortality in sepsis and inhibited pathological inflammation by activating mitophagy and immunometabolic remodeling. The p62 ligands alleviated systemic inflammation in a mouse model of lipopolysaccharide (LPS)-induced septic shock and in the cecal ligation and puncture model of sepsis. In macrophages, the p62 ligand attenuated the production of proinflammatory cytokines and chemokines in response to various innate immune stimuli. Mechanistically, the p62 ligand augmented LPS-induced mitophagy and inhibited the production of mitochondrial reactive oxygen species in macrophages. The p62 ligand-mediated anti-inflammatory, antioxidative, and mitophagy-activating effects depended on p62. In parallel, the p62 ligand significantly downregulated the LPS-induced upregulation of aerobic glycolysis and lactate production. Together, our findings demonstrate that p62 ligands play a critical role in the regulation of inflammatory responses by orchestrating mitophagy and immunometabolic remodeling.
Mesh-Begriff(e)	Animals ; Mice ; Mitophagy ; Ligands ; Lipopolysaccharides/pharmacology ; Autophagy ; Inflammation/drug therapy ; Sepsis/drug therapy
Chemische Substanzen	Ligands ; Lipopolysaccharides
Sprache	Englisch
Erscheinungsdatum	2023-02-01
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/s12276-023-00929-x
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Pexophagy: Molecular Mechanisms and Implications for Health and Diseases.

Cho, Dong-Hyung / Kim, Yi Sak / Jo, Doo Sin / Choe, Seong-Kyu / Jo, Eun-Kyeong

Molecules and cells

2018 Band 41, Heft 1, Seite(n) 55–64

Abstract: Autophagy is an intracellular degradation pathway for large protein aggregates and damaged organelles. Recent studies have indicated that autophagy targets cargoes through a selective degradation pathway called selective autophagy. Peroxisomes are ... ...

Abstract	Autophagy is an intracellular degradation pathway for large protein aggregates and damaged organelles. Recent studies have indicated that autophagy targets cargoes through a selective degradation pathway called selective autophagy. Peroxisomes are dynamic organelles that are crucial for health and development. Pexophagy is selective autophagy that targets peroxisomes and is essential for the maintenance of homeostasis of peroxisomes, which is necessary in the prevention of various peroxisome-related disorders. However, the mechanisms by which pexophagy is regulated and the key players that induce and modulate pexophagy are largely unknown. In this review, we focus on our current understanding of how pexophagy is induced and regulated, and the selective adaptors involved in mediating pexophagy. Furthermore, we discuss current findings on the roles of pexophagy in physiological and pathological responses, which provide insight into the clinical relevance of pexophagy regulation. Understanding how pexophagy interacts with various biological functions will provide fundamental insights into the function of pexophagy and facilitate the development of novel therapeutics against peroxisomal dysfunction-related diseases.
Mesh-Begriff(e)	Animals ; Autophagy ; Endoplasmic Reticulum/metabolism ; Humans ; Membrane Proteins/metabolism ; Mitochondria/metabolism ; Models, Biological ; Peroxisomes/metabolism ; Zellweger Syndrome/metabolism ; Zellweger Syndrome/pathology
Chemische Substanzen	Membrane Proteins
Sprache	Englisch
Erscheinungsdatum	2018-01-23
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Review
ZDB-ID	1148964-9
ISSN	0219-1032 ; 1016-8478
ISSN (online)	0219-1032
ISSN	1016-8478
DOI	10.14348/molcells.2018.2245
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Triamterene induces autophagic degradation of lysosome by exacerbating lysosomal integrity

Park, Na Yeon / Jo, Doo Sin / Kim, Yong Hwan / Bae, Ji-Eun / Kim, Joon Bum / Park, Hyun Jun / Choi, Ji Yeon / Lee, Ha Jung / Chang, Jeong Ho / Bunch, Heeyoun / Jeon, Hong Bae / Jung, Yong-Keun / Cho, Dong-Hyung

Archives of pharmacal research. 2021 June, v. 44, no. 6

2021

Abstract: The maintenance of lysosomal integrity is essential for lysosome function and cell fate. Damaged lysosomes are degraded by lysosomal autophagy, lysophagy. The mechanism underlying lysophagy remains largely unknown; this study aimed to contribute to the ... ...

Abstract	The maintenance of lysosomal integrity is essential for lysosome function and cell fate. Damaged lysosomes are degraded by lysosomal autophagy, lysophagy. The mechanism underlying lysophagy remains largely unknown; this study aimed to contribute to the understanding of this topic. A cell-based screening system was used to identify novel lysophagy modulators. Triamterene (6-phenylpteridine-2,4,7-triamine) was identified as one of the most potent lysophagy inducers from the screening process. We found that triamterene causes lysosomal rupture without affecting other cellular organelles and increases autophagy flux in HepG2 cells. Damaged lysosomes in triamterene-treated cells were removed by autophagy-mediated pathway, which was inhibited by depletion of the autophagy regulator, ATG5 or SQSTM1. In addition, treatment of triamterene decreased the integrity of lysosome and cell viability, which were rescued by removing the triamterene treatment in HepG2 cells. Hence, our data suggest that triamterene is a novel lysophagy inducer through the disruption of lysosomal integrity.
Schlagwörter	cell viability ; lysosomes ; macroautophagy ; research
Sprache	Englisch
Erscheinungsverlauf	2021-06
Umfang	p. 621-631.
Erscheinungsort	Pharmaceutical Society of Korea
Dokumenttyp	Artikel
ZDB-ID	447623-2
ISSN	1976-3786 ; 0253-6269
ISSN (online)	1976-3786
ISSN	0253-6269
DOI	10.1007/s12272-021-01335-5
Datenquelle	NAL Katalog (AGRICOLA)

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