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Article ; Online: A SNX1-SNX2-VAPB partnership regulates endosomal membrane rewiring in response to nutritional stress.

Da Graça, Juliane / Charles, Juliette / Djebar, Morgane / Alvarez-Valadez, Karla / Botti, Joëlle / Morel, Etienne

Life science alliance

2022 Volume 6, Issue 3

Abstract: Nutrient deprivation ("starvation") is a major catabolic stress faced by mammalian cells in both pathological and physiological situations. Starvation induces autophagosome biogenesis in the immediate vicinity of ER and leads to lysosome spatial ... ...

Abstract	Nutrient deprivation ("starvation") is a major catabolic stress faced by mammalian cells in both pathological and physiological situations. Starvation induces autophagosome biogenesis in the immediate vicinity of ER and leads to lysosome spatial repositioning, but little is known about the consequences of nutritional stress on endosomes. Here, we report that starvation induces tethering of endosomal tubules to ER subregions, fostering autophagosome assembly. We show that this endosomal membrane generation is regulated by sorting nexin 1 (SNX1) protein and is important for the autophagic response. These newly formed SNX1 endosomal tubules establish connections with ER subdomains engaged in early autophagic machinery mobilization. Such endosome-ER transient tethers are regulated by a local dialog between SNX2, an endosomal partner of SNX1, and VAPB, an ER protein associated with autophagy initiation stage regulation. We propose that in a very early response to starvation, SNX1 and SNX2 cooperation induces and regulates endosomal membrane tubulation towards VAPB-positive ER subdomains involved in autophagosome biogenesis, highlighting the contribution of early endosomes in the cellular response to nutritional stress.
MeSH term(s)	Animals ; Carrier Proteins/metabolism ; Vesicular Transport Proteins/genetics ; Vesicular Transport Proteins/metabolism ; Endosomes/metabolism ; Intracellular Membranes/metabolism ; Lysosomes/metabolism ; Mammals/metabolism
Chemical Substances	Carrier Proteins ; Vesicular Transport Proteins
Language	English
Publishing date	2022-12-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202201652
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Article: Monitoring lipophagy in kidney epithelial cells in response to shear stress.

Roccio, Federica / Claude-Taupin, Aurore / Botti, Joëlle / Morel, Etienne / Codogno, Patrice / Dupont, Nicolas

Methods in cell biology

2021 Volume 164, Page(s) 11–25

Abstract: Mechanical stress has been shown to induce the degradation of lipid droplets in kidney epithelial cells. Here, we illustrate the technical equipment and devices that are currently used in our laboratory to apply shear stress on cells. We provide a ... ...

Abstract	Mechanical stress has been shown to induce the degradation of lipid droplets in kidney epithelial cells. Here, we illustrate the technical equipment and devices that are currently used in our laboratory to apply shear stress on cells. We provide a detailed protocol to monitor lipophagy in response to shear stress. The aim of this review is to guide and help people understand the challenges in studying acidic lipolysis in cells subjected to fluid flow.
MeSH term(s)	Autophagy ; Epithelial Cells ; Humans ; Kidney ; Lipid Droplets/metabolism ; Lipid Metabolism ; Stress, Mechanical
Language	English
Publishing date	2021-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	0091-679X
ISSN	0091-679X
DOI	10.1016/bs.mcb.2020.12.003
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Article ; Online: The primary cilium protein folliculin is part of the autophagy signaling pathway to regulate epithelial cell size in response to fluid flow.

Zemirli, Naïma / Boukhalfa, Asma / Dupont, Nicolas / Botti, Joëlle / Codogno, Patrice / Morel, Etienne

Cell stress

2019 Volume 3, Issue 3, Page(s) 100–109

Abstract: Autophagy is a conserved molecular pathway directly involved in the degradation and recycling of intracellular components. Autophagy is associated with a response to stress situations, such as nutrients deficit, chemical toxicity, mechanical stress or ... ...

Abstract	Autophagy is a conserved molecular pathway directly involved in the degradation and recycling of intracellular components. Autophagy is associated with a response to stress situations, such as nutrients deficit, chemical toxicity, mechanical stress or microbial host defense. We have recently shown that primary cilium-dependent autophagy is important to control kidney epithelial cell size in response to fluid flow induced shear stress. Here we show that the ciliary protein folliculin (FLCN) actively participates to the signaling cascade leading to the stimulation of fluid flow-dependent autophagy upstream of the cell size regulation in HK2 kidney epithelial cells. The knockdown of FLCN induces a shortening of the primary cilium, inhibits the activation of AMPK and the recruitment of the autophagy protein ATG16L1 at the primary cilium. Altogether, our results suggest that FLCN is essential in the dialog between autophagy and the primary cilium in epithelial cells to integrate shear stress-dependent signaling.
Language	English
Publishing date	2019-02-25
Publishing country	Austria
Document type	Journal Article
ISSN	2523-0204
ISSN (online)	2523-0204
DOI	10.15698/cst2019.03.180
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Article ; Online: The primary cilium protein folliculin is part of the autophagy signaling pathway to regulate epithelial cell size in response to fluid flow

Naïma Zemirli / Asma Boukhalfa / Nicolas Dupont / Joëlle Botti / Patrice Codogno / Etienne Morel

Cell Stress, Vol 3, Iss 3, Pp 100-

2019 Volume 109

Abstract	Autophagy is a conserved molecular pathway directly involved in the degradation and recycling of intracellular components. Autophagy is associated with a response to stress situations, such as nutrients deficit, chemical toxicity, mechanical stress or microbial host defense. We have recently shown that primary cilium-dependent autophagy is important to control kidney epithelial cell size in response to fluid flow induced shear stress. Here we show that the ciliary protein folliculin (FLCN) actively participates to the signaling cascade leading to the stimulation of fluid flow-dependent autophagy upstream of the cell size regulation in HK2 kidney epithelial cells. The knockdown of FLCN induces a shortening of the primary cilium, inhibits the activation of AMPK and the recruitment of the autophagy protein ATG16L1 at the primary cilium. Altogether, our results suggest that FLCN is essential in the dialog between autophagy and the primary cilium in epithelial cells to integrate shear stress-dependent signaling.
Keywords	fluid flow ; shear stress ; autophagy ; folliculin ; primary cilium ; Medicine ; R ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2019-02-01T00:00:00Z
Publisher	Shared Science Publishers OG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: To be or not to be cell autonomous? Autophagy says both.

Fenouille, Nina / Nascimbeni, Anna Chiara / Botti-Millet, Joëlle / Dupont, Nicolas / Morel, Etienne / Codogno, Patrice

Essays in biochemistry

2017 Volume 61, Issue 6, Page(s) 649–661

Abstract: Although cells are a part of the whole organism, classical dogma emphasizes that individual cells function autonomously. Many physiological and pathological conditions, including cancer, and metabolic and neurodegenerative diseases, have been considered ... ...

Abstract	Although cells are a part of the whole organism, classical dogma emphasizes that individual cells function autonomously. Many physiological and pathological conditions, including cancer, and metabolic and neurodegenerative diseases, have been considered mechanistically as cell-autonomous pathologies, meaning those that damage or defect within a selective population of affected cells suffice to produce disease. It is becoming clear, however, that cells and cellular processes cannot be considered in isolation. Best known for shuttling cytoplasmic content to the lysosome for degradation and repurposing of recycled building blocks such as amino acids, nucleotides, and fatty acids, autophagy serves a housekeeping function in every cell and plays key roles in cell development, immunity, tissue remodeling, and homeostasis with the surrounding environment and the distant organs. In this review, we underscore the importance of taking interactions with the microenvironment into consideration while addressing the cell autonomous and non-autonomous functions of autophagy between cells of the same and different types and in physiological and pathophysiological situations.
MeSH term(s)	Animals ; Autophagy/genetics ; Autophagy/physiology ; Cytoplasm/metabolism ; Humans ; Lysosomes/genetics ; Lysosomes/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism
Language	English
Publishing date	2017--12
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	1744-1358 ; 0071-1365
ISSN (online)	1744-1358
ISSN	0071-1365
DOI	10.1042/EBC20170025
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Article ; Online: Novel function of PiT1/SLC20A1 in LPS-related inflammation and wound healing.

Koumakis, Eugénie / Millet-Botti, Joëlle / Benna, Jamel El / Leroy, Christine / Boitez, Valérie / Codogno, Patrice / Friedlander, Gérard / Forand, Anne

Scientific reports

2019 Volume 9, Issue 1, Page(s) 1808

Abstract: PiT1/SLC20A1 is an inorganic phosphate transporter with additional functions including the regulation of TNFα-induced apoptosis, erythropoiesis, cell proliferation and insulin signaling. Recent data suggest a relationship between PiT1 and NF-κB-dependent ...

Abstract	PiT1/SLC20A1 is an inorganic phosphate transporter with additional functions including the regulation of TNFα-induced apoptosis, erythropoiesis, cell proliferation and insulin signaling. Recent data suggest a relationship between PiT1 and NF-κB-dependent inflammation: (i) Pit1 mRNA is up-regulated in the context of NF-κB pathway activation; (ii) NF-κB target gene transcription is decreased in PiT1-deficient conditions. This led us to investigate the role of PiT1 in lipopolysaccharide (LPS)-induced inflammation. MCP-1 and IL-6 concentrations were impaired in PiT1-deficient bone marrow derived macrophages (BMDMs) upon LPS stimulation. Lower MCP-1 and IL-6 serum levels were observed in Mx1-Cre; Pit1
MeSH term(s)	Animals ; Apoptosis/drug effects ; Inflammation/chemically induced ; Inflammation/metabolism ; Lipopolysaccharides/pharmacology ; Macrophages/drug effects ; Macrophages/metabolism ; Male ; Mice ; NADPH Oxidase 2/metabolism ; NF-kappa B/metabolism ; Peritonitis/chemically induced ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects ; Sodium-Phosphate Cotransporter Proteins, Type III/metabolism ; Thioglycolates/toxicity ; Transcription Factor Pit-1/genetics ; Transcription Factor Pit-1/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Wound Healing/drug effects
Chemical Substances	Lipopolysaccharides ; NF-kappa B ; Pit1 protein, mouse ; Reactive Oxygen Species ; Slc20a1 protein, mouse ; Sodium-Phosphate Cotransporter Proteins, Type III ; Thioglycolates ; Transcription Factor Pit-1 ; Tumor Necrosis Factor-alpha ; NADPH Oxidase 2 (EC 1.6.3.-)
Language	English
Publishing date	2019-02-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-37551-1
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Article ; Online: Fine-tuning autophagy: from transcriptional to posttranslational regulation.

Botti-Millet, Joëlle / Nascimbeni, Anna Chiara / Dupont, Nicolas / Morel, Etienne / Codogno, Patrice

American journal of physiology. Cell physiology

2016 Volume 311, Issue 3, Page(s) C351–62

Abstract: Macroautophagy (hereafter called autophagy) is a vacuolar lysosomal pathway for degradation of intracellular material in eukaryotic cells. Autophagy plays crucial roles in tissue homeostasis, in adaptation to stress situations, and in immune and ... ...

Abstract	Macroautophagy (hereafter called autophagy) is a vacuolar lysosomal pathway for degradation of intracellular material in eukaryotic cells. Autophagy plays crucial roles in tissue homeostasis, in adaptation to stress situations, and in immune and inflammatory responses. Alteration of autophagy is associated with cancer, diabetes and obesity, cardiovascular disease, neurodegenerative disease, autoimmune disease, infection, and chronic inflammatory disease. Autophagy is controlled by autophagy-related (ATG) proteins that act in a coordinated manner to build up the initial autophagic vacuole named the autophagosome. It is now known that the activities of ATG proteins are modulated by posttranslational modifications such as phosphorylation, ubiquitination, and acetylation. Moreover, transcriptional and epigenetic controls are involved in the regulation of autophagy in stress situations. Here we summarize and discuss how posttranslational modifications and transcriptional and epigenetic controls regulate the involvement of autophagy in the proteostasis network.
MeSH term(s)	Animals ; Autophagy/genetics ; Epigenesis, Genetic/genetics ; Homeostasis/genetics ; Humans ; Protein Processing, Post-Translational/genetics ; Transcription, Genetic/genetics
Language	English
Publishing date	2016-06-22
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00129.2016
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Article ; Online: Autophagy: A Druggable Process.

Morel, Etienne / Mehrpour, Maryam / Botti, Joëlle / Dupont, Nicolas / Hamaï, Ahmed / Nascimbeni, Anna Chiara / Codogno, Patrice

Annual review of pharmacology and toxicology

2017 Volume 57, Page(s) 375–398

Abstract: Macroautophagy (hereafter called autophagy) is a vacuolar, lysosomal pathway for catabolism of intracellular material that is conserved among eukaryotic cells. Autophagy plays a crucial role in tissue homeostasis, adaptation to stress situations, immune ... ...

Abstract	Macroautophagy (hereafter called autophagy) is a vacuolar, lysosomal pathway for catabolism of intracellular material that is conserved among eukaryotic cells. Autophagy plays a crucial role in tissue homeostasis, adaptation to stress situations, immune responses, and the regulation of the inflammatory response. Blockade or uncontrolled activation of autophagy is associated with cancer, diabetes, obesity, cardiovascular disease, neurodegenerative disease, autoimmune disease, infection, and chronic inflammatory disease. During the past decade, researchers have made major progress in understanding the three levels of regulation of autophagy in mammalian cells: signaling, autophagosome formation, and autophagosome maturation and lysosomal degradation. As we discuss in this review, each of these levels is potentially druggable, and, depending on the indication, may be able to stimulate or inhibit autophagy. We also summarize the different modulators of autophagy and their potential and limitations in the treatment of life-threatening diseases.
Language	English
Publishing date	2017-01-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	196587-6
ISSN	1545-4304 ; 0362-1642
ISSN (online)	1545-4304
ISSN	0362-1642
DOI	10.1146/annurev-pharmtox-010716-104936
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Article ; Online: Regulation of autophagy by extracellular matrix glycoproteins in HeLa cells.

Tuloup-Minguez, Véronique / Greffard, Anne / Codogno, Patrice / Botti, Joëlle

Autophagy

2011 Volume 7, Issue 1, Page(s) 27–39

Abstract: Macroautophagy is a major lysosomal degradation pathway for cellular components in eukaryotic cells. Baseline macroautophagy is important for quality control of the cytoplasm in order to avoid the accumulation of cytotoxic products. Its stimulation by ... ...

Abstract	Macroautophagy is a major lysosomal degradation pathway for cellular components in eukaryotic cells. Baseline macroautophagy is important for quality control of the cytoplasm in order to avoid the accumulation of cytotoxic products. Its stimulation by various stressful situations, including nutrient starvation, is important in maintaining cell survival. Here we demonstrate that macroautophagy is regulated differently depending on whether HeLa cells adhere to collagen I or collagen IV, proteins typical of connective tissue and basal membrane, respectively. We observed that the basal levels of macroautophagy were higher in cells plated on collagen IV than in cells plated on collagen I or on uncoated substrate. However, the stimulation of macroautophagy by nutrient starvation, as reflected by the buildup of autophagosomes and the increase in the autophagic flux, was higher in cells plated on collagen I than in cells plated on collagen IV. These contrasting results were not due to differences in the starvation-dependent inhibition of mTOR complex 1 signaling. Interestingly, cells plated on collagen IV formed numerous focal adhesions (FAs), whereas fewer FAs were observed in cells plated on the other substrates. This implies that focal adhesion kinase (FAK) was more robustly activated by collagen IV. Silencing the expression of FAK by siRNA in cells plated on collagen IV shifted the autophagic phenotype of these cells to an "uncoated substrate autophagic phenotype" under both basal and starvation-induced conditions. Moreover, cells plated on collagen IV were less dependent on autophagy to survive in the absence of nutrients. We conclude that extracellular matrix components can modulate macroautophagy and mitigate its role in cell survival.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Autophagy/drug effects ; Cattle ; Cell Adhesion/drug effects ; Cell Movement/drug effects ; Cell Shape/drug effects ; Cell Survival/drug effects ; Collagen Type IV/pharmacology ; Extracellular Matrix Proteins/metabolism ; Focal Adhesion Protein-Tyrosine Kinases/antagonists & inhibitors ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Focal Adhesions/drug effects ; Focal Adhesions/metabolism ; Gene Silencing/drug effects ; Glycoproteins/metabolism ; HeLa Cells ; Humans ; Integrins/metabolism ; Mechanistic Target of Rapamycin Complex 1 ; Multiprotein Complexes ; Plastics/pharmacology ; Proteins/metabolism ; Sequestosome-1 Protein ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases
Chemical Substances	Adaptor Proteins, Signal Transducing ; Collagen Type IV ; Extracellular Matrix Proteins ; Glycoproteins ; Integrins ; Multiprotein Complexes ; Plastics ; Proteins ; SQSTM1 protein, human ; Sequestosome-1 Protein ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2011-01-01
Publishing country	United States
Document type	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	10.4161/auto.7.1.13851
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Article ; Online: Autophagy modulates cell migration and β1 integrin membrane recycling.

Tuloup-Minguez, Véronique / Hamaï, Ahmed / Greffard, Anne / Nicolas, Valérie / Codogno, Patrice / Botti, Joëlle

Cell cycle (Georgetown, Tex.)

2013 Volume 12, Issue 20, Page(s) 3317–3328

Abstract: Cell migration is dependent on a series of integrated cellular events including the membrane recycling of the extracellular matrix receptor integrins. In this paper, we investigate the role of autophagy in regulating cell migration. In a wound-healing ... ...

Abstract	Cell migration is dependent on a series of integrated cellular events including the membrane recycling of the extracellular matrix receptor integrins. In this paper, we investigate the role of autophagy in regulating cell migration. In a wound-healing assay, we observed that autophagy was reduced in cells at the leading edge than in cells located rearward. These differences in autophagy were correlated with the robustness of MTOR activity. The spatial difference in the accumulation of autophagic structures was not detected in rapamycin-treated cells, which had less migration capacity than untreated cells. In contrast, the knockdown of the autophagic protein ATG7 stimulated cell migration of HeLa cells. Accordingly, atg3(-/-) and atg5(-/-) MEFs have greater cell migration properties than their wild-type counterparts. Stimulation of autophagy increased the co-localization of β1 integrin-containing vesicles with LC3-stained autophagic vacuoles. Moreover, inhibition of autophagy slowed down the lysosomal degradation of internalized β1 integrins and promoted its membrane recycling. From these findings, we conclude that autophagy regulates cell migration, a central mechanism in cell development, angiogenesis, and tumor progression, by mitigating the cell surface expression of β1 integrins.
MeSH term(s)	Animals ; Autophagy ; Autophagy-Related Protein 7 ; Cell Adhesion ; Cell Membrane/metabolism ; Cell Movement ; Endocytosis ; Green Fluorescent Proteins/metabolism ; HeLa Cells ; Humans ; Integrin beta1/metabolism ; Lysosomes/metabolism ; Mice ; Microtubule-Associated Proteins/metabolism ; Phagosomes/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Ubiquitin-Activating Enzymes/metabolism
Chemical Substances	Integrin beta1 ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; Green Fluorescent Proteins (147336-22-9) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; ATG7 protein, human (EC 6.2.1.45) ; Autophagy-Related Protein 7 (EC 6.2.1.45) ; Ubiquitin-Activating Enzymes (EC 6.2.1.45)
Language	English
Publishing date	2013-09-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.26298
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