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Article ; Online: Activating the abscission checkpoint: Top2α senses chromatin bridges in cytokinesis: Top2α binds to DNA knots on chromatin bridges to activate the abscission checkpoint in human cells.

Petsalaki, Eleni / Zachos, George

BioEssays : news and reviews in molecular, cellular and developmental biology

2024 Volume 46, Issue 5, Page(s) e2400011

Abstract: How chromatin bridges are detected by the abscission checkpoint during mammalian cell division is unknown. Here, we discuss recent findings from our lab showing that the DNA topoisomerase IIα (Top2α) enzyme binds to catenated ("knotted") DNA next to the ... ...

Abstract	How chromatin bridges are detected by the abscission checkpoint during mammalian cell division is unknown. Here, we discuss recent findings from our lab showing that the DNA topoisomerase IIα (Top2α) enzyme binds to catenated ("knotted") DNA next to the midbody and forms abortive Top2-DNA cleavage complexes (Top2ccs) on chromatin bridges. Top2ccs are then processed by the proteasome to promote localization of the DNA damage sensor protein Rad17 to Top2-generated double-strand DNA ends on DNA knots. In turn, Rad17 promotes local recruitment of the MRN protein complex and downstream ATM-Chk2-INCENP signaling to delay abscission and prevent chromatin bridge breakage in cytokinesis.
MeSH term(s)	Humans ; DNA Topoisomerases, Type II/metabolism ; Cytokinesis/physiology ; Chromatin/metabolism ; DNA-Binding Proteins/metabolism ; Poly-ADP-Ribose Binding Proteins/metabolism ; DNA/metabolism ; Signal Transduction
Chemical Substances	DNA Topoisomerases, Type II (EC 5.99.1.3) ; Chromatin ; DNA-Binding Proteins ; Poly-ADP-Ribose Binding Proteins ; TOP2A protein, human (EC 5.99.1.3) ; DNA (9007-49-2)
Language	English
Publishing date	2024-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.202400011
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Article: An ATM-CHK2-INCENP pathway prevents chromatin breakage by regulating the abscission checkpoint.

Petsalaki, Eleni / Zachos, George

Molecular & cellular oncology

2021 Volume 8, Issue 2, Page(s) 1877999

Abstract: In response to chromatin bridges, the chromosomal passenger complex (CPC) delays completion of cytokinesis (abscission) to prevent chromosome breakage. Here, we discuss recent findings from our lab showing that an ATM-CHK2-INCENP pathway imposes the ... ...

Abstract	In response to chromatin bridges, the chromosomal passenger complex (CPC) delays completion of cytokinesis (abscission) to prevent chromosome breakage. Here, we discuss recent findings from our lab showing that an ATM-CHK2-INCENP pathway imposes the abscission checkpoint in human cells by regulating CPC midbody-localization.
Language	English
Publishing date	2021-02-08
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2021.1877999
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Article ; Online: The Abscission Checkpoint: A Guardian of Chromosomal Stability.

Petsalaki, Eleni / Zachos, George

Cells

2021 Volume 10, Issue 12

Abstract: The abscission checkpoint contributes to the fidelity of chromosome segregation by delaying completion of cytokinesis (abscission) when there is chromatin lagging in the intercellular bridge between dividing cells. Although additional triggers of an ... ...

Abstract	The abscission checkpoint contributes to the fidelity of chromosome segregation by delaying completion of cytokinesis (abscission) when there is chromatin lagging in the intercellular bridge between dividing cells. Although additional triggers of an abscission checkpoint-delay have been described, including nuclear pore defects, replication stress or high intercellular bridge tension, this review will focus only on chromatin bridges. In the presence of such abnormal chromosomal tethers in mammalian cells, the abscission checkpoint requires proper localization and optimal kinase activity of the Chromosomal Passenger Complex (CPC)-catalytic subunit Aurora B at the midbody and culminates in the inhibition of Endosomal Sorting Complex Required for Transport-III (ESCRT-III) components at the abscission site to delay the final cut. Furthermore, cells with an active checkpoint stabilize the narrow cytoplasmic canal that connects the two daughter cells until the chromatin bridges are resolved. Unsuccessful resolution of chromatin bridges in checkpoint-deficient cells or in cells with unstable intercellular canals can lead to chromatin bridge breakage or tetraploidization by regression of the cleavage furrow. In turn, these outcomes can lead to accumulation of DNA damage, chromothripsis, generation of hypermutation clusters and chromosomal instability, which are associated with cancer formation or progression. Recently, many important questions regarding the mechanisms of the abscission checkpoint have been investigated, such as how the presence of chromatin bridges is signaled to the CPC, how Aurora B localization and kinase activity is regulated in late midbodies, the signaling pathways by which Aurora B implements the abscission delay, and how the actin cytoskeleton is remodeled to stabilize intercellular canals with DNA bridges. Here, we review recent progress toward understanding the mechanisms of the abscission checkpoint and its role in guarding genome integrity at the chromosome level, and consider its potential implications for cancer therapy.
MeSH term(s)	Animals ; Cell Cycle Checkpoints ; Chromatin/metabolism ; Chromosomal Instability ; Cytokinesis ; Humans ; Models, Biological ; Signal Transduction
Chemical Substances	Chromatin
Language	English
Publishing date	2021-11-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10123350
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Article ; Online: Cell division: TIPs for shaping Aurora B activity.

Zachos, George

Nature chemical biology

2016 Volume 12, Issue 4, Page(s) 204–205

MeSH term(s)	Aurora Kinase B/metabolism ; Chromosome Segregation/physiology ; Histone Acetyltransferases/metabolism ; Humans ; Kinetochores/enzymology ; Mitosis/physiology
Chemical Substances	Histone Acetyltransferases (EC 2.3.1.48) ; Aurora Kinase B (EC 2.7.11.1)
Language	English
Publishing date	2016-04
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2202962-X
ISSN	1552-4469 ; 1552-4450
ISSN (online)	1552-4469
ISSN	1552-4450
DOI	10.1038/nchembio.2041
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Article ; Online: The abscission checkpoint senses chromatin bridges through Top2α recruitment to DNA knots.

Petsalaki, Eleni / Balafouti, Sofia / Kyriazi, Athina A / Zachos, George

The Journal of cell biology

2023 Volume 222, Issue 11

Abstract: In response to chromatin bridges, the abscission checkpoint delays completion of cytokinesis to prevent chromosome breakage or tetraploidization. Here, we show that spontaneous or replication stress-induced chromatin bridges exhibit "knots" of catenated ... ...

Abstract	In response to chromatin bridges, the abscission checkpoint delays completion of cytokinesis to prevent chromosome breakage or tetraploidization. Here, we show that spontaneous or replication stress-induced chromatin bridges exhibit "knots" of catenated and overtwisted DNA next to the midbody. Topoisomerase IIα (Top2α) forms abortive Top2-DNA cleavage complexes (Top2ccs) on DNA knots; furthermore, impaired Top2α-DNA cleavage activity correlates with chromatin bridge breakage in cytokinesis. Proteasomal degradation of Top2ccs is required for Rad17 localization to Top2-generated double-strand DNA ends on DNA knots; in turn, Rad17 promotes local recruitment of the MRN complex and downstream ATM-Chk2-INCENP signaling to delay abscission and prevent chromatin breakage. In contrast, dicentric chromosomes that do not exhibit knotted DNA fail to activate the abscission checkpoint in human cells. These findings are the first to describe a mechanism by which the abscission checkpoint detects chromatin bridges, through generation of abortive Top2ccs on DNA knots, to preserve genome integrity.
MeSH term(s)	Humans ; Cell Cycle Proteins/genetics ; Cell Nucleus ; Chromatin/genetics ; Chromosome Breakage ; Cytokinesis ; DNA/genetics ; Cell Cycle Checkpoints ; DNA Topoisomerases, Type II/genetics
Chemical Substances	Cell Cycle Proteins ; Chromatin ; DNA (9007-49-2) ; Rad17 protein, human ; TOP2A protein, human (EC 5.99.1.3) ; DNA Topoisomerases, Type II (EC 5.99.1.3)
Language	English
Publishing date	2023-08-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.202303123
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Article: Descending aorta to right atrial fistula: Transcatheter embolization of a very rare anomaly with coils.

Despotopoulos, Stefanos / Apostolopoulou, Sotiria / Vagenakis, George / Kanakis, Meletios / Samanidis, George / Zachos, Panagiotis / Chatziantoniou, Anastasios / Papagiannis, John / Rammos, Spyridon / Tsoutsinos, Alexandros

Clinical case reports

2024 Volume 12, Issue 2, Page(s) e8529

Abstract: Key clinical message: Descending aorta to right atrial (RA) fistula is a rare and distinct clinical entity mimicking patent ductus arteriosus (PDA) and it may lead to rapid development of pulmonary vascular disease. Correct diagnosis and treatment, ... ...

Abstract	Key clinical message: Descending aorta to right atrial (RA) fistula is a rare and distinct clinical entity mimicking patent ductus arteriosus (PDA) and it may lead to rapid development of pulmonary vascular disease. Correct diagnosis and treatment, especially in the presence of other congenital heart defects, is very important. Interventional management is the treatment of choice. Abstract: We present a case report of a trisomy 21 infant with atrial and ventricular septal defects and small patent ductus arteriosus (PDA) complicated by the presence of descending aorta to right atrial (RA) fistula with large left to right shunt leading to rapid increase in pulmonary vascular resistance. Transcatheter occlusion of the fistula followed by closure of the PDA with Nit-Occlud coil systems led to decreased pulmonary pressure and resistance permitting successful surgical repair of the patient's intracardiac defects with good outcome over 3 years of follow-up. Descending aorta to RA fistula is a rare and distinct clinical entity mimicking PDA and its correct diagnosis and treatment, especially in the presence of other congenital heart defects, is very important as it may lead to rapid development of pulmonary vascular disease.
Language	English
Publishing date	2024-02-13
Publishing country	England
Document type	Case Reports
ZDB-ID	2740234-4
ISSN	2050-0904
ISSN	2050-0904
DOI	10.1002/ccr3.8529
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Article ; Online: DNA damage response proteins regulating mitotic cell division: double agents preserving genome stability.

Petsalaki, Eleni / Zachos, George

The FEBS journal

2020 Volume 287, Issue 9, Page(s) 1700–1721

Abstract: The DNA damage response recognizes DNA lesions and coordinates a cell cycle arrest with the repair of the damaged DNA, or removal of the affected cells to prevent the passage of genetic alterations to the next generation. The mitotic cell division, on ... ...

Abstract	The DNA damage response recognizes DNA lesions and coordinates a cell cycle arrest with the repair of the damaged DNA, or removal of the affected cells to prevent the passage of genetic alterations to the next generation. The mitotic cell division, on the other hand, is a series of processes that aims to accurately segregate the genomic material from the maternal to the two daughter cells. Despite their great importance in safeguarding genomic integrity, the DNA damage response and the mitotic cell division were long viewed as unrelated processes, mainly because animal cells that are irradiated during mitosis continue cell division without repairing the broken chromosomes. However, recent studies have demonstrated that DNA damage proteins play an important role in mitotic cell division. This is performed through regulation of the onset of mitosis, mitotic spindle formation, correction of misattached kinetochore-microtubules, spindle checkpoint signaling, or completion of cytokinesis (abscission), in the absence of DNA damage. In this review, we summarize the roles of DNA damage proteins in unperturbed mitosis, analyze the molecular mechanisms involved, and discuss the potential implications of these findings in cancer therapy.
MeSH term(s)	Animals ; Cell Cycle Proteins/metabolism ; Cell Division ; DNA Damage ; Genomic Instability ; Humans ; Mitosis/genetics
Chemical Substances	Cell Cycle Proteins
Language	English
Publishing date	2020-02-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15240
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Article ; Online: An ATM-Chk2-INCENP pathway activates the abscission checkpoint.

Petsalaki, Eleni / Zachos, George

The Journal of cell biology

2020 Volume 220, Issue 2

Abstract: During cell division, in response to chromatin bridges, the chromosomal passenger complex (CPC) delays abscission to prevent chromosome breakage or tetraploidization. Here, we show that inhibition of ATM or Chk2 kinases impairs CPC localization to the ... ...

Abstract	During cell division, in response to chromatin bridges, the chromosomal passenger complex (CPC) delays abscission to prevent chromosome breakage or tetraploidization. Here, we show that inhibition of ATM or Chk2 kinases impairs CPC localization to the midbody center, accelerates midbody resolution in normally segregating cells, and correlates with premature abscission and chromatin breakage in cytokinesis with trapped chromatin. In cultured human cells, ATM activates Chk2 at late midbodies. In turn, Chk2 phosphorylates human INCENP-Ser91 to promote INCENP binding to Mklp2 kinesin and CPC localization to the midbody center through Mklp2 association with Cep55. Expression of truncated Mklp2 that does not bind to Cep55 or nonphosphorylatable INCENP-Ser91A impairs CPC midbody localization and accelerates abscission. In contrast, expression of phosphomimetic INCENP-Ser91D or a chimeric INCENP protein that is targeted to the midbody center rescues the abscission delay in Chk2-deficient or ATM-deficient cells. Furthermore, the Mre11-Rad50-Nbs1 complex is required for ATM activation at the midbody in cytokinesis with chromatin bridges. These results identify an ATM-Chk2-INCENP pathway that imposes the abscission checkpoint by regulating CPC midbody localization.
MeSH term(s)	Ataxia Telangiectasia Mutated Proteins/metabolism ; Aurora Kinase B/metabolism ; Cell Cycle Checkpoints ; Cell Proliferation ; Checkpoint Kinase 2/antagonists & inhibitors ; Checkpoint Kinase 2/metabolism ; Chromatin/metabolism ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosome Segregation ; Cytokinesis ; Green Fluorescent Proteins/metabolism ; HeLa Cells ; Humans ; Kinesin/metabolism ; MRE11 Homologue Protein/metabolism ; Multiprotein Complexes/metabolism ; Mutation/genetics ; Phosphorylation ; Signal Transduction
Chemical Substances	Chromatin ; Chromosomal Proteins, Non-Histone ; INCENP protein, human ; KIF20A protein, human ; MRE11 protein, human ; Multiprotein Complexes ; Green Fluorescent Proteins (147336-22-9) ; Checkpoint Kinase 2 (EC 2.7.1.11) ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Aurora Kinase B (EC 2.7.11.1) ; CHEK2 protein, human (EC 2.7.11.1) ; MRE11 Homologue Protein (EC 3.1.-) ; Kinesin (EC 3.6.4.4)
Language	English
Publishing date	2020-12-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.202008029
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Article ; Online: The Abscission Checkpoint

Eleni Petsalaki / George Zachos

Cells, Vol 10, Iss 3350, p

A Guardian of Chromosomal Stability

2021 Volume 3350

Abstract	The abscission checkpoint contributes to the fidelity of chromosome segregation by delaying completion of cytokinesis (abscission) when there is chromatin lagging in the intercellular bridge between dividing cells. Although additional triggers of an abscission checkpoint-delay have been described, including nuclear pore defects, replication stress or high intercellular bridge tension, this review will focus only on chromatin bridges. In the presence of such abnormal chromosomal tethers in mammalian cells, the abscission checkpoint requires proper localization and optimal kinase activity of the Chromosomal Passenger Complex (CPC)-catalytic subunit Aurora B at the midbody and culminates in the inhibition of Endosomal Sorting Complex Required for Transport-III (ESCRT-III) components at the abscission site to delay the final cut. Furthermore, cells with an active checkpoint stabilize the narrow cytoplasmic canal that connects the two daughter cells until the chromatin bridges are resolved. Unsuccessful resolution of chromatin bridges in checkpoint-deficient cells or in cells with unstable intercellular canals can lead to chromatin bridge breakage or tetraploidization by regression of the cleavage furrow. In turn, these outcomes can lead to accumulation of DNA damage, chromothripsis, generation of hypermutation clusters and chromosomal instability, which are associated with cancer formation or progression. Recently, many important questions regarding the mechanisms of the abscission checkpoint have been investigated, such as how the presence of chromatin bridges is signaled to the CPC, how Aurora B localization and kinase activity is regulated in late midbodies, the signaling pathways by which Aurora B implements the abscission delay, and how the actin cytoskeleton is remodeled to stabilize intercellular canals with DNA bridges. Here, we review recent progress toward understanding the mechanisms of the abscission checkpoint and its role in guarding genome integrity at the chromosome level, and consider its potential ...
Keywords	chromatin bridges ; abscission checkpoint ; cytokinesis ; actin patches ; midbody ; DNA damage ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2021-11-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Building bridges between chromosomes: novel insights into the abscission checkpoint.

Petsalaki, Eleni / Zachos, George

Cellular and molecular life sciences : CMLS

2019 Volume 76, Issue 21, Page(s) 4291–4307

Abstract: In the presence of chromatin bridges, mammalian cells delay completion of cytokinesis (abscission) to prevent chromatin breakage or tetraploidization by regression of the cleavage furrow. This abscission delay is called "the abscission checkpoint" and is ...

Abstract	In the presence of chromatin bridges, mammalian cells delay completion of cytokinesis (abscission) to prevent chromatin breakage or tetraploidization by regression of the cleavage furrow. This abscission delay is called "the abscission checkpoint" and is dependent on Aurora B kinase. Furthermore, cells stabilize the narrow cytoplasmic canal between the two daughter cells until the DNA bridges are resolved. Impaired abscission checkpoint signaling or unstable intercellular canals can lead to accumulation of DNA damage, aneuploidy, or generation of polyploid cells which are associated with tumourigenesis. However, the molecular mechanisms involved have only recently started to emerge. In this review, we focus on the molecular pathways of the abscission checkpoint and describe newly identified triggers, Aurora B-regulators and effector proteins in abscission checkpoint signaling. We also describe mechanisms that control intercellular bridge stabilization, DNA bridge resolution, or abscission checkpoint silencing upon satisfaction, and discuss how abscission checkpoint proteins can be targeted to potentially improve cancer therapy.
MeSH term(s)	Animals ; Aurora Kinase B/metabolism ; Aurora Kinase B/physiology ; Chromatin/metabolism ; Chromosomes/metabolism ; Cytokinesis/physiology ; Genes, cdc/physiology ; Humans ; Signal Transduction
Chemical Substances	Chromatin ; AURKB protein, human (EC 2.7.11.1) ; Aurora Kinase B (EC 2.7.11.1)
Language	English
Publishing date	2019-07-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-019-03224-z
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