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Article: P-glycoprotein inhibition by glibenclamide and related compounds.

Golstein, P E / Boom, A / van Geffel, J / Jacobs, P / Masereel, B / Beauwens, R

Pflugers Archiv : European journal of physiology

1999 Volume 437, Issue 5, Page(s) 652–660

Abstract: ... was examined on P-glycoprotein, the major ABC transporter responsible for multidrug resistance (MDR ... in cancer cells. To this end, we employed different cell lines that do or do not express P-glycoprotein ... of the opossum kidney (OK). Glibenclamide and the two related derivatives inhibited P-glycoprotein ...

Abstract	Glibenclamide is well known to interact with the sulphonylurea receptor (SUR) and has been shown more recently to inhibit the cystic fibrosis transmembrane conductance regulator protein (CFTR), both proteins that are members of the ABC [adenosine 5'-triphosphate (ATP)-binding cassette] transporters. The effect of glibenclamide and two synthetic sulphonylcyanoguanidine derivatives (dubbed BM-208 and BM-223) was examined on P-glycoprotein, the major ABC transporter responsible for multidrug resistance (MDR) in cancer cells. To this end, we employed different cell lines that do or do not express P-glycoprotein, as confirmed by Western blotting: first, a tumour cell line (VBL600) selected from a human T-cell line (CEM) derived from an acute leukaemia; second, an epithelial cell line derived from a rat colonic adenocarcinoma (CC531(mdr+)) and finally, a non tumour epithelial cell line derived from the proximal tubule of the opossum kidney (OK). Glibenclamide and the two related derivatives inhibited P-glycoprotein because firstly, they acutely increased [3H]colchicine accumulation in P-glycoprotein-expressing cell lines only; secondly BM-223 reversed the MDR phenomenon, quite similarly to verapamil, by enhancing the cytotoxicity of colchicine, taxol and vinblastine and thirdly, BM-208 and BM-223 blocked the photoaffinity-labelling of P-glycoprotein by [3H]azidopine. Furthermore, glibenclamide is itself a substrate for P-glycoprotein, since the cellular accumulation of [3H]glibenclamide was low and substantially increased by addition of P-glycoprotein substrates (e. g., vinblastine and cyclosporine) only in the P-glycoprotein-expressing cell lines. We conclude that glibenclamide and two sulphonylcyanoguanidine derivatives inhibit P-glycoprotein and that sulphonylurea drugs would appear to be general inhibitors of ABC transporters, suggesting an interaction with some conserved motif.
MeSH term(s)	ATP-Binding Cassette Transporters/metabolism ; ATP-Binding Cassette, Sub-Family B, Member 1/antagonists & inhibitors ; Animals ; Cell Adhesion/physiology ; Cell Line ; Cell Membrane/metabolism ; Cell Survival/drug effects ; Colchicine/metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Glyburide/analogs & derivatives ; Glyburide/metabolism ; Glyburide/pharmacology ; Humans ; Hypoglycemic Agents/metabolism ; Hypoglycemic Agents/pharmacology ; Immunochemistry ; Opossums ; Photoaffinity Labels ; Potassium Channels/metabolism ; Potassium Channels, Inwardly Rectifying ; Protein Binding ; Rats ; Receptors, Drug/metabolism ; Sulfonylurea Compounds/metabolism ; Sulfonylurea Receptors
Chemical Substances	ATP-Binding Cassette, Sub-Family B, Member 1 ; CFTR protein, human ; Hypoglycemic Agents ; Photoaffinity Labels ; Potassium Channels ; Potassium Channels, Inwardly Rectifying ; Receptors, Drug ; Sulfonylurea Compounds ; Sulfonylurea Receptors ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Colchicine (SML2Y3J35T) ; Glyburide (SX6K58TVWC)
Language	English
Publishing date	1999-04
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s004240050829
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Article ; Online: Conserved nucleolar stress at the onset of cell death.

Golstein, Pierre

The FEBS journal

2017 Volume 284, Issue 22, Page(s) 3791–3800

Abstract: Cell death pervasiveness among multicellular eukaryotes suggested that some core steps of cell death may be conserved. This could be addressed by comparing the course of cell death in organisms belonging to distinct eukaryotic kingdoms. A search for ... ...

Abstract	Cell death pervasiveness among multicellular eukaryotes suggested that some core steps of cell death may be conserved. This could be addressed by comparing the course of cell death in organisms belonging to distinct eukaryotic kingdoms. A search for early cell death events in a protist revealed nucleolar disorganization similar to the nucleolar stress often reported in dying animal cells. This indicated a conserved role for the nucleolus at the onset of eukaryotic cell death and leads one to consider the course of cell death as a succession of unequally conserved modules.
Language	English
Publishing date	2017-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.14095
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Article: Conserved nucleolar stress at the onset of cell death

Golstein, Pierre

FEBS journal. 2017 Nov., v. 284, no. 22

2017

Abstract	Cell death pervasiveness among multicellular eukaryotes suggested that some core steps of cell death may be conserved. This could be addressed by comparing the course of cell death in organisms belonging to distinct eukaryotic kingdoms. A search for early cell death events in a protist revealed nucleolar disorganization similar to the nucleolar stress often reported in dying animal cells. This indicated a conserved role for the nucleolus at the onset of eukaryotic cell death and leads one to consider the course of cell death as a succession of unequally conserved modules.
Keywords	cell death ; cell nucleolus ; eukaryotic cells ; protists
Language	English
Dates of publication	2017-11
Size	p. 3791-3800.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.14095
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Article ; Online: An early history of T cell-mediated cytotoxicity.

Golstein, Pierre / Griffiths, Gillian M

Nature reviews. Immunology

2018 Volume 18, Issue 8, Page(s) 527–535

Abstract: After 60 years of intense fundamental research into T cell-mediated cytotoxicity, we have gained a detailed knowledge of the cells involved, specific recognition mechanisms and post-recognition perforin-granzyme-based and FAS-based molecular mechanisms. ... ...

Abstract	After 60 years of intense fundamental research into T cell-mediated cytotoxicity, we have gained a detailed knowledge of the cells involved, specific recognition mechanisms and post-recognition perforin-granzyme-based and FAS-based molecular mechanisms. What could not be anticipated at the outset was how discovery of the mechanisms regulating the activation and function of cytotoxic T cells would lead to new developments in cancer immunotherapy. Given the profound recent interest in therapeutic manipulation of cytotoxic T cell responses, it is an opportune time to look back on the early history of the field. This Timeline describes how the early findings occurred and eventually led to current therapeutic applications.
MeSH term(s)	Animals ; Cytotoxicity, Immunologic ; Fas Ligand Protein/immunology ; Granzymes/immunology ; History, 20th Century ; History, 21st Century ; Humans ; Immunity, Cellular ; Immunotherapy/history ; Immunotherapy/trends ; Isoantigens/immunology ; Models, Immunological ; Perforin/immunology ; Receptors, Antigen, T-Cell/history ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction/immunology ; T-Lymphocytes, Cytotoxic/immunology ; fas Receptor/immunology
Chemical Substances	Fas Ligand Protein ; Isoantigens ; Receptors, Antigen, T-Cell ; fas Receptor ; Perforin (126465-35-8) ; Granzymes (EC 3.4.21.-)
Language	English
Publishing date	2018-05-02
Publishing country	England
Document type	Historical Article ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2062776-2
ISSN	1474-1741 ; 1474-1733
ISSN (online)	1474-1741
ISSN	1474-1733
DOI	10.1038/s41577-018-0009-3
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Zs.A 5565: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Cell death in unusual but informative and beautiful model organisms.

Golstein, Pierre

Seminars in cancer biology

2007 Volume 17, Issue 2, Page(s) 91–93

Abstract: Cancer depends on cell death. It can emerge when cell death is deficient, and it could be treated through cancer-cell-specific induction of cell death. However, our understanding of cell death is still incomplete. While a few classical animal models have ...

Abstract	Cancer depends on cell death. It can emerge when cell death is deficient, and it could be treated through cancer-cell-specific induction of cell death. However, our understanding of cell death is still incomplete. While a few classical animal models have helped greatly in this respect, more may be learnt from non-classical model organisms from all eukaryotic kingdoms. We describe in this volume some of these non-classical models of cell death, which are at least potentially scientifically informative and often aesthetically pleasing.
MeSH term(s)	Animals ; Cell Death/physiology ; Models, Animal
Language	English
Publishing date	2007-04
Publishing country	England
Document type	Editorial
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2006.11.001
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Article: Signal transduction. FasL binds preassembled Fas.

Golstein, P

Science (New York, N.Y.)

2000 Volume 288, Issue 5475, Page(s) 2328–2329

Abstract: ... for signal transduction to ensue. However, as Golstein explains in his Perspective, new findings (Chan et al. and Siegel ...

Abstract	The binding of a ligand to its receptor has always been viewed as the trigger for signal transduction to ensue. However, as Golstein explains in his Perspective, new findings (Chan et al. and Siegel et al.) suggest that the Fas receptor preassembles into trimers without the help of its ligand, and that this preassembly conditions ligand binding, and thus subsequent signal transduction of a death signal.
MeSH term(s)	Animals ; Apoptosis ; Binding Sites ; Cell Membrane/metabolism ; Dimerization ; Fas Ligand Protein ; Humans ; Ligands ; Macromolecular Substances ; Membrane Glycoproteins/chemistry ; Membrane Glycoproteins/metabolism ; Mutation ; Protein Conformation ; Protein Structure, Tertiary ; Signal Transduction ; fas Receptor/chemistry ; fas Receptor/genetics ; fas Receptor/metabolism
Chemical Substances	FASLG protein, human ; Fas Ligand Protein ; Ligands ; Macromolecular Substances ; Membrane Glycoproteins ; fas Receptor
Language	English
Publishing date	2000-06-30
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.288.5475.2328
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Zs.A 27: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Cell death in us and others.

Golstein, P

Science (New York, N.Y.)

1998 Volume 281, Issue 5381, Page(s) 1283

MeSH term(s)	Animals ; Apoptosis ; Cell Death ; Cysteine Endopeptidases/metabolism ; Fungi/cytology ; Humans ; Plant Cells
Chemical Substances	Cysteine Endopeptidases (EC 3.4.22.-)
Language	English
Publishing date	1998-08-28
Publishing country	United States
Document type	Editorial
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.281.5381.1283
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Article ; Online: Early nucleolar disorganization in Dictyostelium cell death.

Luciani, M F / Song, Y / Sahrane, A / Kosta, A / Golstein, P

Cell death & disease

2017 Volume 8, Issue 1, Page(s) e2528

Abstract: Cell death occurs in all eukaryotes, but it is still not known whether some core steps of the cell death process are conserved. We investigated this using the protist Dictyostelium. The dissection of events in Dictyostelium vacuolar developmental cell ... ...

Abstract	Cell death occurs in all eukaryotes, but it is still not known whether some core steps of the cell death process are conserved. We investigated this using the protist Dictyostelium. The dissection of events in Dictyostelium vacuolar developmental cell death was facilitated by the sequential requirement for two distinct exogenous signals. An initial exogenous signal (starvation and cAMP) recruited some cells into clumps. Only within these clumps did subsequent cell death events take place. Contrary to our expectations, already this initial signal provoked nucleolar disorganization and irreversible inhibition of rRNA and DNA synthesis, reflecting marked cell dysfunction. The initial signal also primed clumped cells to respond to a second exogenous signal (differentiation-inducing factor-1 or c-di-GMP), which led to vacuolization and synthesis of cellulose encasings. Thus, the latter prominent hallmarks of developmental cell death were induced separately from initial cell dysfunction. We propose that (1) in Dictyostelium vacuolization and cellulose encasings are late, organism-specific, hallmarks, and (2) on the basis of our observations in this protist and of similar previous observations in some cases of mammalian cell death, early inhibition of rRNA synthesis and nucleolar disorganization may be conserved in some eukaryotes to usher in developmental cell death.
MeSH term(s)	Animals ; Apoptosis/genetics ; Autophagy/genetics ; Cell Death/genetics ; Cell Nucleolus/genetics ; Cell Nucleolus/pathology ; Cyclic AMP/genetics ; Dictyostelium/genetics ; Dictyostelium/growth & development ; Protozoan Proteins/genetics ; Protozoan Proteins/metabolism ; Vacuoles/metabolism
Chemical Substances	Protozoan Proteins ; Cyclic AMP (E0399OZS9N)
Language	English
Publishing date	2017-01-05
Publishing country	England
Document type	Journal Article
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2016.444
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Article ; Online: Do we need retarded delivery of bone growth factors in facial bone repair? An experimental study in rats.

Moser, N / Lohse, N / Golstein, J / Kauffmann, P / Sven, B / Epple, M / Schliephake, H

European cells & materials

2017 Volume 34, Page(s) 162–179

Abstract: The aim of the present study was to evaluate the effect of different dosages of retarded vs. rapid release of bone morphogenic protein 2 (BMP2) at different recipient sites. Porous composite poly(D,L-lactic acid) (PDLLA)/CaCO3 scaffolds were loaded with ... ...

Abstract	The aim of the present study was to evaluate the effect of different dosages of retarded vs. rapid release of bone morphogenic protein 2 (BMP2) at different recipient sites. Porous composite poly(D,L-lactic acid) (PDLLA)/CaCO3 scaffolds were loaded with three different dosages of rhBMP2 (24 µg, 48 µg and 96 µg) and implanted, together with blank controls, both into non-healing defects of the mandibles and into the gluteal muscles of 24 adult male Wistar rats. After 26 weeks, bone formation and expression of bone specific markers [alkaline phosphatase (AP) and Runx2] were evaluated by histomorphometry and immunohistochemistry. Results showed that the mode of delivery had no quantitative effect on bone formation in mandibular sites. Expression of AP and Runx2 showed significant differences among the three dosage groups. There were significant correlations between the expression of both AP and Runx2 as well as the extent of bone formation, with both retarded and rapid release of rhBMP2. In ectopic sites, retarded release significantly enhanced bone formation in the low and medium dosage groups, compared to rapid release. Expression of AP was significantly higher and Runx2 significantly lower in ectopic sites, compared to mandibular sites. Significant correlations between the expression of bone specific markers and bone formation occurred only in the retarded delivery groups, but not in the rapid release groups. Within the limitations of the experimental model, it was concluded that retarded delivery of BMP2 was effective, preferably in sites with low or non-existing pristine osteogenic activity. Expression of bone specific markers indicated that osteogenic pathways might be different in mandibular vs. ectopic sites.
MeSH term(s)	Alkaline Phosphatase/metabolism ; Animals ; Bone Morphogenetic Protein 2/pharmacology ; Bone and Bones/drug effects ; Bone and Bones/metabolism ; Calcium Carbonate/chemistry ; Core Binding Factor Alpha 1 Subunit/metabolism ; Facial Bones/drug effects ; Facial Bones/pathology ; Male ; Mandible/drug effects ; Mandible/pathology ; Osteogenesis/drug effects ; Polyesters/chemistry ; Porosity ; Rats, Wistar ; Recombinant Proteins/pharmacology ; Time Factors ; Tissue Scaffolds/chemistry ; Transforming Growth Factor beta/pharmacology ; Treatment Outcome
Chemical Substances	Bone Morphogenetic Protein 2 ; Core Binding Factor Alpha 1 Subunit ; Polyesters ; Recombinant Proteins ; Transforming Growth Factor beta ; recombinant human bone morphogenetic protein-2 ; poly(lactide) (459TN2L5F5) ; Alkaline Phosphatase (EC 3.1.3.1) ; Calcium Carbonate (H0G9379FGK)
Language	English
Publishing date	2017-10-05
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2046669-9
ISSN	1473-2262 ; 1473-2262
ISSN (online)	1473-2262
ISSN	1473-2262
DOI	10.22203/eCM.v034a11
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Article: Controlling cell death.

Golstein, P

Science (New York, N.Y.)

1997 Volume 275, Issue 5303, Page(s) 1081–1082

MeSH term(s)	Animals ; Apoptosis ; Apoptosis Regulatory Proteins ; Caenorhabditis elegans/cytology ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins ; Calcium-Binding Proteins/metabolism ; Caspase 1 ; Caspases ; Cysteine Endopeptidases/metabolism ; Cytochrome c Group/metabolism ; Cytosol/metabolism ; Helminth Proteins/metabolism ; Membrane Glycoproteins/metabolism ; Mitochondria/metabolism ; Perforin ; Pore Forming Cytotoxic Proteins ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Signal Transduction ; Transfection ; bcl-X Protein
Chemical Substances	Apoptosis Regulatory Proteins ; Caenorhabditis elegans Proteins ; Calcium-Binding Proteins ; Ced-4 protein, C elegans ; Ced-9 protein, C elegans ; Cytochrome c Group ; Helminth Proteins ; Membrane Glycoproteins ; Pore Forming Cytotoxic Proteins ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2 ; bcl-X Protein ; Perforin (126465-35-8) ; Caspases (EC 3.4.22.-) ; Cysteine Endopeptidases (EC 3.4.22.-) ; ced-3 protein, C elegans (EC 3.4.22.-) ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	1997-02-21
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.275.5303.1081
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