LIVIVO - Search results -

Search results

Result 1 - 10 of total 155

Search options

Article ; Online: Nitric oxide mediated redox regulation of protein homeostasis.

Tegeder, Irmgard

2018 Volume 53, Page(s) 348–356

Abstract: Nitric oxide is a versatile diffusible signaling molecule, whose biosynthesis by three NO synthases (NOS) is tightly regulated at transcriptional and posttranslational levels, availability of co-factors, and calcium binding. Above normal levels of NO ... ...

Abstract	Nitric oxide is a versatile diffusible signaling molecule, whose biosynthesis by three NO synthases (NOS) is tightly regulated at transcriptional and posttranslational levels, availability of co-factors, and calcium binding. Above normal levels of NO have beneficial protective effects for example in the cardiovascular system, but also contribute to the pathophysiology in the context of inflammatory diseases, and to aging and neurodegeneration in the nervous system. The effect specificity relies on the functional and spatial specificity of the NOS isoenzymes, and on the duality of two major signaling mechanisms (i) activation of soluble guanylycylase (sGC)-dependent cGMP production and (ii) direct S-nitrosylation of redox sensitive cysteines of susceptible proteins. The present review summarizes the functional implications of S-nitrosylation in the context of proteostasis, and focuses on two NO target proteins, heat shock cognate of 70 kDa (Hsc70/HSPA8) and the ubiquitin 2 ligase (UBE2D), because both are modified on functionally critical cysteines and are key regulators of chaperone mediated and assisted autophagy and proteasomal protein degradation. SNO modifications of these candidates are associated with protein accumulations and adoption of a senescent phenotype of neuronal cells suggesting that S-nitrosylations of protein homeostatic machineries contribute to aging phenomena.
MeSH term(s)	Aging ; Animals ; HSC70 Heat-Shock Proteins/metabolism ; Humans ; Nitric Oxide/metabolism ; Oxidation-Reduction ; Proteostasis ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	HSC70 Heat-Shock Proteins ; Ubiquitin ; Nitric Oxide (31C4KY9ESH) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2018-11-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2018.10.019
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2579: 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)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Failure of Diphtheria Toxin Model to Induce Parkinson-Like Behavior in Mice.

Valek, Lucie / Tegeder, Irmgard

International journal of molecular sciences

2021 Volume 22, Issue 17

Abstract: Rodent models of Parkinson's disease are based on transgenic expression of mutant synuclein, deletion of PD genes, injections of MPTP or rotenone, or seeding of synuclein fibrils. The models show histopathologic features of PD such as Lewi bodies but ... ...

Abstract	Rodent models of Parkinson's disease are based on transgenic expression of mutant synuclein, deletion of PD genes, injections of MPTP or rotenone, or seeding of synuclein fibrils. The models show histopathologic features of PD such as Lewi bodies but mostly only subtle in vivo manifestations or systemic toxicity. The models only partly mimic a predominant loss of dopaminergic neurons in the substantia nigra. We therefore generated mice that express the transgenic diphtheria toxin receptor (DTR) specifically in DA neurons by crossing DAT-Cre mice with Rosa26 loxP-STOP-loxP DTR mice. After defining a well-tolerated DTx dose, DAT-DTR and DTR-flfl controls were subjected to non-toxic DTx treatment (5 × 100 pg/g) and subsequent histology and behavioral tests. DAT protein levels were reduced in the midbrain, and tyrosine hydroxylase-positive neurons were reduced in the substantia nigra, whereas the pan-neuronal marker NeuN was not affected. Despite the promising histologic results, there was no difference in motor function tests or open field behavior. These are tests in which double mutant Pink1
MeSH term(s)	Animals ; Brain/pathology ; Corpus Striatum/metabolism ; Diphtheria Toxin/metabolism ; Diphtheria Toxin/pharmacology ; Disease Models, Animal ; Dopamine/metabolism ; Dopaminergic Neurons/pathology ; Female ; Heparin-binding EGF-like Growth Factor/genetics ; Heparin-binding EGF-like Growth Factor/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Parkinson Disease/metabolism ; Parkinson Disease/physiopathology ; Parkinsonian Disorders/chemically induced ; Parkinsonian Disorders/metabolism ; Substantia Nigra/pathology ; Tyrosine 3-Monooxygenase/metabolism ; alpha-Synuclein/metabolism
Chemical Substances	Diphtheria Toxin ; Heparin-binding EGF-like Growth Factor ; alpha-Synuclein ; Tyrosine 3-Monooxygenase (EC 1.14.16.2) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2021-08-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22179496
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Nucleoredoxin Knockdown in SH-SY5Y Cells Promotes Cell Renewal.

Valek, Lucie / Tegeder, Irmgard

Antioxidants (Basel, Switzerland)

2021 Volume 10, Issue 3

Abstract: Nucleoredoxin (NXN) is a redox regulator of Disheveled and thereby of WNT signaling. Deficiency in mice leads to cranial dysmorphisms and defects of heart, brain, and bone, suggesting defects of cell fate determination. We used shRNA-mediated knockdown ... ...

Abstract	Nucleoredoxin (NXN) is a redox regulator of Disheveled and thereby of WNT signaling. Deficiency in mice leads to cranial dysmorphisms and defects of heart, brain, and bone, suggesting defects of cell fate determination. We used shRNA-mediated knockdown of NXN in SH-SY5Y neuroblastoma cells to study its impact on neuronal cells. We expected that shNXN cells would easily succumb to redox stress, but there were no differences in viability on stimulation with hydrogen peroxide. Instead, the proliferation of naïve shNXN cells was increased with a higher rate of mitotic cells in cell cycle analyses. In addition, basal respiratory rates were higher, whereas the relative change in oxygen consumption upon mitochondrial stressors was similar to control cells. shNXN cells had an increased expression of redox-sensitive heat shock proteins, Hsc70/HSPA8 and HSP90, and autophagy markers suggested an increase in autophagosome formation upon stimulation with bafilomycin and higher flux under low dose rapamycin. A high rate of self-renewal, autophagy, and upregulation of redox-sensitive chaperones appears to be an attractive anti-aging combination if it were to occur in neurons in vivo for which SH-SY5Y cells are a model.
Language	English
Publishing date	2021-03-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10030449
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Yeast-2-Hybrid data file showing progranulin interactions in human fetal brain and bone marrow libraries.

Tegeder, Irmgard

Data in brief

2016 Volume 9, Page(s) 1060–1062

Abstract: Progranulin deficiency in humans is associated with neurodegeneration. Its mechanisms are not yet fully understood. We performed a Yeast-2-Hybrid screen using human full-length progranulin as bait to assess the interactions of progranulin. Progranulin ... ...

Abstract	Progranulin deficiency in humans is associated with neurodegeneration. Its mechanisms are not yet fully understood. We performed a Yeast-2-Hybrid screen using human full-length progranulin as bait to assess the interactions of progranulin. Progranulin was screened against human fetal brain and human bone marrow libraries using the standard Matchmaker technology (Clontech). This article contains the full Y2H data table, including blast results and sequences, a sorted table according to selection criteria for likely positive, putatively positive, likely false and false preys, and tables showing the gene ontology terms associated with the likely and putative preys of the brain and bone marrow libraries. The interactions with autophagy proteins were confirmed and functionally analyzed in "Progranulin overexpression in sensory neurons attenuates neuropathic pain in mice: Role of autophagy" (C. Altmann, S. Hardt, C. Fischer, J. Heidler, H.Y. Lim, A. Haussler, B. Albuquerque, B. Zimmer, C. Moser, C. Behrends, F. Koentgen, I. Wittig, M.H. Schmidt, A.M. Clement, T. Deller, I. Tegeder, 2016) [1].
Language	English
Publishing date	2016-11-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2016.11.031
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Endocannabinoids as Guardians of Metastasis.

Tegeder, Irmgard

International journal of molecular sciences

2016 Volume 17, Issue 2, Page(s) 230

Abstract: Endocannabinoids including anandamide and 2-arachidonoylglycerol are involved in cancer pathophysiology in several ways, including tumor growth and progression, peritumoral inflammation, nausea and cancer pain. Recently we showed that the endocannabinoid ...

Abstract	Endocannabinoids including anandamide and 2-arachidonoylglycerol are involved in cancer pathophysiology in several ways, including tumor growth and progression, peritumoral inflammation, nausea and cancer pain. Recently we showed that the endocannabinoid profiles are deranged during cancer to an extent that this manifests in alterations of plasma endocannabinoids in cancer patients, which was mimicked by similar changes in rodent models of local and metastatic cancer. The present topical review summarizes the complexity of endocannabinoid signaling in the context of tumor growth and metastasis.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Arachidonic Acids/blood ; Arachidonic Acids/metabolism ; Cannabinoids/pharmacology ; Cannabinoids/therapeutic use ; Endocannabinoids/blood ; Endocannabinoids/metabolism ; Ethanolamine/metabolism ; Glycerides/blood ; Glycerides/metabolism ; Humans ; Neoplasm Metastasis ; Neoplasms/drug therapy ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Oleic Acids/blood ; Oleic Acids/metabolism ; Receptors, Cannabinoid/metabolism ; Tumor Microenvironment
Chemical Substances	Antineoplastic Agents ; Arachidonic Acids ; Cannabinoids ; Endocannabinoids ; Glycerides ; Oleic Acids ; Oleylethanolamide ; Receptors, Cannabinoid ; Ethanolamine (5KV86114PT) ; glyceryl 2-arachidonate (8D239QDW64)
Language	English
Publishing date	2016-02-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms17020230
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Full text

Order via subito

Details ▾
- Full text online
- Order with fees

Article: Nucleoredoxin Knockdown in SH-SY5Y Cells Promotes Cell Renewal

Valek, Lucie / Tegeder, Irmgard

Antioxidants. 2021 Mar. 13, v. 10, no. 3

2021

Abstract	Nucleoredoxin (NXN) is a redox regulator of Disheveled and thereby of WNT signaling. Deficiency in mice leads to cranial dysmorphisms and defects of heart, brain, and bone, suggesting defects of cell fate determination. We used shRNA-mediated knockdown of NXN in SH-SY5Y neuroblastoma cells to study its impact on neuronal cells. We expected that shNXN cells would easily succumb to redox stress, but there were no differences in viability on stimulation with hydrogen peroxide. Instead, the proliferation of naïve shNXN cells was increased with a higher rate of mitotic cells in cell cycle analyses. In addition, basal respiratory rates were higher, whereas the relative change in oxygen consumption upon mitochondrial stressors was similar to control cells. shNXN cells had an increased expression of redox-sensitive heat shock proteins, Hsc70/HSPA8 and HSP90, and autophagy markers suggested an increase in autophagosome formation upon stimulation with bafilomycin and higher flux under low dose rapamycin. A high rate of self-renewal, autophagy, and upregulation of redox-sensitive chaperones appears to be an attractive anti-aging combination if it were to occur in neurons in vivo for which SH-SY5Y cells are a model.
Keywords	autophagosomes ; autophagy ; brain ; heart ; heat stress ; hydrogen peroxide ; mitochondria ; mitosis ; models ; neurons ; oxygen consumption ; rapamycin ; viability
Language	English
Dates of publication	2021-0313
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10030449
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article ; Online: Repurposing of pexidartinib for microglia depletion and renewal.

Weyer, Marc-Philipp / Strehle, Jenny / Schäfer, Michael K E / Tegeder, Irmgard

Pharmacology & therapeutics

2023 Volume 253, Page(s) 108565

Abstract: Pexidartinib (PLX3397) is a small molecule receptor tyrosine kinase inhibitor of colony stimulating factor 1 receptor (CSF1R) with moderate selectivity over other members of the platelet derived growth factor receptor family. It is approved for treatment ...

Abstract	Pexidartinib (PLX3397) is a small molecule receptor tyrosine kinase inhibitor of colony stimulating factor 1 receptor (CSF1R) with moderate selectivity over other members of the platelet derived growth factor receptor family. It is approved for treatment of tenosynovial giant cell tumors (TGCT). CSF1R is highly expressed by microglia, which are macrophages of the central nervous system (CNS) that defend the CNS against injury and pathogens and contribute to synapse development and plasticity. Challenged by pathogens, apoptotic cells, debris, or inflammatory molecules they adopt a responsive state to propagate the inflammation and eventually return to a homeostatic state. The phenotypic switch may fail, and disease-associated microglia contribute to the pathophysiology in neurodegenerative or neuropsychiatric diseases or long-lasting detrimental brain inflammation after brain, spinal cord or nerve injury or ischemia/hemorrhage. Microglia also contribute to the growth permissive tumor microenvironment of glioblastoma (GBM). In rodents, continuous treatment for 1-2 weeks via pexidartinib food pellets leads to a depletion of microglia and subsequent repopulation from the remaining fraction, which is aided by peripheral monocytes that search empty niches for engraftment. The putative therapeutic benefit of such microglia depletion or forced renewal has been assessed in almost any rodent model of CNS disease or injury or GBM with heterogeneous outcomes, but a tendency of partial beneficial effects. So far, microglia monitoring e.g. via positron emission imaging is not standard of care for patients receiving Pexidartinib (e.g. for TGCT), so that the depletion and repopulation efficiency in humans is still largely unknown. Considering the virtuous functions of microglia, continuous depletion is likely no therapeutic option but short-lasting transient partial depletion to stimulate microglia renewal or replace microglia in genetic disease in combination with e.g. stem cell transplantation or as part of a multimodal concept in treatment of glioblastoma appears feasible. The present review provides an overview of the preclinical evidence pro and contra microglia depletion as a therapeutic approach.
MeSH term(s)	Humans ; Microglia ; Glioblastoma ; Aminopyridines/pharmacology ; Pyrroles/metabolism ; Pyrroles/pharmacology ; Tumor Microenvironment
Chemical Substances	pexidartinib (6783M2LV5X) ; Aminopyridines ; Pyrroles
Language	English
Publishing date	2023-12-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2023.108565
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1183: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Cold avoidance and heat pain hypersensitivity in neuronal nucleoredoxin knockout mice.

Valek, Lucie / Tran, Bao Ngoc / Tegeder, Irmgard

Free radical biology & medicine

2022 Volume 192, Page(s) 84–97

Abstract: Nucleoredoxin is a thioredoxin-like oxidoreductase that mainly acts as oxidase and thereby regulates calcium calmodulin kinase Camk2a, an effector of nitric oxide mediated synaptic potentiation and nociceptive sensitization. We asked here if and how NXN ... ...

Abstract	Nucleoredoxin is a thioredoxin-like oxidoreductase that mainly acts as oxidase and thereby regulates calcium calmodulin kinase Camk2a, an effector of nitric oxide mediated synaptic potentiation and nociceptive sensitization. We asked here if and how NXN affects thermal sensation and nociception in mice using pan-neuronal NXN deletion driven by Nestin-Cre, and sensory neuron specific deletion driven by Advillin-Cre. In a thermal gradient ring, where mice can freely choose the temperature of well-being, Nestin-NXN
MeSH term(s)	Animals ; Calcium ; Cold Temperature ; Ganglia, Spinal ; Hot Temperature ; Mice ; Mice, Knockout ; Nestin ; Nitric Oxide ; Oxidoreductases ; Thioredoxins
Chemical Substances	Nestin ; Nitric Oxide (31C4KY9ESH) ; Thioredoxins (52500-60-4) ; Oxidoreductases (EC 1.-) ; nucleoredoxin (EC 1.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-09-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2022.09.010
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2109: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: When lipid homeostasis runs havoc: Lipotoxicity links lysosomal dysfunction to autophagy.

Tegeder, Irmgard / Kögel, Donat

Matrix biology : journal of the International Society for Matrix Biology

2020 Volume 100-101, Page(s) 99–117

Abstract: Autophagy is one of the major cellular degradation pathways, which prevents accumulation of cellular wastes including "hazardous" material such as oxidized proteins and lipids and allows removal of aggregates and dysfunctional organelles. Hence, ... ...

Abstract	Autophagy is one of the major cellular degradation pathways, which prevents accumulation of cellular wastes including "hazardous" material such as oxidized proteins and lipids and allows removal of aggregates and dysfunctional organelles. Hence, autophagy is meant to preserve cell survival, and is mostly protective. However, autophagy may trigger a feedforward, exaggerated cycle in which cells continue to degrade proteins and organelles, finally leading to autophagy-dependent cell death (ADCD), a process that can be initiated with lysosomotropic detergents, which are protonated within the lysosome and cause a permeabilization of the membrane. Such drugs may be useful to combat cancer. In some paradigms of ADCD, there is evidence that the cellular fate is determined by the integrity of lysosomal membranes, transporters, enzymes and ion gradients. Detergent-like effects of lysosomotropic drugs can over-activate autophagy. A disruption of the lysosomal membrane barrier with leakage of lysosomal enzymes or lipids may trigger a vicious cycle via proteases and accumulation of lipids, which impair the functions of the plasma - and organelle membranes. This review summarizes the current evidence for a crosstalk between lysosomal dysfunction and autophagy and the lysosomal events, which progress toward ADCD with a focus on the role of sphingolipids and cholesterol as cargo and as regulators of ADCD.
MeSH term(s)	Autophagy ; Homeostasis ; Lipids ; Lysosomes ; Sphingolipids
Chemical Substances	Lipids ; Sphingolipids
Language	English
Publishing date	2020-12-05
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1183793-7
ISSN	1569-1802 ; 0945-053X
ISSN (online)	1569-1802
ISSN	0945-053X
DOI	10.1016/j.matbio.2020.11.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1694: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Book ; Thesis: Antibiotika- und Wismutempfindlichkeit von Helicobacter pylori

Tegeder, Irmgard

1991

Author's details	vorgelegt von Irmgard Tegeder
Size	122 Bl. : graph. Darst.
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Bochum, Univ., Diss., 1992
HBZ-ID	HT004231243
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

Shelf mark	Loan status	Location
92 E 3124	order for loan	Magazin

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito