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Article ; Online: Combinatorial targeting of a specific EMT/MET network by macroH2A variants safeguards mesenchymal identity.

Valakos, Dimitrios / Klagkou, Eleftheria / Kokkalis, Antonis / Polyzos, Alexandros / Kyrilis, Fotis L / Banos, Aggelos / Vatsellas, Giannis / Pliatska, Maria / Ford, Ethan / Stravopodis, Dimitrios J / Thanos, Dimitris

PloS one

2023 Volume 18, Issue 7, Page(s) e0288005

Abstract: Generation of induced pluripotent stem cells from specialized cell types provides an excellent model to study how cells maintain their stability, and how they can change identity, especially in the context of disease. Previous studies have shown that ... ...

Abstract	Generation of induced pluripotent stem cells from specialized cell types provides an excellent model to study how cells maintain their stability, and how they can change identity, especially in the context of disease. Previous studies have shown that chromatin safeguards cell identity by acting as a barrier to reprogramming. We investigated mechanisms by which the histone macroH2A variants inhibit reprogramming and discovered that they work as gate keepers of the mesenchymal cell state by blocking epithelial transition, a step required for reprogramming of mouse fibroblasts. More specifically, we found that individual macroH2A variants regulate the expression of defined sets of genes, whose overall function is to stabilize the mesenchymal gene expression program, thus resisting reprogramming. We identified a novel gene network (MSCN, mesenchymal network) composed of 63 macroH2A-regulated genes related to extracellular matrix, cell membrane, signaling and the transcriptional regulators Id2 and Snai2, all of which function as guardians of the mesenchymal phenotype. ChIP-seq and KD experiments revealed a macroH2A variant-specific combinatorial targeting of the genes reconstructing the MSCN, thus generating robustness in gene expression programs to resist cellular reprogramming.
MeSH term(s)	Animals ; Mice ; Chromatin/genetics ; Cell Membrane ; Cellular Reprogramming/genetics ; Chromatin Immunoprecipitation Sequencing ; Extracellular Matrix
Chemical Substances	Chromatin
Language	English
Publishing date	2023-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0288005
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Article: Perturbation of transcriptome in non-neoplastic salivary gland epithelial cell lines derived from patients with primary Sjögren's syndrome

Vakrakou, Aigli G. / Polyzos, Alexandros / Kapsogeorgou, Efstathia K. / Thanos, Dimitris / Manoussakis, Menelaos N.

Data in Brief. 2018 Apr., v. 17

2018

Abstract: The data presented here are related to the research article titled “Impaired anti-inflammatory activity of PPARγ in the salivary epithelia of Sjögren's syndrome patients imposed by intrinsic NF-κB activation” (Vakrakou et al., Journal of Autoimmunity, in ...

Abstract	The data presented here are related to the research article titled “Impaired anti-inflammatory activity of PPARγ in the salivary epithelia of Sjögren's syndrome patients imposed by intrinsic NF-κB activation” (Vakrakou et al., Journal of Autoimmunity, in press, 2017). In the cited manuscript, using comparative analyses of salivary gland biopsy specimens and ductal salivary gland epithelial cell (SGEC) lines from SS patients and disease controls, we have demonstrated that the ductal epithelia of SS patients display constitutively reduced PPARγ expression, transcriptional activity and anti-inflammatory function that were associated with cell-autonomously activated NF-κB and IL-1β pathways in these cells. Herein, the comparative transcriptome analysis of SGEC lines is presented. We show that the ductal epithelia of SS patients with severe lymphoepithelial lesions manifest constitutive perturbation in various inflammation- and metabolism related signaling pathways.
Keywords	anti-inflammatory activity ; autoimmunity ; biopsy ; epithelial cells ; metabolism ; salivary glands ; transcription (genetics) ; transcriptome ; transcriptomics
Language	English
Dates of publication	2018-04
Size	p. 194-199.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2017.12.023
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Article ; Online: Effects of cryopreservation on antiviral responses of primary airway epithelial cells.

Taka, Styliani / Nikopoulou, Chrysa / Polyzos, Alexandros / Megremis, Spyridon / Skevaki, Chrysanthi L / Roumpedaki, Eirini / Trochoutsou, Aikaterini / Thanos, Dimitris / Papadopoulos, Nikolaos G

Allergy

2020 Volume 75, Issue 6, Page(s) 1486–1489

MeSH term(s)	Antiviral Agents ; Cells, Cultured ; Cryopreservation ; Epithelial Cells ; Respiratory System ; Rhinovirus
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2020-02-08
Publishing country	Denmark
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.14163
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Article: Perturbation of transcriptome in non-neoplastic salivary gland epithelial cell lines derived from patients with primary Sjögren's syndrome.

Vakrakou, Aigli G / Polyzos, Alexandros / Kapsogeorgou, Efstathia K / Thanos, Dimitris / Manoussakis, Menelaos N

Data in brief

2017 Volume 17, Page(s) 194–199

Abstract: The data presented here are related to the research article ... ...

Abstract	The data presented here are related to the research article titled
Language	English
Publishing date	2017-12-12
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2017.12.023
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Article ; Online: Impaired anti-inflammatory activity of PPARγ in the salivary epithelia of Sjögren's syndrome patients imposed by intrinsic NF-κB activation.

Vakrakou, Aigli G / Polyzos, Alexandros / Kapsogeorgou, Efstathia K / Thanos, Dimitris / Manoussakis, Menelaos N

Journal of autoimmunity

2017 Volume 86, Page(s) 62–74

Abstract: Sjögren's syndrome (SS) patients manifest inflammation in the salivary glands (SG) and evidence of persistent intrinsic activation of ductal SG epithelial cells (SGEC), demonstrable in non-neoplastic SGEC lines derived from patients (SS-SGEC). The ... ...

Abstract	Sjögren's syndrome (SS) patients manifest inflammation in the salivary glands (SG) and evidence of persistent intrinsic activation of ductal SG epithelial cells (SGEC), demonstrable in non-neoplastic SGEC lines derived from patients (SS-SGEC). The peroxisome-proliferator-activated receptor-γ (PPARγ) mediates important anti-inflammatory activities in epithelial cells. Herein, the comparative analysis of SG biopsies and SGEC lines obtained from SS patients and controls had revealed constitutively reduced PPARγ expression, transcriptional activity and anti-inflammatory function in the ductal epithelia of SS patients that were associated with cell-autonomously activated NF-κB and IL-1β pathways. Transcriptome profiling analysis revealed several differentially expressed proinflammatory and metabolism-related gene sets in SS-SGEC lines. These aberrations largely correlated with the severity of histopathologic lesions, the disease activity and the occurrence of adverse manifestations in SS patients studied, a fact which corroborates the key role of the persistently-activated epithelia in the pathogenesis of both local and systemic features of this disease. The treatment of control SGEC lines with PPARγ agonists was found to diminish the NF-κB activation and apoptosis induced by proinflammatory agents. In addition, the in-vitro application of PPARγ agonists and pharmacologic inhibitors of IL-1β and NF-κB had significant beneficial effects on SS-SGEC lines, such as the restoration of PPARγ functions and the reduction of their intrinsic activation, a fact which may advocate the future clinical study of the above agents as therapeutic modalities for SS.
MeSH term(s)	Apoptosis ; Cell Line ; Disease Progression ; Epithelium/physiology ; Gene Expression Profiling ; Gene Expression Regulation ; Humans ; Interleukin-1beta/metabolism ; NF-kappa B/metabolism ; PPAR gamma/agonists ; PPAR gamma/metabolism ; Rosiglitazone/pharmacology ; Salivary Glands/pathology ; Signal Transduction ; Sjogren's Syndrome/immunology ; Tissue Array Analysis
Chemical Substances	Interleukin-1beta ; NF-kappa B ; PPAR gamma ; Rosiglitazone (05V02F2KDG)
Language	English
Publishing date	2017-10-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2017.09.007
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Article: Pleiotrophin and its receptor protein tyrosine phosphatase beta/zeta as regulators of angiogenesis and cancer.

Papadimitriou, Evangelia / Pantazaka, Evangelia / Castana, Penelope / Tsalios, Thomas / Polyzos, Alexandros / Beis, Dimitris

Biochimica et biophysica acta

2016 Volume 1866, Issue 2, Page(s) 252–265

Abstract: Pleiotrophin (PTN) is a secreted heparin-binding growth factor that through its receptor protein tyrosine phosphatase beta/zeta (RPTPβ/ζ) has a significant regulatory effect on angiogenesis and cancer. PTN and RPTPβ/ζ are over-expressed in several types ... ...

Abstract	Pleiotrophin (PTN) is a secreted heparin-binding growth factor that through its receptor protein tyrosine phosphatase beta/zeta (RPTPβ/ζ) has a significant regulatory effect on angiogenesis and cancer. PTN and RPTPβ/ζ are over-expressed in several types of human cancers and regulate important cancer cell functions in vitro and cancer growth in vivo. This review begins with a brief introduction of PTN and the regulation of its expression. PTN receptors are described with special emphasis on RPTPβ/ζ, which also interacts with and/or affects the function of other important targets for cancer therapy, such as vascular endothelial growth factor A, α
MeSH term(s)	Animals ; Carrier Proteins/genetics ; Carrier Proteins/physiology ; Cytokines/genetics ; Cytokines/physiology ; Gene Expression Regulation ; Humans ; Neoplasms/blood supply ; Neoplasms/etiology ; Neovascularization, Pathologic/etiology ; Neovascularization, Physiologic ; Receptor-Like Protein Tyrosine Phosphatases, Class 5/physiology
Chemical Substances	Carrier Proteins ; Cytokines ; pleiotrophin (134034-50-7) ; Receptor-Like Protein Tyrosine Phosphatases, Class 5 (EC 3.1.3.48)
Language	English
Publishing date	2016
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbcan.2016.09.007
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Article ; Online: RbAp48 Protein Is a Critical Component of GPR158/OCN Signaling and Ameliorates Age-Related Memory Loss.

Kosmidis, Stylianos / Polyzos, Alexandros / Harvey, Lucas / Youssef, Mary / Denny, Christine A / Dranovsky, Alex / Kandel, Eric R

Cell reports

2018 Volume 25, Issue 4, Page(s) 959–973.e6

Abstract: Precisely deciphering the molecular mechanisms of age-related memory loss is crucial to create appropriate therapeutic interventions. We have previously shown that the histone-binding protein RbAp48/Rbbp4 is a molecular determinant of Age-Related Memory ... ...

Abstract	Precisely deciphering the molecular mechanisms of age-related memory loss is crucial to create appropriate therapeutic interventions. We have previously shown that the histone-binding protein RbAp48/Rbbp4 is a molecular determinant of Age-Related Memory Loss. By exploring how this protein regulates the genomic landscape of the hippocampal circuit, we find that RbAp48 controls the expression of BDNF and GPR158 proteins, both critical components of osteocalcin (OCN) signaling in the mouse hippocampus. We show that inhibition of RbAp48 in the hippocampal formation inhibits OCN's beneficial functions in cognition and causes deficits in discrimination memory. In turn, disruption of OCN/GPR158 signaling leads to the downregulation of RbAp48 protein, mimicking the discrimination memory deficits observed in the aged hippocampus. We also show that activation of the OCN/GPR158 pathway increases the expression of RbAp48 in the aged dentate gyrus and rescues age-related memory loss.
MeSH term(s)	Aging/metabolism ; Animals ; Conditioning, Psychological ; Dentate Gyrus/metabolism ; Fear ; HEK293 Cells ; Humans ; Memory ; Memory Disorders/metabolism ; Memory Disorders/physiopathology ; Mice ; Mice, Inbred C57BL ; Osteocalcin/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Retinoblastoma-Binding Protein 4/metabolism ; Signal Transduction ; Up-Regulation
Chemical Substances	GPR158 protein, mouse ; Receptors, G-Protein-Coupled ; Retinoblastoma-Binding Protein 4 ; Osteocalcin (104982-03-8)
Language	English
Publishing date	2018-10-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2018.09.077
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Article: A recurrent chromosomal inversion suffices for driving escape from oncogene-induced senescence via subTAD reorganization

Zampetidis, Christos P. / Galanos, Panagiotis / Angelopoulou, Andriani / Zhu, Yajie / Polyzou, Aikaterini / Karamitros, Timokratis / Kotsinas, Athanassios / Lagopati, Nefeli / Mourkioti, Ioanna / Mirzazadeh, Reza / Polyzos, Alexandros / Garnerone, Silvano / Mizi, Athanasia / Gusmao, Eduardo G. / Sofiadis, Konstantinos / Gál, Zita / Larsen, Dorthe H. / Pefani, Dafni-Eleftheria / Demaria, Marco /

Tsirigos, Aristotelis / Crosetto, Nicola / Maya-Mendoza, Apolinar / Papaspyropoulos, Angelos / Evangelou, Konstantinos / Bartek, Jiri / Papantonis, Argyris / Gorgoulis, Vassilis G.

Molecular cell. 2021 Dec. 02, v. 81, no. 23

2021

Abstract: Oncogene-induced senescence (OIS) is an inherent and important tumor suppressor mechanism. However, if not removed timely via immune surveillance, senescent cells also have detrimental effects. Although this has mostly been attributed to the senescence- ... ...

Abstract	Oncogene-induced senescence (OIS) is an inherent and important tumor suppressor mechanism. However, if not removed timely via immune surveillance, senescent cells also have detrimental effects. Although this has mostly been attributed to the senescence-associated secretory phenotype (SASP) of these cells, we recently proposed that “escape” from the senescent state is another unfavorable outcome. The mechanism underlying this phenomenon remains elusive. Here, we exploit genomic and functional data from a prototypical human epithelial cell model carrying an inducible CDC6 oncogene to identify an early-acquired recurrent chromosomal inversion that harbors a locus encoding the circadian transcription factor BHLHE40. This inversion alone suffices for BHLHE40 activation upon CDC6 induction and driving cell cycle re-entry of senescent cells, and malignant transformation. Ectopic overexpression of BHLHE40 prevented induction of CDC6-triggered senescence. We provide strong evidence in support of replication stress-induced genomic instability being a causative factor underlying “escape” from oncogene-induced senescence.
Keywords	cell cycle ; chromosome inversions ; epithelial cells ; genetic instability ; genomics ; humans ; loci ; models ; monitoring ; neoplasms ; oncogenes ; phenotype ; transcription factors
Language	English
Dates of publication	2021-1202
Size	p. 4907-4923.e8.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2021.10.017
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Article ; Online: CRH Promotes the Neurogenic Activity of Neural Stem Cells in the Adult Hippocampus.

Koutmani, Yassemi / Gampierakis, Ioannis A / Polissidis, Alexia / Ximerakis, Methodios / Koutsoudaki, Paraskevi N / Polyzos, Alexandros / Agrogiannis, George / Karaliota, Sevasti / Thomaidou, Dimitra / Rubin, Lee L / Politis, Panagiotis K / Karalis, Katia P

Cell reports

2019 Volume 29, Issue 4, Page(s) 932–945.e7

Abstract: Local cues in the adult neurogenic niches dynamically regulate homeostasis in neural stem cells, whereas their identity and associated molecular mechanisms remain poorly understood. Here, we show that corticotropin-releasing hormone (CRH), the major ... ...

Abstract	Local cues in the adult neurogenic niches dynamically regulate homeostasis in neural stem cells, whereas their identity and associated molecular mechanisms remain poorly understood. Here, we show that corticotropin-releasing hormone (CRH), the major mediator of mammalian stress response and a key neuromodulator in the adult brain, is necessary for hippocampal neural stem cell (hiNSC) activity under physiological conditions. In particular, we demonstrate functionality of the CRH/CRH receptor (CRHR) system in mouse hiNSCs and conserved expression in humans. Most important, we show that genetic deficiency of CRH impairs hippocampal neurogenesis, affects spatial memory, and compromises hiNSCs' responsiveness to environmental stimuli. These deficits have been partially restored by virus-mediated CRH expression. Additionally, we provide evidence that local disruption of the CRH/CRHR system reduces neurogenesis, while exposure of adult hiNSCs to CRH promotes neurogenic activity via BMP4 suppression. Our findings suggest a critical role of CRH in adult neurogenesis, independently of its stress-related systemic function.
MeSH term(s)	Animals ; Cell Line ; Cells, Cultured ; Corticotropin-Releasing Hormone/genetics ; Corticotropin-Releasing Hormone/metabolism ; Hippocampus/cytology ; Hippocampus/metabolism ; Hippocampus/physiology ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Neural Stem Cells/cytology ; Neural Stem Cells/metabolism ; Neurogenesis ; Receptors, Corticotropin-Releasing Hormone/genetics ; Receptors, Corticotropin-Releasing Hormone/metabolism ; Spatial Memory
Chemical Substances	Receptors, Corticotropin-Releasing Hormone ; Corticotropin-Releasing Hormone (9015-71-8)
Language	English
Publishing date	2019-10-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.09.037
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Article ; Online: Transcriptomics in tissue glucocorticoid sensitivity.

Nicolaides, Nicolas C / Polyzos, Alexandros / Koniari, Eleni / Lamprokostopoulou, Agaristi / Papageorgiou, Ifigeneia / Golfinopoulou, Eleni / Papathanasiou, Chrysanthi / Sertedaki, Amalia / Thanos, Dimitris / Chrousos, George P / Charmandari, Evangelia

European journal of clinical investigation

2019 Volume 49, Issue 8, Page(s) e13129

Abstract: Background: Synthetic glucocorticoids are widely used in the treatment of several inflammatory, autoimmune and lymphoproliferative disorders. However, considerable variation in response to therapeutic doses of glucocorticoids has been documented among ... ...

Abstract	Background: Synthetic glucocorticoids are widely used in the treatment of several inflammatory, autoimmune and lymphoproliferative disorders. However, considerable variation in response to therapeutic doses of glucocorticoids has been documented among individuals. The aim of our study was to identify novel glucocorticoid sensitivity-determining genes using genome-wide expression profiling in healthy subjects. Methods: One hundred one healthy subjects [mean age ± standard error of the mean (SEM); 26.52 ± 0.50 years] were given 0.25 mg dexamethasone at midnight, and serum cortisol concentrations were determined at 08:00 hours the following morning. Subjects were stratified into the 10% most glucocorticoid-sensitive and 10% most glucocorticoid-resistant according to the serum cortisol concentrations. Genomic DNA, RNA and plasma samples were obtained in the 22 subjects one month later. Results: Transcriptomic analysis showed variability between glucocorticoid-resistant and glucocorticoid-sensitive subjects. One hundred thirty-three genes were upregulated and 49 downregulated in the glucocorticoid-resistant compared to the glucocorticoid-sensitive group. Further analysis revealed differences between 3 glucocorticoid-resistant and 3 glucocorticoid-sensitive subjects. The majority of the 1058 upregulated genes and 1139 downregulated genes were found to participate in telomere maintenance, systemic lupus erythematosus and Alzheimer's disease. Interestingly, Synuclein A, a key molecule in Parkinson's disease, was upregulated in the subgroup of glucocorticoid-sensitive subjects. Conclusions: We have identified differences in tissue sensitivity to glucocorticoids among healthy subjects at the transcriptomic level. These differences are associated with differential expression of genes related to autoimmune and neurological disorders.
MeSH term(s)	Adult ; Alzheimer Disease/blood ; Alzheimer Disease/genetics ; Dexamethasone/pharmacology ; Down-Regulation/drug effects ; Female ; Gene Expression Profiling ; Glucocorticoids/pharmacology ; Humans ; Hydrocortisone/blood ; Lupus Erythematosus, Systemic/blood ; Lupus Erythematosus, Systemic/genetics ; Male ; Receptors, Glucocorticoid/genetics ; Telomere Homeostasis/drug effects ; Telomere Homeostasis/genetics ; Transcriptome/drug effects ; Up-Regulation/drug effects ; alpha-Synuclein/blood
Chemical Substances	Glucocorticoids ; NR3C1 protein, human ; Receptors, Glucocorticoid ; SNCA protein, human ; alpha-Synuclein ; Dexamethasone (7S5I7G3JQL) ; Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2019-05-30
Publishing country	England
Document type	Journal Article
ZDB-ID	186196-7
ISSN	1365-2362 ; 0014-2972 ; 0960-135X
ISSN (online)	1365-2362
ISSN	0014-2972 ; 0960-135X
DOI	10.1111/eci.13129
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