LIVIVO - Search results -

Search results

Result 1 - 10 of total 16

Search options

Article: Neuroserpin, a crucial regulator for axogenesis, synaptic modelling and cell–cell interactions in the pathophysiology of neurological disease

Godinez, Angela / Rajput, Rashi / Chitranshi, Nitin / Gupta, Veer / Basavarajappa, Devaraj / Sharma, Samridhi / You, Yuyi / Pushpitha, Kanishka / Dhiman, Kunal / Mirzaei, Mehdi / Graham, Stuart / Gupta, Vivek

Cellular and molecular life sciences. 2022 Mar., v. 79, no. 3

2022

Abstract: Neuroserpin is an axonally secreted serpin that is involved in regulating plasminogen and its enzyme activators, such as tissue plasminogen activator (tPA). The protein has been increasingly shown to play key roles in neuronal development, plasticity, ... ...

Abstract	Neuroserpin is an axonally secreted serpin that is involved in regulating plasminogen and its enzyme activators, such as tissue plasminogen activator (tPA). The protein has been increasingly shown to play key roles in neuronal development, plasticity, maturation and synaptic refinement. The proteinase inhibitor may function both independently and through tPA-dependent mechanisms. Herein, we discuss the recent evidence regarding the role of neuroserpin in healthy and diseased conditions and highlight the participation of the serpin in various cellular signalling pathways. Several polymorphisms and mutations have also been identified in the protein that may affect the serpin conformation, leading to polymer formation and its intracellular accumulation. The current understanding of the involvement of neuroserpin in Alzheimer’s disease, cancer, glaucoma, stroke, neuropsychiatric disorders and familial encephalopathy with neuroserpin inclusion bodies (FENIB) is presented. To truly understand the detrimental consequences of neuroserpin dysfunction and the effective therapeutic targeting of this molecule in pathological conditions, a cross-disciplinary understanding of neuroserpin alterations and its cellular signaling networks is essential.
Keywords	encephalopathy ; glaucoma ; neurons ; pathophysiology ; plasminogen ; plasticity ; polymers ; proteinase inhibitors ; stroke ; t-plasminogen activator ; therapeutics
Language	English
Dates of publication	2022-03
Size	p. 172.
Publishing place	Springer International Publishing
Document type	Article
Note	Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-022-04185-6
Database	NAL-Catalogue (AGRICOLA)

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Bonn / Germany

Z 4' 47/14: Show issues

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.

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article: Oxidative Stress Induced Dysfunction of Protein Synthesis in 661W Mice Photoreceptor Cells.

Deng, Liting / Gupta, Vivek / Abyadeh, Morteza / Chitranshi, Nitin / Pushpitha, Kanishka / Wu, Yunqi / Gupta, Veer / You, Yuyi / Paulo, Joao A / Graham, Stuart L / Mirzaei, Mehdi / Haynes, Paul A

Proteomes

2023 Volume 11, Issue 2

Abstract: Photoreceptor cells are highly susceptible to oxidative-stress-induced damage due to their high metabolic rate. Oxidative stress plays a key role in driving pathological events in several different ocular diseases, which lead to retinal degeneration and ... ...

Abstract	Photoreceptor cells are highly susceptible to oxidative-stress-induced damage due to their high metabolic rate. Oxidative stress plays a key role in driving pathological events in several different ocular diseases, which lead to retinal degeneration and ultimately blindness. A growing number of studies have been performed to understand downstream events caused by ROS induced oxidative stress in photoreceptor cells; however, the underlying mechanisms of ROS toxicity are not fully understood. To shed light on ROS induced downstream pathological events, we employed a tandem mass tag (TMT) labelling-based quantitative mass-spectrometric approach to determine proteome changes in 661W photoreceptor cells following oxidative stress induction via the application of different concentrations of H
Language	English
Publishing date	2023-04-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720995-7
ISSN	2227-7382
ISSN	2227-7382
DOI	10.3390/proteomes11020012
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Neuroserpin gene therapy inhibits retinal ganglion cell apoptosis and promotes functional preservation in glaucoma.

Chitranshi, Nitin / Rajput, Rashi / Godinez, Angela / Pushpitha, Kanishka / Mirzaei, Mehdi / Basavarajappa, Devaraj / Gupta, Veer / Sharma, Samridhi / You, Yuyi / Galliciotti, Giovanna / Salekdeh, Ghasem H / Baker, Mark S / Graham, Stuart L / Gupta, Vivek K

Molecular therapy : the journal of the American Society of Gene Therapy

2023 Volume 31, Issue 7, Page(s) 2056–2076

Abstract: Our research has proven that the inhibitory activity of the serine protease inhibitor neuroserpin (NS) is impaired because of its oxidation deactivation in glaucoma. Using genetic NS knockout ( ... ...

Abstract	Our research has proven that the inhibitory activity of the serine protease inhibitor neuroserpin (NS) is impaired because of its oxidation deactivation in glaucoma. Using genetic NS knockout (NS
MeSH term(s)	Mice ; Animals ; Retinal Ganglion Cells/metabolism ; Beclin-1/metabolism ; Disease Models, Animal ; Glaucoma/genetics ; Glaucoma/therapy ; Glaucoma/metabolism ; Apoptosis/genetics ; Intraocular Pressure ; Neuroserpin
Chemical Substances	Beclin-1
Language	English
Publishing date	2023-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1016/j.ymthe.2023.03.008
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5640: 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

Details ▾

Article: Siponimod exerts neuroprotective effects on the retina and higher visual pathway through neuronal S1PR1 in experimental glaucoma.

Basavarajappa, Devaraj / Gupta, Vivek / Chitranshi, Nitin / Wall, Roshana Vander / Rajput, Rashi / Pushpitha, Kanishka / Sharma, Samridhi / Mirzaei, Mehdi / Klistorner, Alexander / Graham, Stuart L

Neural regeneration research

2022 Volume 18, Issue 4, Page(s) 840–848

Abstract: Sphingosine-1-phosphate receptor (S1PR) signaling regulates diverse pathophysiological processes in the central nervous system. The role of S1PR signaling in neurodegenerative conditions is still largely unidentified. Siponimod is a specific modulator of ...

Abstract	Sphingosine-1-phosphate receptor (S1PR) signaling regulates diverse pathophysiological processes in the central nervous system. The role of S1PR signaling in neurodegenerative conditions is still largely unidentified. Siponimod is a specific modulator of S1P1 and S1P5 receptors, an immunosuppressant drug for managing secondary progressive multiple sclerosis. We investigated its neuroprotective properties in vivo on the retina and the brain in an optic nerve injury model induced by a chronic increase in intraocular pressure or acute N-methyl-D-aspartate excitotoxicity. Neuronal-specific deletion of sphingosine-1-phosphate receptor (S1PR1) was carried out by expressing AAV-PHP.eB-Cre recombinase under Syn1 promoter in S1PR1
Language	English
Publishing date	2022-10-17
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.344952
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Neuroserpin, a crucial regulator for axogenesis, synaptic modelling and cell-cell interactions in the pathophysiology of neurological disease.

Cellular and molecular life sciences : CMLS

2022 Volume 79, Issue 3, Page(s) 172

Abstract	Neuroserpin is an axonally secreted serpin that is involved in regulating plasminogen and its enzyme activators, such as tissue plasminogen activator (tPA). The protein has been increasingly shown to play key roles in neuronal development, plasticity, maturation and synaptic refinement. The proteinase inhibitor may function both independently and through tPA-dependent mechanisms. Herein, we discuss the recent evidence regarding the role of neuroserpin in healthy and diseased conditions and highlight the participation of the serpin in various cellular signalling pathways. Several polymorphisms and mutations have also been identified in the protein that may affect the serpin conformation, leading to polymer formation and its intracellular accumulation. The current understanding of the involvement of neuroserpin in Alzheimer's disease, cancer, glaucoma, stroke, neuropsychiatric disorders and familial encephalopathy with neuroserpin inclusion bodies (FENIB) is presented. To truly understand the detrimental consequences of neuroserpin dysfunction and the effective therapeutic targeting of this molecule in pathological conditions, a cross-disciplinary understanding of neuroserpin alterations and its cellular signaling networks is essential.
MeSH term(s)	Axons/metabolism ; Cell Communication ; Humans ; Neoplasms/metabolism ; Neoplasms/pathology ; Nervous System Diseases/metabolism ; Nervous System Diseases/pathology ; Neuronal Plasticity ; Neuropeptides/chemistry ; Neuropeptides/metabolism ; Plasminogen/metabolism ; Serpins/chemistry ; Serpins/metabolism ; Signal Transduction ; Tissue Plasminogen Activator/metabolism ; Neuroserpin
Chemical Substances	Neuropeptides ; Serpins ; Plasminogen (9001-91-6) ; Tissue Plasminogen Activator (EC 3.4.21.68)
Language	English
Publishing date	2022-03-04
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/s00018-022-04185-6
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 195: 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 ▾

Article ; Online: Inner retinal injury in experimental glaucoma is prevented upon AAV mediated Shp2 silencing in a caveolin dependent manner.

Abbasi, Mojdeh / Gupta, Vivek K / Chitranshi, Nitin / Gupta, Veer / Ranjbaran, Reza / Rajput, Rashi / Pushpitha, Kanishka / Kb, Devaraj / You, Yuyi / Salekdeh, Ghasem Hosseini / Parton, Robert G / Mirzaei, Mehdi / Graham, Stuart L

Theranostics

2021 Volume 11, Issue 13, Page(s) 6154–6172

Abstract: SH2 domain containing tyrosine phosphatase 2 (Shp2; PTPN11) regulates several intracellular pathways downstream of multiple growth factor receptors. Our studies implicate that Shp2 interacts with Caveolin-1 (Cav-1) protein in retinal ganglion cells (RGCs) ...

Abstract	SH2 domain containing tyrosine phosphatase 2 (Shp2; PTPN11) regulates several intracellular pathways downstream of multiple growth factor receptors. Our studies implicate that Shp2 interacts with Caveolin-1 (Cav-1) protein in retinal ganglion cells (RGCs) and negatively regulates BDNF/TrkB signaling. This study aimed to investigate the mechanisms underlying the protective effects of shp2 silencing in the RGCs in glaucomatous conditions.
MeSH term(s)	Alpha-Globulins/genetics ; Animals ; Apoptosis ; Brain-Derived Neurotrophic Factor/physiology ; Caveolin 1/deficiency ; Caveolin 1/genetics ; Caveolin 1/physiology ; DNA, Complementary/genetics ; Dependovirus/genetics ; Focal Adhesion Kinase 1/physiology ; Gene Knockdown Techniques ; Genes, Reporter ; Genes, Synthetic ; Genetic Therapy ; Genetic Vectors/therapeutic use ; Glaucoma/metabolism ; Glaucoma/pathology ; Glaucoma/therapy ; Integrin beta1/physiology ; Intraocular Pressure ; Intravitreal Injections ; Membrane Glycoproteins/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Promoter Regions, Genetic ; Protein Tyrosine Phosphatase, Non-Receptor Type 11/antagonists & inhibitors ; Protein Tyrosine Phosphatase, Non-Receptor Type 11/biosynthesis ; Protein Tyrosine Phosphatase, Non-Receptor Type 11/genetics ; Protein-Tyrosine Kinases/physiology ; Retina/pathology ; Up-Regulation
Chemical Substances	Alpha-Globulins ; Bdnf protein, mouse ; Brain-Derived Neurotrophic Factor ; Caveolin 1 ; DNA, Complementary ; Integrin beta1 ; Membrane Glycoproteins ; chorionic alpha(2)-microglobulin ; Ntrk2 protein, mouse (EC 2.7.10.1) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Focal Adhesion Kinase 1 (EC 2.7.10.2) ; Ptk2 protein, mouse (EC 2.7.10.2) ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 (EC 3.1.3.48) ; Ptpn11 protein, mouse (EC 3.1.3.48)
Language	English
Publishing date	2021-04-15
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.55472
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Mouse model of Alzheimer's disease demonstrates differential effects of early disease pathology on various brain regions.

Deng, Liting / Gupta, Vivek K / Wu, Yunqi / Pushpitha, Kanishka / Chitranshi, Nitin / Gupta, Veer B / Fitzhenry, Matthew J / Moghaddam, Masoud Zabet / Karl, Tim / Salekdeh, Ghasem Hosseini / Graham, Stuart L / Haynes, Paul A / Mirzaei, Mehdi

Proteomics

2021 Volume 21, Issue 7-8, Page(s) e2000213

Abstract: Different parts of the brain are affected distinctively in various stages of the Alzheimer's disease (AD) pathogenesis. Identifying the biochemical changes in specific brain regions is key to comprehend the neuropathological mechanisms in early pre- ... ...

Abstract	Different parts of the brain are affected distinctively in various stages of the Alzheimer's disease (AD) pathogenesis. Identifying the biochemical changes in specific brain regions is key to comprehend the neuropathological mechanisms in early pre-symptomatic phases of AD. Quantitative proteomics profiling of four distinct areas of the brain of young APP/PS1 mouse model of AD was performed followed by biochemical pathway enrichment analysis. Findings revealed fundamental compositional and functional shifts even in the early stages of the disease. This novel study highlights unique proteome and biochemical pathway alterations in specific regions of the brain that underlie the early stages of AD pathology and will provide a framework for future longitudinal studies. The proteomics data were deposited into the ProteomeXchange Consortium via PRIDE with the identifier PXD019192.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Protein Precursor/genetics ; Animals ; Brain/metabolism ; Brain/pathology ; Disease Models, Animal ; Mice ; Presenilin-1/genetics ; Proteome/metabolism
Chemical Substances	Amyloid beta-Protein Precursor ; Presenilin-1 ; Proteome
Language	English
Publishing date	2021-03-09
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2032093-0
ISSN	1615-9861 ; 1615-9853
ISSN (online)	1615-9861
ISSN	1615-9853
DOI	10.1002/pmic.202000213
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5386: 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)
Zs.A 1868: 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 ▾

Article: Amyloid-beta peptide neurotoxicity in human neuronal cells is associated with modulation of insulin-like growth factor transport, lysosomal machinery and extracellular matrix receptor interactions.

Deng, Liting / Haynes, Paul A / Wu, Yunqi / Amirkhani, Ardeshir / Kamath, Karthik Shantharam / Wu, Jemma X / Pushpitha, Kanishka / Gupta, Veer / Graham, Stuart / Gupta, Vivek K / Mirzaei, Mehdi

Neural regeneration research

2020 Volume 15, Issue 11, Page(s) 2131–2142

Abstract: Extracellular deposits of the amyloid-beta peptide (Aβ) are known as the main pathological hallmark of Alzheimer's disease. In Alzheimer's disease, neurons are injured and die throughout the brain, a process in which Aβ neurotoxicity is considered to ... ...

Abstract	Extracellular deposits of the amyloid-beta peptide (Aβ) are known as the main pathological hallmark of Alzheimer's disease. In Alzheimer's disease, neurons are injured and die throughout the brain, a process in which Aβ neurotoxicity is considered to play an important role. However, the molecular mechanisms underlying Aβ toxicity that lead to neurodegeneration are not clearly established. Here we have elucidated the molecular pathways and networks which are impacted by Aβ in neurons using SH-SY5Y human neuroblastoma cells as a model. These cells were treated with Aβ
Language	English
Publishing date	2020-05-11
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.282261
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Evolving geographic diversity in SARS-CoV2 and in silico analysis of replicating enzyme 3CL

Chitranshi, Nitin / Gupta, Vivek K / Rajput, Rashi / Godinez, Angela / Pushpitha, Kanishka / Shen, Ting / Mirzaei, Mehdi / You, Yuyi / Basavarajappa, Devaraj / Gupta, Veer / Graham, Stuart L

Journal of translational medicine

2020 Volume 18, Issue 1, Page(s) 278

Abstract: Background: Severe acute respiratory syndrome (SARS) has been initiating pandemics since the beginning of the century. In December 2019, the world was hit again by a devastating SARS episode that has so far infected almost four million individuals ... ...

Abstract	Background: Severe acute respiratory syndrome (SARS) has been initiating pandemics since the beginning of the century. In December 2019, the world was hit again by a devastating SARS episode that has so far infected almost four million individuals worldwide, with over 200,000 fatalities having already occurred by mid-April 2020, and the infection rate continues to grow exponentially. SARS coronavirus 2 (SARS-CoV-2) is a single stranded RNA pathogen which is characterised by a high mutation rate. It is vital to explore the mutagenic capability of the viral genome that enables SARS-CoV-2 to rapidly jump from one host immunity to another and adapt to the genetic pool of local populations. Methods: For this study, we analysed 2301 complete viral sequences reported from SARS-CoV-2 infected patients. SARS-CoV-2 host genomes were collected from The Global Initiative on Sharing All Influenza Data (GISAID) database containing 9 genomes from pangolin-CoV origin and 3 genomes from bat-CoV origin, Wuhan SARS-CoV2 reference genome was collected from GeneBank database. The Multiple sequence alignment tool, Clustal Omega was used for genomic sequence alignment. The viral replicating enzyme, 3-chymotrypsin-like cysteine protease (3CL Results: Our results demonstrate that bat-CoV shares > 96% similar identity, while pangolin-CoV shares 85.98% identity with Wuhan SARS-CoV-2 genome. This in-depth analysis has identified 12 novel recurrent mutations in South American and African viral genomes out of which 3 were unique in South America, 4 unique in Africa and 5 were present in-patient isolates from both populations. Using state of the art in silico approaches, this study further investigates the interaction of repurposed drugs with the SARS-CoV-2 3CL Conclusions: Overall, this study provides insights into the evolving mutations, with implications to understand viral pathogenicity and possible new strategies for repurposing compounds to combat the nCovid-19 pandemic.
MeSH term(s)	Betacoronavirus/enzymology ; Betacoronavirus/genetics ; COVID-19 ; Computer Simulation ; Coronavirus 3C Proteases ; Coronavirus Infections/virology ; Cysteine Endopeptidases/metabolism ; DNA Replication ; Drug Repositioning ; Evolution, Molecular ; Genome, Viral ; Geography ; Humans ; Molecular Docking Simulation ; Mutation/genetics ; Mutation Rate ; Pandemics ; Phylogeny ; Pneumonia, Viral/virology ; SARS-CoV-2 ; Viral Nonstructural Proteins/metabolism ; Virus Assembly
Chemical Substances	Viral Nonstructural Proteins ; Cysteine Endopeptidases (EC 3.4.22.-) ; Coronavirus 3C Proteases (EC 3.4.22.28)
Keywords	covid19
Language	English
Publishing date	2020-07-09
Publishing country	England
Document type	Journal Article
ISSN	1479-5876
ISSN (online)	1479-5876
DOI	10.1186/s12967-020-02448-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Retinoid x receptor modulation protects against ER stress response and rescues glaucoma phenotypes in adult mice.

Dheer, Yogita / Chitranshi, Nitin / Gupta, Veer / Sharma, Samridhi / Pushpitha, Kanishka / Abbasi, Mojdeh / Mirzaei, Mehdi / You, Yuyi / Graham, Stuart L / Gupta, Vivek

Experimental neurology

2019 Volume 314, Page(s) 111–125

Abstract: Retinoid X receptors (RXRs) play an important role in transcription, are involved in numerous cellular networks from cell proliferation to lipid metabolism and are essential for normal eye development. RXRs form homo or heterodimers with other nuclear ... ...

Abstract	Retinoid X receptors (RXRs) play an important role in transcription, are involved in numerous cellular networks from cell proliferation to lipid metabolism and are essential for normal eye development. RXRs form homo or heterodimers with other nuclear receptors, bind to DNA response elements and regulate several biological processes including neurogenesis. Mounting evidence suggests that RXR activation by selective RXR modulators (sRXRms) may be neuroprotective in the central nervous system. However, their potential neuroprotective role in the retina and specifically in glaucoma remains unexplored. This study investigated changes in RXR expression in the human and mouse retina under glaucomatous stress conditions and investigated the effect of RXR modulation on the RGCs using pharmacological approaches. RXR protein levels in retina were downregulated in both human glaucoma and experimental RGC injury models while RXR agonist, bexarotene treatment resulted in upregulation of RXR expression particularly in the inner retinal layers. Retinal electrophysiological recordings and histological analysis indicated that inner retinal function and retinal laminar structure were preserved upon treatment with bexarotene. These protective effects were associated with downregulation of ER stress marker response upon bexarotene treatment under glaucoma conditions. Overall, retinal RXR modulation by bexarotene significantly protected RGCs in vivo in both acute and chronic glaucoma models.
MeSH term(s)	Aged ; Aged, 80 and over ; Aging ; Animals ; Bexarotene/pharmacology ; Bexarotene/therapeutic use ; Electroretinography ; Endoplasmic Reticulum Stress/drug effects ; Female ; Gene Expression/drug effects ; Glaucoma/pathology ; Glaucoma/prevention & control ; Histone Deacetylase Inhibitors/therapeutic use ; Histone Deacetylases/metabolism ; Humans ; In Vitro Techniques ; Male ; Mice ; Mice, Inbred C57BL ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Phenotype ; Retina/drug effects ; Retina/metabolism ; Retina/pathology ; Retinoid X Receptors/agonists ; Retinoid X Receptors/biosynthesis
Chemical Substances	Histone Deacetylase Inhibitors ; Neuroprotective Agents ; Retinoid X Receptors ; Bexarotene (A61RXM4375) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2019-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2019.01.015
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 184: 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 ▾

To top

Full text online

More links

Kategorien

In stock of ZB MED Bonn / Germany

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

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

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito