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Article ; Online: The Inflammasome in Times of COVID-19

de Rivero Vaccari, Juan Carlos / Dietrich, W. Dalton / Keane, Robert W. / de Rivero Vaccari, Juan Pablo

2020 Volume 11

Keywords	covid19
Publisher	Frontiers Media SA
Publishing country	ch
Document type	Article ; Online
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.583373
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The Inflammasome in Times of COVID-19.

de Rivero Vaccari, Juan Carlos / Dietrich, W Dalton / Keane, Robert W / de Rivero Vaccari, Juan Pablo

Frontiers in immunology

2020 Volume 11, Page(s) 583373

Abstract: Coronaviruses (CoVs) are members of the genus Betacoronavirus and the Coronaviridiae family responsible for infections such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and more recently, coronavirus disease-2019 ( ...

Abstract	Coronaviruses (CoVs) are members of the genus Betacoronavirus and the Coronaviridiae family responsible for infections such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and more recently, coronavirus disease-2019 (COVID-19). CoV infections present mainly as respiratory infections that lead to acute respiratory distress syndrome (ARDS). However, CoVs, such as COVID-19, also present as a hyperactivation of the inflammatory response that results in increased production of inflammatory cytokines such as interleukin (IL)-1β and its downstream molecule IL-6. The inflammasome is a multiprotein complex involved in the activation of caspase-1 that leads to the activation of IL-1β in a variety of diseases and infections such as CoV infection and in different tissues such as lungs, brain, intestines and kidneys, all of which have been shown to be affected in COVID-19 patients. Here we review the literature regarding the mechanism of inflammasome activation by CoV infection, the role of the inflammasome in ARDS, ventilator-induced lung injury (VILI), and Disseminated Intravascular Coagulation (DIC) as well as the potential mechanism by which the inflammasome may contribute to the damaging effects of inflammation in the cardiac, renal, digestive, and nervous systems in COVID-19 patients.
MeSH term(s)	Betacoronavirus/immunology ; COVID-19 ; Caspase 1/metabolism ; Coronavirus Infections/immunology ; Coronavirus Infections/pathology ; Cytokine Release Syndrome/pathology ; Disseminated Intravascular Coagulation/pathology ; Humans ; Inflammasomes/immunology ; Inflammation/pathology ; Interleukin-1beta/metabolism ; Pandemics ; Pneumonia, Viral/immunology ; Pneumonia, Viral/pathology ; SARS-CoV-2 ; Severe Acute Respiratory Syndrome/pathology ; Ventilator-Induced Lung Injury/pathology
Chemical Substances	IL1B protein, human ; Inflammasomes ; Interleukin-1beta ; Caspase 1 (EC 3.4.22.36)
Keywords	covid19
Language	English
Publishing date	2020-10-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.583373
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Inflammasome Proteins as Inflammatory Biomarkers of Age-Related Macular Degeneration.

Weaver, Cailey / Cyr, Brianna / de Rivero Vaccari, Juan Carlos / de Rivero Vaccari, Juan Pablo

Translational vision science & technology

2020 Volume 9, Issue 13, Page(s) 27

Abstract: Purpose: Age-related macular degeneration (AMD) can result in severe vision loss and blurriness in the older population. The early and intermediate stages of AMD typically start without noticeable symptoms and can only be detected with a comprehensive ... ...

Abstract	Purpose: Age-related macular degeneration (AMD) can result in severe vision loss and blurriness in the older population. The early and intermediate stages of AMD typically start without noticeable symptoms and can only be detected with a comprehensive eye exam. Because of the quiet onset of the disease, it is necessary to identify potential biomarkers to aid in the diagnosis, staging, and association with disease onset. Inflammasome signaling proteins are prominent biomarkers in the central nervous system, and the inflammasome has been shown to play a role in the innate inflammatory response in aging and AMD. Methods: Serum from healthy controls and AMD patients were analyzed for the protein levels of Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), interleukin (IL)-18 and C-reactive protein (CRP) to determine cutoff points, positive and negative predictive values, and receiver operator characteristic curves, as well as univariate and multivariate linear and logistic regression models. Results: ASC, IL-18, and CRP were elevated in the serum of AMD patients when compared to healthy controls. The area under the curve (AUC) for ASC was 0.98 with a cutoff point of 365.6 pg/mL, whereas IL-18 had an AUC of 0.73 and a cutoff point of 242.4 pg/mL, and the AUC for CRP was 0.67 with a cutoff point of 8,684,152 pg/mL. Levels of IL-18 had a statistically significant linear correlation with that of ASC with an adjusted Conclusions: ASC, IL-18, and CRP are elevated in patients with AMD, and the protein levels of IL-18 are partially the result of ASC protein expression. Moreover, elevated protein levels of ASC in serum and a diagnosis of HTN increase the odds of patients having a diagnosis of AMD. Translational relevance: Biomarkers of AMD may be used to monitor disease risk, response to treatment and disease progression.
MeSH term(s)	Biomarkers ; C-Reactive Protein ; Humans ; Inflammasomes ; Interleukin-18 ; Macular Degeneration/diagnosis
Chemical Substances	Biomarkers ; Inflammasomes ; Interleukin-18 ; C-Reactive Protein (9007-41-4)
Language	English
Publishing date	2020-12-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2674602-5
ISSN	2164-2591 ; 2164-2591
ISSN (online)	2164-2591
ISSN	2164-2591
DOI	10.1167/tvst.9.13.27
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The Inflammasome in Times of COVID-19

de Rivero Vaccari, Juan Carlos / Dietrich, W Dalton / Keane, Robert W / de Rivero Vaccari, Juan Pablo

Front Immunol

Abstract	Coronaviruses (CoVs) are members of the genus Betacoronavirus and the Coronaviridiae family responsible for infections such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and more recently, coronavirus disease-2019 (COVID-19). CoV infections present mainly as respiratory infections that lead to acute respiratory distress syndrome (ARDS). However, CoVs, such as COVID-19, also present as a hyperactivation of the inflammatory response that results in increased production of inflammatory cytokines such as interleukin (IL)-1ß and its downstream molecule IL-6. The inflammasome is a multiprotein complex involved in the activation of caspase-1 that leads to the activation of IL-1ß in a variety of diseases and infections such as CoV infection and in different tissues such as lungs, brain, intestines and kidneys, all of which have been shown to be affected in COVID-19 patients. Here we review the literature regarding the mechanism of inflammasome activation by CoV infection, the role of the inflammasome in ARDS, ventilator-induced lung injury (VILI), and Disseminated Intravascular Coagulation (DIC) as well as the potential mechanism by which the inflammasome may contribute to the damaging effects of inflammation in the cardiac, renal, digestive, and nervous systems in COVID-19 patients.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #902402
Database	COVID19

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Article ; Online: The Inflammasome in Times of COVID-19

Juan Carlos de Rivero Vaccari / W. Dalton Dietrich / Robert W. Keane / Juan Pablo de Rivero Vaccari

Frontiers in Immunology, Vol

2020 Volume 11

Abstract	Coronaviruses (CoVs) are members of the genus Betacoronavirus and the Coronaviridiae family responsible for infections such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and more recently, coronavirus disease-2019 (COVID-19). CoV infections present mainly as respiratory infections that lead to acute respiratory distress syndrome (ARDS). However, CoVs, such as COVID-19, also present as a hyperactivation of the inflammatory response that results in increased production of inflammatory cytokines such as interleukin (IL)-1β and its downstream molecule IL-6. The inflammasome is a multiprotein complex involved in the activation of caspase-1 that leads to the activation of IL-1β in a variety of diseases and infections such as CoV infection and in different tissues such as lungs, brain, intestines and kidneys, all of which have been shown to be affected in COVID-19 patients. Here we review the literature regarding the mechanism of inflammasome activation by CoV infection, the role of the inflammasome in ARDS, ventilator-induced lung injury (VILI), and Disseminated Intravascular Coagulation (DIC) as well as the potential mechanism by which the inflammasome may contribute to the damaging effects of inflammation in the cardiac, renal, digestive, and nervous systems in COVID-19 patients.
Keywords	inflammasome ; COVID-19 ; inflammation ; coronavirus ; caspase-1 ; IL-1beta ; Immunologic diseases. Allergy ; RC581-607 ; covid19
Subject code	610
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: RIG-I contributes to the innate immune response after cerebral ischemia.

Brand, Frank J / de Rivero Vaccari, Juan Carlos / Mejias, Nancy H / Alonso, Ofelia F / de Rivero Vaccari, Juan Pablo

Journal of inflammation (London, England)

2015 Volume 12, Page(s) 52

Abstract: Background: Focal cerebral ischemia induces an inflammatory response that when exacerbated contributes to deleterious outcomes. The molecular basis regarding the regulation of the innate immune response after focal cerebral ischemia remains poorly ... ...

Abstract	Background: Focal cerebral ischemia induces an inflammatory response that when exacerbated contributes to deleterious outcomes. The molecular basis regarding the regulation of the innate immune response after focal cerebral ischemia remains poorly understood. Methods: In this study we examined the expression of retinoic acid-inducible gene (RIG)-like receptor-I (RIG-I) and its involvement in regulating inflammation after ischemia in the brain of rats subjected to middle cerebral artery occlusion (MCAO). In addition, we studied the regulation of RIG-I after oxygen glucose deprivation (OGD) in astrocytes in culture. Results: In this study we show that in the hippocampus of rats, RIG-I and IFN-α are elevated after MCAO. Consistent with these results was an increased in RIG-I and IFN-α after OGD in astrocytes in culture. These data are consistent with immunohistochemical analysis of hippocampal sections, indicating that in GFAP-positive cells there was an increase in RIG-I after MCAO. In addition, in this study we have identified n-propyl gallate as an inhibitor of IFN-α signaling in astrocytes. Conclusion: Our findings suggest a role for RIG-I in contributing to the innate immune response after focal cerebral ischemia.
Language	English
Publishing date	2015-09-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2164385-4
ISSN	1476-9255
ISSN	1476-9255
DOI	10.1186/s12950-015-0101-4
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Mincle signaling in the innate immune response after traumatic brain injury.

de Rivero Vaccari, Juan Carlos / Brand, Frank J / Berti, Aldo F / Alonso, Ofelia F / Bullock, M Ross / de Rivero Vaccari, Juan Pablo

Journal of neurotrauma

2015 Volume 32, Issue 4, Page(s) 228–236

Abstract: The innate immune response contributes to the inflammatory activity after traumatic brain injury (TBI). In the present study we identify macrophage-inducible C-type lectin (mincle) as a pattern recognition receptor that contributes to innate immunity in ... ...

Abstract	The innate immune response contributes to the inflammatory activity after traumatic brain injury (TBI). In the present study we identify macrophage-inducible C-type lectin (mincle) as a pattern recognition receptor that contributes to innate immunity in neurons after TBI. Here we report that mincle is activated by SAP130 in cortical neurons in culture, resulting in production of the inflammatory cytokine TNF. In addition, mincle and SAP130 are elevated in the brain and cerebrospinal fluid of humans after TBI and the brain of rodents after fluid percussion brain injury. Thus, these findings suggest the involvement of mincle to the pathology of TBI. Importantly, blocking mincle with a neutralizing antibody against mincle in cortical neurons in culture treated with SAP130 resulted in inhibition of mincle signaling and decreased TNF production. Therefore, our findings identify mincle as a contributor to the inflammatory response after TBI.
MeSH term(s)	Adolescent ; Adult ; Animals ; Brain Injuries/immunology ; Female ; Humans ; Immunity, Innate/immunology ; Immunoblotting ; Immunohistochemistry ; Lectins, C-Type/immunology ; Male ; Microscopy, Confocal ; Middle Aged ; Rats ; Rats, Sprague-Dawley ; Receptors, Immunologic/immunology ; Signal Transduction/immunology ; Young Adult
Chemical Substances	CLEC4D protein, human ; Lectins, C-Type ; Receptors, Immunologic
Language	English
Publishing date	2015-02-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2014.3436
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Article ; Online: Astrogliosis involves activation of retinoic acid-inducible gene-like signaling in the innate immune response after spinal cord injury.

de Rivero Vaccari, Juan Pablo / Minkiewicz, Julia / Wang, Xiaoliang / De Rivero Vaccari, Juan Carlos / German, Ramon / Marcillo, Alex E / Dietrich, W Dalton / Keane, Robert W

Glia

2011 Volume 60, Issue 3, Page(s) 414–421

Abstract: Spinal cord injury (SCI) induces a glial response in which astrocytes become activated and produce inflammatory mediators. The molecular basis for regulation of glial-innate immune responses remains poorly understood. Here, we examined the activation of ... ...

Abstract	Spinal cord injury (SCI) induces a glial response in which astrocytes become activated and produce inflammatory mediators. The molecular basis for regulation of glial-innate immune responses remains poorly understood. Here, we examined the activation of retinoic acid-inducible gene (RIG)-like receptors (RLRs) and their involvement in regulating inflammation after SCI. We show that astrocytes express two intracellular RLRs: RIG-I and melanoma differentiation-associated gene 5. SCI and stretch injury of cultured astrocytes stimulated RLR signaling as determined by phosphorylation of interferon regulatory factor 3 (IRF3) leading to production of type I interferons (IFNs). RLR signaling stimulation with synthetic ribonucleic acid resulted in RLR activation, phosphorylation of IRF3, and increased expression of glial fibrillary acidic protein (GFAP) and vimentin, two hallmarks of reactive astrocytes. Moreover, mitochondrial E3 ubiquitin protein ligase 1, an RLR inhibitor, decreased production of GFAP and vimentin after RIG-I signaling stimulation. Our findings identify a role for RLR signaling and type I IFN in regulating astrocyte innate immune responses after SCI.
MeSH term(s)	Analysis of Variance ; Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Astrocytes/physiology ; Cells, Cultured ; DEAD-box RNA Helicases/metabolism ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Enzyme Activation/drug effects ; Female ; Gene Expression Regulation/drug effects ; Glial Fibrillary Acidic Protein/metabolism ; Immunity, Innate/drug effects ; Immunity, Innate/physiology ; Interferon Regulatory Factor-3/metabolism ; Interferon Type I/genetics ; Interferon Type I/metabolism ; Interferon-Induced Helicase, IFIH1 ; Poly I-C/pharmacology ; RNA Helicases/metabolism ; RNA Helicases/pharmacology ; RNA, Double-Stranded/pharmacology ; Rats ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Spinal Cord Injuries/immunology ; Spinal Cord Injuries/metabolism ; Stress, Mechanical ; Time Factors ; Vimentin/metabolism
Chemical Substances	Glial Fibrillary Acidic Protein ; Interferon Regulatory Factor-3 ; Interferon Type I ; RNA, Double-Stranded ; Vimentin ; RIG-I protein, rat (EC 2.7.7.-) ; IFIH1 protein, human (EC 3.6.1.-) ; DEAD-box RNA Helicases (EC 3.6.4.13) ; Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13) ; RNA Helicases (EC 3.6.4.13) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2011-12-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.22275
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Article: Gap junctions are required for NMDA receptor dependent cell death in developing neurons.

de Rivero Vaccari, Juan Carlos / Corriveau, Roderick A / Belousov, Andrei B

Journal of neurophysiology

2007 Volume 98, Issue 5, Page(s) 2878–2886

Abstract: A number of studies have indicated an important role for N-methyl-D-aspartate (NMDA) receptors in cell survival versus cell death decisions during neuronal development, trauma, and ischemia. Coupling of neurons by electrical synapses (gap junctions) is ... ...

Abstract	A number of studies have indicated an important role for N-methyl-D-aspartate (NMDA) receptors in cell survival versus cell death decisions during neuronal development, trauma, and ischemia. Coupling of neurons by electrical synapses (gap junctions) is high or increases in neuronal networks during all three of these conditions. However, whether neuronal gap junctions contribute to NMDA receptor-regulated cell death is not known. Here we address the role of neuronal gap junction coupling in NMDA receptor-regulated cell death in developing neurons. We report that inactivation or hyperactivation of NMDA receptors induces neuronal cell death in primary hypothalamic cultures, specifically during the peak of developmental gap junction coupling. In contrast, increasing or decreasing NMDA receptor function when gap junction coupling is low has no or greatly reduced impact on cell survival. Pharmacological inactivation of gap junctions or knockout of neuronal connexin 36 prevents the cell death caused by NMDA receptor hypofunction or hyperfunction. The results indicate the critical role of neuronal gap junctions in cell death caused by increased or decreased NMDA receptor function in developing neurons. Based on these data, we propose the novel hypothesis that NMDA receptors and gap junctions work in concert to regulate neuronal survival.
MeSH term(s)	Analysis of Variance ; Animals ; Bicuculline/pharmacology ; Cell Death/physiology ; Cells, Cultured ; Connexins/deficiency ; Drug Interactions ; Embryo, Mammalian ; Excitatory Amino Acid Agents/pharmacology ; Female ; GABA Antagonists/pharmacology ; Gap Junctions/physiology ; Hypothalamus, Middle/cytology ; Male ; Mice ; Mice, Knockout ; Neurons/physiology ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/physiology ; Time Factors ; Gap Junction delta-2 Protein
Chemical Substances	Connexins ; Excitatory Amino Acid Agents ; GABA Antagonists ; Receptors, N-Methyl-D-Aspartate ; Bicuculline (Y37615DVKC)
Language	English
Publishing date	2007-09-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80161-6
ISSN	1522-1598 ; 0022-3077
ISSN (online)	1522-1598
ISSN	0022-3077
DOI	10.1152/jn.00362.2007
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Article ; Online: Ataxin-1 poly(Q)-induced proteotoxic stress and apoptosis are attenuated in neural cells by docosahexaenoic acid-derived neuroprotectin D1.

Calandria, Jorgelina M / Mukherjee, Pranab K / de Rivero Vaccari, Juan Carlos / Zhu, Min / Petasis, Nicos A / Bazan, Nicolas G

The Journal of biological chemistry

2012 Volume 287, Issue 28, Page(s) 23726–23739

Abstract: Neurodegenerative diseases share two common features: enhanced oxidative stress and cellular inability to scavenge structurally damaged abnormal proteins. Pathogenesis of polyglutamine (poly(Q)) diseases involves increased protein misfolding, along with ... ...

Abstract	Neurodegenerative diseases share two common features: enhanced oxidative stress and cellular inability to scavenge structurally damaged abnormal proteins. Pathogenesis of polyglutamine (poly(Q)) diseases involves increased protein misfolding, along with ubiquitin and chaperon protein-containing nuclear aggregates. In spinocerebellar ataxia, the brain and retina undergo degeneration. Neuroprotectin D1 (NPD1) is made on-demand in the nervous system and retinal pigment epithelial (RPE) cells in response to oxidative stress, which activates prosurvival signaling via regulation of gene expression and other processes. We hypothesized that protein misfolding-induced proteotoxic stress triggers NPD1 synthesis. We used ARPE-19 cells as a cellular model to assess stress due to ataxin-1 82Q protein expression and determine whether NPD1 prevents apoptosis. Ectopic ataxin-1 expression induced RPE cell apoptosis, which was abrogated by 100 nm docosahexaenoic acid, 10 ng/ml pigment epithelium-derived factor, or NPD1. Similarly, NPD1 was protective in neurons and primary human RPE cells. Furthermore, when ataxin-1 82Q was expressed in 15-lipoxygenase-1-deficient cells, apoptosis was greatly enhanced, and only NPD1 (50 nm) rescued cells from death. NPD1 reduced misfolded ataxin-1-induced accumulation of proapoptotic Bax in the cytoplasm, suggesting that NPD1 acts by preventing proapoptotic signaling pathways from occurring. Finally, NPD1 signaling interfered with ataxin-1/capicua repression of gene expression and decreased phosphorylated ataxin-1 in an Akt-independent manner, suggesting that NPD1 signaling modulates formation or stabilization of ataxin-1 complexes. These data suggest that 1) NPD1 synthesis is an early response induced by proteotoxic stress due to abnormally folded ataxin-1, and 2) NPD1 promotes cell survival through modulating stabilization of ataxin-1 functional complexes and pro-/antiapoptotic and inflammatory pathways.
MeSH term(s)	Apoptosis/drug effects ; Ataxin-1 ; Ataxins ; Blotting, Western ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; Cyclooxygenase 2/genetics ; Docosahexaenoic Acids/metabolism ; Docosahexaenoic Acids/pharmacology ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Humans ; Luciferases/genetics ; Luciferases/metabolism ; Microscopy, Fluorescence ; Mutation ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neurons/cytology ; Neurons/drug effects ; Neurons/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Peptides/genetics ; Peptides/metabolism ; Phosphorylation/drug effects ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Retinal Pigment Epithelium/cytology ; Retinal Pigment Epithelium/drug effects ; Retinal Pigment Epithelium/metabolism ; Stress, Physiological ; Transfection
Chemical Substances	ATXN1 protein, human ; Ataxin-1 ; Ataxins ; Nerve Tissue Proteins ; Nuclear Proteins ; Peptides ; protectin D1 ; Green Fluorescent Proteins (147336-22-9) ; Docosahexaenoic Acids (25167-62-8) ; polyglutamine (26700-71-0) ; Luciferases (EC 1.13.12.-) ; Cyclooxygenase 2 (EC 1.14.99.1) ; PTGS2 protein, human (EC 1.14.99.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2012-04-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M111.287078
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