LIVIVO - Search results -

Search results

Result 1 - 10 of total 49

Search options

Article: Editorial: Role of Senescence in Neurodegenerative Diseases.

Tüzer, Ferit / Chinta, Shankar J / Viel, Tania Araujo

2022 Volume 14, Page(s) 907670

Language	English
Publishing date	2022-05-17
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2022.907670
Database	MEDical Literature Analysis and Retrieval System OnLINE

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.

Article ; Online: Kavain suppresses human Aβ-induced paralysis in

Chamoli, Manish / Chinta, Shankar J / Andersen, Julie K / Lithgow, Gordon J

microPublication biology

2020 Volume 2020

Language	English
Publishing date	2020-05-21
Publishing country	United States
Document type	Journal Article
ISSN	2578-9430
ISSN (online)	2578-9430
DOI	10.17912/micropub.biology.000254
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: An inducible MAO-B mouse model of Parkinson's disease: a tool towards better understanding basic disease mechanisms and developing novel therapeutics.

Chamoli, Manish / Chinta, Shankar J / Andersen, Julie K

Journal of neural transmission (Vienna, Austria : 1996)

2018 Volume 125, Issue 11, Page(s) 1651–1658

Abstract: Several studies have suggested that increases in astrocytic monoamine oxidase B (MAO-B) levels in conjunction with Parkinson's disease (PD) may contribute to subsequent neuropathology associated with the disorder. MAO-B inhibitors are currently widely ... ...

Abstract	Several studies have suggested that increases in astrocytic monoamine oxidase B (MAO-B) levels in conjunction with Parkinson's disease (PD) may contribute to subsequent neuropathology associated with the disorder. MAO-B inhibitors are currently widely used as symptomatic therapeutics for PD and, although somewhat controversial, these drugs may also exhibit disease-modifying properties. To obtain a better understanding of the potential role of MAO-B in disease neuropathology, we created an inducible astrocyte-specific transgenic MAO-B mouse model. Here, we summarize findings associated with this model, including neuropathological PD features associated with it.
MeSH term(s)	Animals ; Astrocytes/metabolism ; Disease Models, Animal ; Mice ; Mice, Transgenic ; Monoamine Oxidase/genetics ; Monoamine Oxidase/metabolism ; Oxidative Stress/genetics ; Parkinson Disease/genetics ; Parkinson Disease/metabolism
Chemical Substances	Monoamine Oxidase (EC 1.4.3.4)
Language	English
Publishing date	2018-04-30
Publishing country	Austria
Document type	Journal Article ; Review
ZDB-ID	184163-4
ISSN	1435-1463 ; 0300-9564
ISSN (online)	1435-1463
ISSN	0300-9564
DOI	10.1007/s00702-018-1887-z
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

Ui II Zs.150: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: A guide to senolytic intervention in neurodegenerative disease.

Lee, Suckwon / Wang, Ellen Y / Steinberg, Alexandra B / Walton, Chaska C / Chinta, Shankar J / Andersen, Julie K

Mechanisms of ageing and development

2021 Volume 200, Page(s) 111585

Abstract: Cellular senescence is a potential tumor-suppressive mechanism that generally results in an irreversible cell cycle arrest. Senescent cells accumulate with age and actively secrete soluble factors, collectively termed the 'senescence-associated secretory ...

Abstract	Cellular senescence is a potential tumor-suppressive mechanism that generally results in an irreversible cell cycle arrest. Senescent cells accumulate with age and actively secrete soluble factors, collectively termed the 'senescence-associated secretory phenotype' (SASP), which has both beneficial and detrimental effects. Although the contribution of senescent cells to age-related pathologies has been well-established outside the brain, emerging evidence indicates that brain cells also undergo cellular senescence and contribute to neuronal loss in the context of age-related neurodegenerative diseases. Contribution of senescent cells in the pathogenesis of neurological disorders has led to the possibility of eliminating senescence cells via pharmacological compounds called senolytics. Recently several senolytics have been demonstrated to elicit improved cognitive performance and healthspan in mouse models of neurodegeneration. However, their translation for use in the clinic still holds several potential challenges. This review summarizes available senolytics, their purported mode of action, and possible off-target effects. We also discuss possible alternative strategies that may help minimize potential side-effects associated with the senolytics approach.
MeSH term(s)	Aging/drug effects ; Aging/physiology ; Animals ; Cellular Senescence/drug effects ; Cellular Senescence/physiology ; Humans ; Mice ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/metabolism ; Senescence-Associated Secretory Phenotype/drug effects ; Senotherapeutics/pharmacology
Chemical Substances	Senotherapeutics
Language	English
Publishing date	2021-10-08
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	183915-9
ISSN	1872-6216 ; 0047-6374
ISSN (online)	1872-6216
ISSN	0047-6374
DOI	10.1016/j.mad.2021.111585
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 1012: 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: A drug-like molecule engages nuclear hormone receptor DAF-12/FXR to regulate mitophagy and extend lifespan.

Chamoli, Manish / Rane, Anand / Foulger, Anna / Chinta, Shankar J / Shahmirzadi, Azar Asadi / Kumsta, Caroline / Nambiar, Dhanya K / Hall, David / Holcom, Angelina / Angeli, Suzanne / Schmidt, Minna / Pitteri, Sharon / Hansen, Malene / Lithgow, Gordon J / Andersen, Julie K

Nature aging

2023 Volume 3, Issue 12, Page(s) 1529–1543

Abstract: Autophagy-lysosomal function is crucial for maintaining healthy lifespan and preventing age-related diseases. The transcription factor TFEB plays a key role in regulating this pathway. Decreased TFEB expression is associated with various age-related ... ...

Abstract	Autophagy-lysosomal function is crucial for maintaining healthy lifespan and preventing age-related diseases. The transcription factor TFEB plays a key role in regulating this pathway. Decreased TFEB expression is associated with various age-related disorders, making it a promising therapeutic target. In this study, we screened a natural product library and discovered mitophagy-inducing coumarin (MIC), a benzocoumarin compound that enhances TFEB expression and lysosomal function. MIC robustly increases the lifespan of Caenorhabditis elegans in an HLH-30/TFEB-dependent and mitophagy-dependent manner involving DCT-1/BNIP3 while also preventing mitochondrial dysfunction in mammalian cells. Mechanistically, MIC acts by inhibiting ligand-induced activation of the nuclear hormone receptor DAF-12/FXR, which, in turn, induces mitophagy and extends lifespan. In conclusion, our study uncovers MIC as a promising drug-like molecule that enhances mitochondrial function and extends lifespan by targeting DAF-12/FXR. Furthermore, we discovered DAF-12/FXR as a previously unknown upstream regulator of HLH-30/TFEB and mitophagy.
MeSH term(s)	Animals ; Mitophagy ; Longevity/genetics ; Caenorhabditis elegans/genetics ; Autophagy ; Receptors, Cytoplasmic and Nuclear/genetics ; Mammals/metabolism ; Caenorhabditis elegans Proteins/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism
Chemical Substances	Receptors, Cytoplasmic and Nuclear ; DAF-12 protein, C elegans ; Caenorhabditis elegans Proteins ; HLH-30 protein, C elegans ; Basic Helix-Loop-Helix Transcription Factors
Language	English
Publishing date	2023-11-13
Publishing country	United States
Document type	Journal Article
ISSN	2662-8465
ISSN (online)	2662-8465
DOI	10.1038/s43587-023-00524-9
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: Nitrosylation and nitration of mitochondrial complex I in Parkinson's disease.

Chinta, Shankar J / Andersen, Julie K

Free radical research

2011 Volume 45, Issue 1, Page(s) 53–58

Abstract: Impairment of the mitochondrial electron transport chain has been suggested to be a critical factor in the neuropathogenesis of Parkinson's disease (PD), as inhibition of mitochondrial complex I (CI) activity is consistently detected in PD patients as ... ...

Abstract	Impairment of the mitochondrial electron transport chain has been suggested to be a critical factor in the neuropathogenesis of Parkinson's disease (PD), as inhibition of mitochondrial complex I (CI) activity is consistently detected in PD patients as well as in mitochondrial toxin models of the disorder. Increased levels of various reactive oxygen and nitrogen species appear to contribute to CI inhibition and mitochondrial dysfunction in PD. Reactive nitrogen species (RNS) such as nitric oxide (NO) and its metabolite peroxynitrite (PN) may inhibit CI activity via several different mechanisms including S-nitrosylation, nitration, and protein thiol formation. Studies using various cell and animal PD models have demonstrated that selective mitochondrial CI inhibition in dopaminergic cells may be due to both NO-mediated S-nitrosylation and nitration of CI sub-units. Strategies to modulate mitochondrial NO levels will therefore likely be a promising approach to enhance mitochondrial function and protect dopaminergic neurons against oxidative or nitrosative insult.
MeSH term(s)	Electron Transport Complex I/metabolism ; Humans ; Mitochondria/enzymology ; Mitochondria/metabolism ; Mitochondria/pathology ; Nitric Oxide/metabolism ; Oxidative Stress ; Parkinson Disease/enzymology ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Peroxynitrous Acid/metabolism ; Reactive Nitrogen Species/metabolism
Chemical Substances	Reactive Nitrogen Species ; Peroxynitrous Acid (14691-52-2) ; Nitric Oxide (31C4KY9ESH) ; Electron Transport Complex I (EC 1.6.5.3)
Language	English
Publishing date	2011-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1194130-3
ISSN	1029-2470 ; 1071-5762
ISSN (online)	1029-2470
ISSN	1071-5762
DOI	10.3109/10715762.2010.509398
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2236: 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: Dysregulated iron metabolism in C. elegans catp-6/ATP13A2 mutant impairs mitochondrial function.

Anand, Nikhita / Holcom, Angelina / Broussalian, Michael / Schmidt, Minna / Chinta, Shankar J / Lithgow, Gordon J / Andersen, Julie K / Chamoli, Manish

Neurobiology of disease

2020 Volume 139, Page(s) 104786

Abstract: Mutations in the human ATP13A2 gene are associated with an early-onset form of Parkinson's disease (PD) known as Kufor Rakeb Syndrome (KRS). Patients with KRS show increased iron deposition in the basal ganglia, suggesting iron toxicity-induced ... ...

Abstract	Mutations in the human ATP13A2 gene are associated with an early-onset form of Parkinson's disease (PD) known as Kufor Rakeb Syndrome (KRS). Patients with KRS show increased iron deposition in the basal ganglia, suggesting iron toxicity-induced neurodegeneration as a potential pathogenesis associated with the ATP13A2 mutation. Previously we demonstrated that functional losses of ATP13A2 disrupt the lysosomes ability to store excess iron, leading to reduce survival of dopaminergic neuronal cells. To understand the possible mechanisms involved, we studied a Caenorhabditis elegans mutant defective in catp-6 function, an ortholog of human ATP13A2 gene. Here we show that catp-6 mutant worms have defective autophagy and lysosomal function, demonstrate characteristic PD phenotypes including reduced motor function and dysregulated iron metabolism. Additionally, these mutants have defective mitochondrial health, which is rescuable via iron chelation or mitophagy induction.
MeSH term(s)	Adenosine Triphosphatases/metabolism ; Animals ; Autophagy ; Caenorhabditis elegans ; Caenorhabditis elegans Proteins/metabolism ; Dopaminergic Neurons/metabolism ; Humans ; Iron/metabolism ; Lysosomes/metabolism ; Mitochondria/metabolism ; Mutation ; Parkinson Disease/metabolism ; Parkinsonian Disorders/metabolism ; Proton-Translocating ATPases/metabolism
Chemical Substances	ATP13A2 protein, human ; Caenorhabditis elegans Proteins ; Iron (E1UOL152H7) ; Adenosine Triphosphatases (EC 3.6.1.-) ; CATP-6 protein, C elegans (EC 3.6.1.-) ; Proton-Translocating ATPases (EC 3.6.3.14)
Language	English
Publishing date	2020-02-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2020.104786
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 4444: 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 ; Online: Prospects and challenges for the use of stem cell technologies to develop novel therapies for Parkinson disease.

Chinta, Shankar J / Andersen, Julie K

Cell cycle (Georgetown, Tex.)

2011 Volume 10, Issue 24, Page(s) 4179–4180

MeSH term(s)	Adult Stem Cells/physiology ; Cell Differentiation/physiology ; Embryonic Stem Cells/physiology ; Humans ; Induced Pluripotent Stem Cells/physiology ; Models, Biological ; Neurons/cytology ; Parkinson Disease/pathology ; Parkinson Disease/therapy ; Research ; Stem Cell Transplantation/methods ; Stem Cell Transplantation/trends
Language	English
Publishing date	2011-12-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.10.24.18835
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 5881: 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 ; Online: Hsp90 Co-chaperone p23 contributes to dopaminergic mitochondrial stress via stabilization of PHD2: Implications for Parkinson's disease.

Rane, Anand / Rajagopalan, Subramanian / Ahuja, Manuj / Thomas, Bobby / Chinta, Shankar J / Andersen, Julie K

Neurotoxicology

2018 Volume 65, Page(s) 166–173

Abstract: The heat shock factor 90 (hsp90) complex has long been associated with neuropathological phenotypes linked to Parkinson's disease (PD) and its inhibition is neuroprotective in disease models. Hsp90 is conventionally believed to act by suppressing ... ...

Abstract	The heat shock factor 90 (hsp90) complex has long been associated with neuropathological phenotypes linked to Parkinson's disease (PD) and its inhibition is neuroprotective in disease models. Hsp90 is conventionally believed to act by suppressing induction of hsp70. Here, we report a novel hsp70-independent mechanism by which Hsp90 may also contribute to PD-associated neuropathology. We previously reported that inhibition of the enzyme prolyl hydroxylase domain 2 (PHD2) in conjunction with increases in hypoxia-inducible factor 1 alpha (HIF1α) results in protection of vulnerable dopaminergic substantia nigra pars compacta (DAergic SNpc) neurons in in vitro and in vivo models of PD. We discovered an increased interaction between PHD2 and the p23:Hsp90 chaperone complex in response to mitochondrial stress elicited by the mitochondrial neurotoxin 1-methyl-4-phenylpyridine (MPP
MeSH term(s)	1-Methyl-4-phenylpyridinium/antagonists & inhibitors ; Animals ; Cells, Cultured ; Dopaminergic Neurons/drug effects ; Dopaminergic Neurons/pathology ; Gene Knockdown Techniques ; HSP90 Heat-Shock Proteins/metabolism ; Limonins/pharmacology ; Mitochondria/drug effects ; Mitochondria/pathology ; Molecular Chaperones/antagonists & inhibitors ; Molecular Chaperones/genetics ; Molecular Chaperones/metabolism ; Neuroprotective Agents/pharmacology ; Parkinson Disease/metabolism ; Procollagen-Proline Dioxygenase/metabolism ; Rats
Chemical Substances	HSP90 Heat-Shock Proteins ; Limonins ; Molecular Chaperones ; Neuroprotective Agents ; gedunin (2753-30-2) ; Procollagen-Proline Dioxygenase (EC 1.14.11.2) ; Egln1 protein, rat (EC 1.14.11.29) ; 1-Methyl-4-phenylpyridinium (R865A5OY8J)
Language	English
Publishing date	2018-02-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	800820-6
ISSN	1872-9711 ; 0161-813X
ISSN (online)	1872-9711
ISSN	0161-813X
DOI	10.1016/j.neuro.2018.02.012
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 1547: 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: Regulation of ATP13A2 via PHD2-HIF1α Signaling Is Critical for Cellular Iron Homeostasis: Implications for Parkinson's Disease.

Rajagopalan, Subramanian / Rane, Anand / Chinta, Shankar J / Andersen, Julie K

The Journal of neuroscience : the official journal of the Society for Neuroscience

2016 Volume 36, Issue 4, Page(s) 1086–1095

Abstract: We previously reported that pharmacological inhibition of a class of enzymes known as prolyl hydroxylase domain proteins (PHDs) has neuroprotective effects in various in vitro and in vivo models of Parkinson's disease (PD). We hypothesized that this was ... ...

Abstract	We previously reported that pharmacological inhibition of a class of enzymes known as prolyl hydroxylase domain proteins (PHDs) has neuroprotective effects in various in vitro and in vivo models of Parkinson's disease (PD). We hypothesized that this was due to inhibition of the PHD2 isoform, preventing it from hydroxylating the transcription factor hypoxia inducible factor 1 α (HIF1α), targeting it for eventual proteasomal degradation. HIF1α itself induces the transcription of various cellular stress genes, including several involved in iron metabolism. Although all three isoforms of PHD are expressed within vulnerable dopaminergic (DAergic) substantia nigra pars compacta neurons, only select downregulation of the PHD2 isoform was found to protect against in vivo neurodegenerative effects associated with the mitochondrial neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. These findings were corroborated in induced pluripotent stem cell-derived neurons, providing validation in a pertinent human cell model. PHD2 inhibition was found to result in increased expression of ATP13A2, mutation of which is responsible for a rare juvenile form of PD known as Kufor-Rakeb syndrome. Knockdown of ATP13A2 expression within human DAergic cells was found to abrogate restoration of cellular iron homeostasis and neuronal cell viability elicited by inhibition of PHD2 under conditions of mitochondrial stress, likely via effects on lysosomal iron storage. These data suggest that regulation of ATP13A2 by the PHD2-HIF1α signaling pathway affects cellular iron homeostasis and DAergic neuronal survival. This constitutes a heretofore unrecognized process associated with loss of ATP13A2 function that could have wide-ranging implications for it as a therapeutic target for PD and other related conditions. Significance statement: Reductions in PHD2 activity within dopaminergic neurons in vivo and in cultured human induced pluripotent stem cell-derived neurons protects against mitochondrial stress-induced neurotoxicity. Protective effects are dependent on downstream HIF-1α expression. Knockdown of ATP13A2, a gene linked to a rare juvenile form of Parkinson's disease and recently identified as a novel HIF1α target, was found to abrogate maintenance of cellular iron homeostasis and neuronal viability elicited by PHD2 inhibition in vivo and in cultured dopaminergic cells under conditions of mitochondrial stress. Mechanistically, this was due to ATP13A2's role in maintaining lysosomal iron stores. This constitutes a novel mechanism by which alterations in ATP13A2 activity may be driving PD-related neuropathology.
MeSH term(s)	Adenosine Triphosphatases/genetics ; Adenosine Triphosphatases/metabolism ; Animals ; Disease Models, Animal ; Fluoresceins/metabolism ; Gene Expression Regulation/genetics ; Homeostasis/genetics ; Homeostasis/physiology ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Hypoxia-Inducible Factor-Proline Dioxygenases/genetics ; Hypoxia-Inducible Factor-Proline Dioxygenases/metabolism ; Iron/metabolism ; Lysosomes/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Transgenic ; Neuroblastoma/pathology ; Parkinsonian Disorders/chemically induced ; Parkinsonian Disorders/metabolism ; Pluripotent Stem Cells/drug effects ; Pluripotent Stem Cells/physiology ; Proton-Translocating ATPases ; RNA, Messenger/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Signal Transduction/physiology ; Tyrosine 3-Monooxygenase/metabolism
Chemical Substances	Fluoresceins ; Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit ; Membrane Proteins ; RNA, Messenger ; RNA, Small Interfering ; Iron (E1UOL152H7) ; Egln1 protein, mouse (EC 1.14.11.29) ; Hypoxia-Inducible Factor-Proline Dioxygenases (EC 1.14.11.29) ; Tyrosine 3-Monooxygenase (EC 1.14.16.2) ; ATP13A2 protein, mouse (EC 3.6.1.-) ; Adenosine Triphosphatases (EC 3.6.1.-) ; Proton-Translocating ATPases (EC 3.6.3.14) ; fluorexon (V0YM2B16TS)
Language	English
Publishing date	2016-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.3117-15.2016
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1668: 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

To top

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

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

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