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Article ; Online: Phagocytosis increases an oxidative metabolic and immune suppressive signature in tumor macrophages.

Gonzalez, Michael A / Lu, Daniel R / Yousefi, Maryam / Kroll, Ashley / Lo, Chen Hao / Briseño, Carlos G / Watson, J E Vivienne / Novitskiy, Sergey / Arias, Vanessa / Zhou, Hong / Plata Stapper, Andres / Tsai, Min K / Ashkin, Emily L / Murray, Christopher W / Li, Chi-Ming / Winslow, Monte M / Tarbell, Kristin V

The Journal of experimental medicine

2023 Volume 220, Issue 6

Abstract: Phagocytosis is a key macrophage function, but how phagocytosis shapes tumor-associated macrophage (TAM) phenotypes and heterogeneity in solid tumors remains unclear. Here, we utilized both syngeneic and novel autochthonous lung tumor models in which ... ...

Abstract	Phagocytosis is a key macrophage function, but how phagocytosis shapes tumor-associated macrophage (TAM) phenotypes and heterogeneity in solid tumors remains unclear. Here, we utilized both syngeneic and novel autochthonous lung tumor models in which neoplastic cells express the fluorophore tdTomato (tdTom) to identify TAMs that have phagocytosed neoplastic cells in vivo. Phagocytic tdTompos TAMs upregulated antigen presentation and anti-inflammatory proteins, but downregulated classic proinflammatory effectors compared to tdTomneg TAMs. Single-cell transcriptomic profiling identified TAM subset-specific and common gene expression changes associated with phagocytosis. We uncover a phagocytic signature that is predominated by oxidative phosphorylation (OXPHOS), ribosomal, and metabolic genes, and this signature correlates with worse clinical outcome in human lung cancer. Expression of OXPHOS proteins, mitochondrial content, and functional utilization of OXPHOS were increased in tdTompos TAMs. tdTompos tumor dendritic cells also display similar metabolic changes. Our identification of phagocytic TAMs as a distinct myeloid cell state links phagocytosis of neoplastic cells in vivo with OXPHOS and tumor-promoting phenotypes.
MeSH term(s)	Humans ; Macrophages/metabolism ; Phagocytosis/genetics ; Lung Neoplasms/pathology ; Myeloid Cells/metabolism ; Oxidative Stress ; Tumor Microenvironment
Language	English
Publishing date	2023-03-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20221472
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Article ; Online: Systems biology of neurodegenerative diseases.

Wood, Levi B / Winslow, Ashley R / Strasser, Samantha Dale

Integrative biology : quantitative biosciences from nano to macro

2015 Volume 7, Issue 7, Page(s) 758–775

Abstract: Neurodegenerative diseases (NDs) collectively afflict more than 40 million people worldwide. The majority of these diseases lack therapies to slow or stop progression due in large part to the challenge of disentangling the simultaneous presentation of ... ...

Abstract	Neurodegenerative diseases (NDs) collectively afflict more than 40 million people worldwide. The majority of these diseases lack therapies to slow or stop progression due in large part to the challenge of disentangling the simultaneous presentation of broad, multifaceted pathophysiologic changes. Present technologies and computational capabilities suggest an optimistic future for deconvolving these changes to identify novel mechanisms driving ND onset and progression. In particular, integration of highly multi-dimensional omic analytical techniques (e.g., microarray, mass spectrometry) with computational systems biology approaches provides a systematic methodology to elucidate new mechanisms driving NDs. In this review, we begin by summarizing the complex pathophysiology of NDs associated with protein aggregation, emphasizing the shared complex dysregulation found in all of these diseases, and discuss available experimental ND models. Next, we provide an overview of technological and computational techniques used in systems biology that are applicable to studying NDs. We conclude by reviewing prior studies that have applied these approaches to NDs and comment on the necessity of combining analysis from both human tissues and model systems to identify driving mechanisms. We envision that the integration of computational approaches with multiple omic analyses of human tissues, and mouse and in vitro models, will enable the discovery of new therapeutic strategies for these devastating diseases.
MeSH term(s)	Animals ; Brain/metabolism ; Computer Simulation ; Humans ; Models, Neurological ; Nerve Tissue Proteins/metabolism ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Proteome/metabolism ; Signal Transduction ; Systems Biology/methods
Chemical Substances	Nerve Tissue Proteins ; Proteome
Language	English
Publishing date	2015-06-12
Publishing country	England
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. ; Review
ZDB-ID	2480063-6
ISSN	1757-9708 ; 1757-9694
ISSN (online)	1757-9708
ISSN	1757-9694
DOI	10.1039/c5ib00031a
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Article ; Online: The Parkinson disease protein α-synuclein inhibits autophagy.

Winslow, Ashley R / Rubinsztein, David C

Autophagy

2011 Volume 7, Issue 4, Page(s) 429–431

Abstract: Parkinson disease (PD) is the most common movement disorder affecting people. It is characterized by the accumulation of the protein α-synuclein in Lewy body inclusions in vulnerable neurons. α-Synuclein overexpression caused by gene multiplications is ... ...

Abstract	Parkinson disease (PD) is the most common movement disorder affecting people. It is characterized by the accumulation of the protein α-synuclein in Lewy body inclusions in vulnerable neurons. α-Synuclein overexpression caused by gene multiplications is sufficient to cause this disease, suggesting that α-synuclein accumulation is toxic. Here we review our recent study showing that α-synuclein inhibits autophagy. We discuss our mechanistic understanding of this phenomenon and also speculate how a deficiency in autophagy may contribute to a range of pleiotropic features of PD biology.
MeSH term(s)	Animals ; Autophagy ; Autophagy-Related Proteins ; Gene Expression Regulation ; Golgi Apparatus/metabolism ; Humans ; Lewy Bodies/metabolism ; Membrane Proteins/metabolism ; Mitochondria/metabolism ; Models, Biological ; Parkinson Disease/metabolism ; Phagosomes/metabolism ; alpha-Synuclein/metabolism ; rab1 GTP-Binding Proteins/metabolism
Chemical Substances	ATG9B protein, human ; Autophagy-Related Proteins ; Membrane Proteins ; alpha-Synuclein ; rab1 GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2011-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.7.4.14393
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Article ; Online: Self-report data as a tool for subtype identification in genetically-defined Parkinson's Disease.

Winslow, Ashley R / Hyde, Craig L / Wilk, Jemma B / Eriksson, Nicholas / Cannon, Paul / Miller, Melissa R / Hirst, Warren D

Scientific reports

2018 Volume 8, Issue 1, Page(s) 12992

Abstract: Through a targeted recruitment 23andMe has collected DNA and patient-reported symptoms from more than 10,000 subjects reporting a physician-verified diagnosis of PD. This study evaluated the potential of self-report, web-based questionnaires to rapidly ... ...

Abstract	Through a targeted recruitment 23andMe has collected DNA and patient-reported symptoms from more than 10,000 subjects reporting a physician-verified diagnosis of PD. This study evaluated the potential of self-report, web-based questionnaires to rapidly assess disease natural history and symptomology in genetically-defined PD populations. While average age-at-diagnosis was significantly lower in GBA mutation carriers compared to idiopathic PD, or iPD (idiopathic PD, defined as no GBA mutations and no LRRK2 G2019S mutation), there were no significant differences in symptoms. Conversely, LRRK2 G2019S carrier status significantly associated with reporting of milder daily symptoms of lightheadedness and several differences were observed at a false discovery rate < 0.1, including increased reporting of changes in walking as an initial symptom of disease, decreased reporting of lightheadedness upon standing, and milder symptoms related to daily functioning. The subclinical differences in symptoms reported by LRRK2 G2019S carriers suggest differences in underlying pathophysiology and/or disease progression in LRRK2 carriers compared to iPD. Importantly, we confirm previous findings in PD genetic subsets where disease characteristics were ascertained through clinical exam. Overall, these data support the effective use of self-report and genetic data to rapidly analyze information from a large disease population or difficult to identify genetic subgroups.
MeSH term(s)	Activities of Daily Living ; Adult ; Female ; Glucosylceramidase/genetics ; Humans ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Male ; Middle Aged ; Mutation, Missense ; Parkinson Disease/diagnosis ; Parkinson Disease/genetics ; Parkinson Disease/physiopathology ; Self Report ; Surveys and Questionnaires
Chemical Substances	LRRK2 protein, human (EC 2.7.11.1) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; GBA protein, human (EC 3.2.1.45) ; Glucosylceramidase (EC 3.2.1.45)
Language	English
Publishing date	2018-08-28
Publishing country	England
Document type	Clinical Trial ; Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-30843-6
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Article: Autophagy in neurodegeneration and development.

Winslow, Ashley R / Rubinsztein, David C

Biochimica et biophysica acta

2008 Volume 1782, Issue 12, Page(s) 723–729

Abstract: Efficient protein turnover is essential for the maintenance of cellular health. Here we review how autophagy has fundamental functions in cellular homeostasis and possible uses as a therapeutic strategy for neurodegenerative diseases associated with ... ...

Abstract	Efficient protein turnover is essential for the maintenance of cellular health. Here we review how autophagy has fundamental functions in cellular homeostasis and possible uses as a therapeutic strategy for neurodegenerative diseases associated with intracytosolic aggregate formation, like Huntington's disease (HD). Drugs like rapamycin, that induce autophagy, increase the clearance of mutant huntingtin fragments and ameliorate the pathology in cell and animal models of HD and related conditions. In Drosophila, the beneficial effects of rapamycin in diseases related to HD are autophagy-dependent. We will also discuss the importance of autophagy in early stages of development and its possible contribution as a secondary disease mechanism in forms of fronto-temporal dementias, motor neuron disease, and lysosomal storage disorders.
MeSH term(s)	Animals ; Autophagy/physiology ; Humans ; Nerve Degeneration/metabolism ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/therapy
Language	English
Publishing date	2008-07-01
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.bbadis.2008.06.010
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Article: Systems biology of neurodegenerative diseases

Wood, Levi B / Winslow, Ashley R / Strasser, Samantha Dale

Integrative biology. 2015 July 6, v. 7, no. 7

2015

Abstract	Neurodegenerative diseases (NDs) collectively afflict more than 40 million people worldwide. The majority of these diseases lack therapies to slow or stop progression due in large part to the challenge of disentangling the simultaneous presentation of broad, multifaceted pathophysiologic changes. Present technologies and computational capabilities suggest an optimistic future for deconvolving these changes to identify novel mechanisms driving ND onset and progression. In particular, integration of highly multi-dimensional omic analytical techniques (e.g., microarray, mass spectrometry) with computational systems biology approaches provides a systematic methodology to elucidate new mechanisms driving NDs. In this review, we begin by summarizing the complex pathophysiology of NDs associated with protein aggregation, emphasizing the shared complex dysregulation found in all of these diseases, and discuss available experimental ND models. Next, we provide an overview of technological and computational techniques used in systems biology that are applicable to studying NDs. We conclude by reviewing prior studies that have applied these approaches to NDs and comment on the necessity of combining analysis from both human tissues and model systems to identify driving mechanisms. We envision that the integration of computational approaches with multiple omic analyses of human tissues, and mouse and in vitro models, will enable the discovery of new therapeutic strategies for these devastating diseases.
Keywords	humans ; mass spectrometry ; mice ; microarray technology ; models ; neurodegenerative diseases ; pathophysiology ; systems biology ; therapeutics ; tissues
Language	English
Dates of publication	2015-0706
Size	p. 758-775.
Publishing place	The Royal Society of Chemistry
Document type	Article
ZDB-ID	2480063-6
ISSN	1757-9708 ; 1757-9694
ISSN (online)	1757-9708
ISSN	1757-9694
DOI	10.1039/c5ib00031a
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Article ; Online: Convergence of pathology in dementia with Lewy bodies and Alzheimer's disease: a role for the novel interaction of alpha-synuclein and presenilin 1 in disease.

Winslow, Ashley R / Moussaud, Simon / Zhu, Liya / Post, Kathryn L / Post, Katherine L / Dickson, Dennis W / Berezovska, Oksana / McLean, Pamela J

Brain : a journal of neurology

2014 Volume 137, Issue Pt 7, Page(s) 1958–1970

Abstract: A growing number of PSEN1 mutations have been associated with dementia with Lewy bodies and familial Alzheimer's disease with concomitant α-synuclein pathology. The objective of this study was to determine if PSEN1 plays a direct role in the development ... ...

Abstract	A growing number of PSEN1 mutations have been associated with dementia with Lewy bodies and familial Alzheimer's disease with concomitant α-synuclein pathology. The objective of this study was to determine if PSEN1 plays a direct role in the development of α-synuclein pathology in these diseases. Using mass spectrometry, immunoelectron microscopy and fluorescence lifetime image microscopy based on Forster resonance energy transfer (FLIM-FRET) we identified α-synuclein as a novel interactor of PSEN1 in wild-type mouse brain tissue. The interaction of α-synuclein with PSEN1 was detected in post-mortem brain tissue from cognitively normal cases and was significantly increased in tissue from cases with dementia with Lewy bodies and familial Alzheimer's disease associated with known PSEN1 mutations. We confirmed an increased interaction of PSEN1 and α-synuclein in cell lines expressing well characterized familial Alzheimer's disease PSEN1 mutations, L166P and delta exon 9, and demonstrated that PSEN1 mutations associate with increased membrane association and accumulation of α-synuclein. Our data provides evidence of a molecular interaction of PSEN1 and α-synuclein that may explain the clinical and pathophysiological overlap seen in synucleinopathies, including Parkinson's disease, dementia with Lewy bodies, and some forms of Alzheimer's disease.
MeSH term(s)	Alzheimer Disease/pathology ; Amyloid Precursor Protein Secretases/metabolism ; Animals ; Brain/metabolism ; Brain/pathology ; Brain/ultrastructure ; CHO Cells ; Cells, Cultured ; Cerebral Cortex ; Cricetulus ; Female ; Glutathione Transferase/genetics ; Humans ; Lewy Body Disease/pathology ; Male ; Mice ; Mice, Knockout ; Microscopy, Immunoelectron ; Mutation/genetics ; Neurons/drug effects ; Neurons/metabolism ; Presenilin-1/deficiency ; Presenilin-1/genetics ; Presenilin-1/metabolism ; alpha-Synuclein/metabolism
Chemical Substances	PSEN1 protein, human ; Presenilin-1 ; alpha-Synuclein ; Glutathione Transferase (EC 2.5.1.18) ; Amyloid Precursor Protein Secretases (EC 3.4.-)
Language	English
Publishing date	2014-05-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awu119
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Article ; Online: Identification of 15 genetic loci associated with risk of major depression in individuals of European descent.

Hyde, Craig L / Nagle, Michael W / Tian, Chao / Chen, Xing / Paciga, Sara A / Wendland, Jens R / Tung, Joyce Y / Hinds, David A / Perlis, Roy H / Winslow, Ashley R

Nature genetics

2016 Volume 48, Issue 9, Page(s) 1031–1036

Abstract: Despite strong evidence supporting the heritability of major depressive disorder (MDD), previous genome-wide studies were unable to identify risk loci among individuals of European descent. We used self-report data from 75,607 individuals reporting ... ...

Abstract	Despite strong evidence supporting the heritability of major depressive disorder (MDD), previous genome-wide studies were unable to identify risk loci among individuals of European descent. We used self-report data from 75,607 individuals reporting clinical diagnosis of depression and 231,747 individuals reporting no history of depression through 23andMe and carried out meta-analysis of these results with published MDD genome-wide association study results. We identified five independent variants from four regions associated with self-report of clinical diagnosis or treatment for depression. Loci with a P value <1.0 × 10(-5) in the meta-analysis were further analyzed in a replication data set (45,773 cases and 106,354 controls) from 23andMe. A total of 17 independent SNPs from 15 regions reached genome-wide significance after joint analysis over all three data sets. Some of these loci were also implicated in genome-wide association studies of related psychiatric traits. These studies provide evidence for large-scale consumer genomic data as a powerful and efficient complement to data collected from traditional means of ascertainment for neuropsychiatric disease genomics.
MeSH term(s)	Adult ; Case-Control Studies ; Depressive Disorder, Major/genetics ; European Continental Ancestry Group/genetics ; Female ; Genetic Loci/genetics ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotype ; Humans ; Male ; Meta-Analysis as Topic ; Middle Aged ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Risk Factors
Language	English
Publishing date	2016-08-01
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/ng.3623
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Article ; Online: Identification of neurotoxic cytokines by profiling Alzheimer's disease tissues and neuron culture viability screening.

Wood, Levi B / Winslow, Ashley R / Proctor, Elizabeth A / McGuone, Declan / Mordes, Daniel A / Frosch, Matthew P / Hyman, Bradley T / Lauffenburger, Douglas A / Haigis, Kevin M

Scientific reports

2015 Volume 5, Page(s) 16622

Abstract: Alzheimer's disease (AD) therapeutics based on the amyloid hypothesis have shown minimal efficacy in patients, suggesting that the activity of amyloid beta (Aβ) represents only one aspect of AD pathogenesis. Since neuroinflammation is thought to play an ... ...

Abstract	Alzheimer's disease (AD) therapeutics based on the amyloid hypothesis have shown minimal efficacy in patients, suggesting that the activity of amyloid beta (Aβ) represents only one aspect of AD pathogenesis. Since neuroinflammation is thought to play an important role in AD, we hypothesized that cytokines may play a direct role in promoting neuronal death. Here, we profiled cytokine expression in a small cohort of human AD and control brain tissues. We identified AD-associated cytokines using partial least squares regression to correlate cytokine expression with quantified pathologic disease state and then used neuron cultures to test whether cytokines up-regulated in AD tissues could affect neuronal viability. This analysis identified cytokines that were associated with the pathological severity. Of the top correlates, only TNF-α reduced viability in neuron culture when applied alone. VEGF also reduced viability when applied together with Aβ, which was surprising because VEGF has been viewed as a neuro-protective protein. We found that this synthetic pro-death effect of VEGF in the context of Aβ was commensurate with VEGFR-dependent changes in multiple signaling pathways that govern cell fate. Our findings suggest that profiling of tissues combined with a culture-based screening approach can successfully identify new mechanisms driving neuronal death.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Peptides/pharmacology ; Brain/metabolism ; Cell Survival/drug effects ; Cell Survival/genetics ; Cells, Cultured ; Cytokines/genetics ; Cytokines/metabolism ; Cytokines/pharmacology ; Female ; Gene Expression Profiling/methods ; Gene Regulatory Networks/genetics ; Humans ; Inflammation Mediators/metabolism ; Inflammation Mediators/pharmacology ; Interleukin-5/genetics ; Interleukin-5/metabolism ; Interleukin-5/pharmacology ; Least-Squares Analysis ; Male ; Middle Aged ; Multivariate Analysis ; Neurons/drug effects ; Neurons/metabolism ; Regression Analysis ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/pharmacology ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor A/pharmacology
Chemical Substances	Amyloid beta-Peptides ; Cytokines ; Inflammation Mediators ; Interleukin-5 ; Tumor Necrosis Factor-alpha ; Vascular Endothelial Growth Factor A
Language	English
Publishing date	2015-11-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep16622
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Article ; Online: Autophagic substrate clearance requires activity of the syntaxin-5 SNARE complex.

Renna, Maurizio / Schaffner, Catherine / Winslow, Ashley R / Menzies, Fiona M / Peden, Andrew A / Floto, R Andres / Rubinsztein, David C

Journal of cell science

2011 Volume 124, Issue Pt 3, Page(s) 469–482

Abstract: Autophagy is a lysosome-dependent cellular catabolic mechanism that mediates the turnover of intracellular organelles and long-lived proteins. Reduced autophagic activity has been shown to lead to the accumulation of misfolded proteins in neurons and ... ...

Abstract	Autophagy is a lysosome-dependent cellular catabolic mechanism that mediates the turnover of intracellular organelles and long-lived proteins. Reduced autophagic activity has been shown to lead to the accumulation of misfolded proteins in neurons and might be involved in chronic neurodegenerative diseases. Here, we uncover an essential role for the syntaxin-5 SNARE complex in autophagy. Using genetic knockdown, we show that the syntaxin-5 SNARE complex regulates the later stages of autophagy after the initial formation of autophagosomes. This SNARE complex acts on autophagy by regulating ER-to-Golgi transport through the secretory pathway, which is essential for the activity of lysosomal proteases such as cathepsins. Depletion of syntaxin-5 complex components results in the accumulation of autophagosomes as a result of lysosomal dysfunction, leading to decreased degradation of autophagic substrates. Our findings provide a novel link between a fundamental process such as intracellular trafficking and human diseases that might be affected by defective biogenesis and/or homeostasis of the autophagosome-lysosome degradation system.
MeSH term(s)	Adaptor Proteins, Vesicular Transport ; Autophagy/physiology ; Biological Transport/physiology ; HeLa Cells ; Humans ; Lysosomes/enzymology ; Microtubule-Associated Proteins/physiology ; Qa-SNARE Proteins/physiology ; R-SNARE Proteins/physiology ; Vesicular Transport Proteins/physiology
Chemical Substances	Adaptor Proteins, Vesicular Transport ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; Qa-SNARE Proteins ; R-SNARE Proteins ; SCFD1 protein, human ; Vesicular Transport Proteins
Language	English
Publishing date	2011-01-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.076489
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