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Article ; Online: Synaptic Formation, Neural Circuits and Neurodevelopmental Disorders Controlled by Signaling, Translation, and Epigenetic Regulation.

Hsueh, Yi-Ping

2019 Volume 79, Issue 1, Page(s) 2–7

MeSH term(s)	Animals ; Epigenesis, Genetic/physiology ; Humans ; Nerve Net/pathology ; Neurodevelopmental Disorders/genetics ; Neurodevelopmental Disorders/pathology ; Signal Transduction ; Synapses/pathology
Language	English
Publishing date	2019-01-22
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2256184-5
ISSN	1932-846X ; 1097-4695 ; 1932-8451 ; 0022-3034
ISSN (online)	1932-846X ; 1097-4695
ISSN	1932-8451 ; 0022-3034
DOI	10.1002/dneu.22655
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Zs.A 853: Show issues

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Article ; Online: Vcp overexpression and leucine supplementation extend lifespan and ameliorate neuromuscular junction phenotypes of a SOD1G93A-ALS mouse model.

Huang, Tzyy-Nan / Shih, Yu-Tzu / Yen, Tzu-Li / Hsueh, Yi-Ping

Human molecular genetics

2024 Volume 33, Issue 11, Page(s) 935–944

Abstract: Many genes with distinct molecular functions have been linked to genetically heterogeneous amyotrophic lateral sclerosis (ALS), including SuperOxide Dismutase 1 (SOD1) and Valosin-Containing Protein (VCP). SOD1 converts superoxide to oxygen and hydrogen ... ...

Abstract	Many genes with distinct molecular functions have been linked to genetically heterogeneous amyotrophic lateral sclerosis (ALS), including SuperOxide Dismutase 1 (SOD1) and Valosin-Containing Protein (VCP). SOD1 converts superoxide to oxygen and hydrogen peroxide. VCP acts as a chaperon to regulate protein degradation and synthesis and various other cellular responses. Although the functions of these two genes differ, in the current report we show that overexpression of wild-type VCP in mice enhances lifespan and maintains the size of neuromuscular junctions (NMJs) of both male and female SOD1G93A mice, a well-known ALS mouse model. Although VCP exerts multiple functions, its regulation of ER formation and consequent protein synthesis has been shown to play the most important role in controlling dendritic spine formation and social and memory behaviors. Given that SOD1 mutation results in protein accumulation and aggregation, it may direct VCP to the protein degradation pathway, thereby impairing protein synthesis. Since we previously showed that the protein synthesis defects caused by Vcp deficiency can be improved by leucine supplementation, to confirm the role of the VCP-protein synthesis pathway in SOD1-linked ALS, we applied leucine supplementation to SOD1G93A mice and, similar to Vcp overexpression, we found that it extends SOD1G93A mouse lifespan. In addition, the phenotypes of reduced muscle strength and fewer NMJs of SOD1G93A mice are also improved by leucine supplementation. These results support the existence of crosstalk between SOD1 and VCP and suggest a critical role for protein synthesis in ASL. Our study also implies a potential therapeutic treatment for ALS.
MeSH term(s)	Animals ; Valosin Containing Protein/metabolism ; Valosin Containing Protein/genetics ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Disease Models, Animal ; Mice ; Neuromuscular Junction/metabolism ; Female ; Male ; Longevity/genetics ; Mice, Transgenic ; Leucine/pharmacology ; Leucine/metabolism ; Superoxide Dismutase-1/genetics ; Superoxide Dismutase-1/metabolism ; Phenotype ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Humans ; Adenosine Triphosphatases/genetics ; Adenosine Triphosphatases/metabolism
Chemical Substances	Vcp protein, mouse ; Sod1 protein, mouse
Language	English
Publishing date	2024-02-19
Publishing country	England
Document type	Journal Article
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddae022
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Zs.A 3469: Show issues

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Article ; Online: Quantification of the density and morphology of dendritic spines and synaptic protein distribution using Thy1-YFP transgenic mice.

Lin, Yung-Jui / Huang, Tzyy-Nan / Hsueh, Yi-Ping

STAR protocols

2023 Volume 4, Issue 2, Page(s) 102290

Abstract: Synaptopathy, which encompasses morphological deficits and any abnormal protein distribution of synapses, is a critical feature of many neurological diseases. We here provide a protocol using mice stably expressing a Thy1-YFP transgene to assess synaptic ...

Abstract	Synaptopathy, which encompasses morphological deficits and any abnormal protein distribution of synapses, is a critical feature of many neurological diseases. We here provide a protocol using mice stably expressing a Thy1-YFP transgene to assess synaptic features in vivo. We describe steps for recording the entire morphology of projection neurons using confocal microscopy based on YFP signals. We detail assessment of the density and size of dendritic spines and the distributions of synaptic proteins using ImageJ and statistical analysis using Prism. For complete details on the use and execution of this protocol, please refer to Shih et al. (2020).
Language	English
Publishing date	2023-05-06
Publishing country	United States
Document type	Journal Article
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2023.102290
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Article ; Online: TLR7 and IL-6 differentially regulate the effects of rotarod exercise on the transcriptomic profile and neurogenesis to influence anxiety and memory.

Hung, Yun-Fen / Hsueh, Yi-Ping

iScience

2021 Volume 24, Issue 4, Page(s) 102384

Abstract: Voluntary exercise is well known to benefit brain performance. In contrast, forced exercise induces inflammation-related stress responses and may cause psychiatric disorders. Here, we unexpectedly found that rotarod testing, a frequently applied assay ... ...

Abstract	Voluntary exercise is well known to benefit brain performance. In contrast, forced exercise induces inflammation-related stress responses and may cause psychiatric disorders. Here, we unexpectedly found that rotarod testing, a frequently applied assay for evaluating rodent motor coordination, induces anxiety and alters spatial learning/memory performance of mice. Rotarod testing upregulated genes involved in the unfolded protein response and stress responses and downregulated genes associated with neurogenesis and neuronal differentiation. It impacts two downstream pathways. The first is the IL-6-dependent pathway, which mediates rotarod-induced anxiety. The second is the Toll-like receptor 7 (TLR7)-dependent pathway, which is involved in the effect of rotarod exercise on gene expression and its impact on contextual learning and memory of mice. Thus, although rotarod exercise does not induce systemic inflammation, it influences innate immunity-related responses in the brain, controls gene expression and, consequently, regulates anxiety and contextual learning and memory.
Language	English
Publishing date	2021-03-31
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2021.102384
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Article: Editorial: Autism Signaling Pathways.

Hsueh, Yi-Ping / Lin, Yu-Chih

Frontiers in cellular neuroscience

2021 Volume 15, Page(s) 760994

Language	English
Publishing date	2021-09-28
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2021.760994
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Article ; Online: Protein synthesis as a modifiable target for autism-related dendritic spine pathophysiologies.

Lu, Ming-Hsuan / Hsueh, Yi-Ping

The FEBS journal

2021 Volume 289, Issue 8, Page(s) 2282–2300

Abstract: Autism spectrum disorder (ASD) is increasingly recognized as a condition of altered brain connectivity. As synapses are fundamental subcellular structures for neuronal connectivity, synaptic pathophysiology has become one of central themes in autism ... ...

Abstract	Autism spectrum disorder (ASD) is increasingly recognized as a condition of altered brain connectivity. As synapses are fundamental subcellular structures for neuronal connectivity, synaptic pathophysiology has become one of central themes in autism research. Reports disagree upon whether the density of dendritic spines, namely excitatory synapses, is increased or decreased in ASD and whether the protein synthesis that is critical for dendritic spine formation and function is upregulated or downregulated. Here, we review recent evidence supporting a subgroup of ASD models with decreased dendritic spine density (hereafter ASD-DSD), including Nf1 and Vcp mutant mice. We discuss the relevance of branched-chain amino acid (BCAA) insufficiency in relation to unmet protein synthesis demand in ASD-DSD. In contrast to ASD-DSD, ASD models with hyperactive mammalian target of rapamycin (mTOR) may represent the opposite end of the disease spectrum, often characterized by increases in protein synthesis and dendritic spine density (denoted ASD-ISD). Finally, we propose personalized dietary leucine as a strategy tailored to balancing protein synthesis demand, thereby ameliorating dendritic spine pathophysiologies and autism-related phenotypes in susceptible patients, especially those with ASD-DSD.
MeSH term(s)	Animals ; Autism Spectrum Disorder/genetics ; Autism Spectrum Disorder/metabolism ; Autistic Disorder/genetics ; Autistic Disorder/metabolism ; Dendritic Spines/genetics ; Dendritic Spines/metabolism ; Humans ; Mammals ; Mice ; Neurons/metabolism ; Synapses/metabolism
Language	English
Publishing date	2021-02-22
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15733
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Zs.A 260: Show issues

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Article: Protein synthesis as a modifiable target for autism‐related dendritic spine pathophysiologies

Lu, Ming‐Hsuan / Hsueh, Yi‐Ping

FEBS journal. 2022 Apr., v. 289, no. 8

2022

Abstract	Autism spectrum disorder (ASD) is increasingly recognized as a condition of altered brain connectivity. As synapses are fundamental subcellular structures for neuronal connectivity, synaptic pathophysiology has become one of central themes in autism research. Reports disagree upon whether the density of dendritic spines, namely excitatory synapses, is increased or decreased in ASD and whether the protein synthesis that is critical for dendritic spine formation and function is upregulated or downregulated. Here, we review recent evidence supporting a subgroup of ASD models with decreased dendritic spine density (hereafter ASD‐DSD), including Nf1 and Vcp mutant mice. We discuss the relevance of branched‐chain amino acid (BCAA) insufficiency in relation to unmet protein synthesis demand in ASD‐DSD. In contrast to ASD‐DSD, ASD models with hyperactive mammalian target of rapamycin (mTOR) may represent the opposite end of the disease spectrum, often characterized by increases in protein synthesis and dendritic spine density (denoted ASD‐ISD). Finally, we propose personalized dietary leucine as a strategy tailored to balancing protein synthesis demand, thereby ameliorating dendritic spine pathophysiologies and autism‐related phenotypes in susceptible patients, especially those with ASD‐DSD.
Keywords	autism ; brain ; dendrites ; leucine ; mutants ; pathophysiology ; protein synthesis ; rapamycin
Language	English
Dates of publication	2022-04
Size	p. 2282-2300.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15733
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Article ; Online: Noncanonical usage of stop codons in ciliates expands proteins with structurally flexible Q-rich motifs.

Chuang, Chi-Ning / Liu, Hou-Cheng / Woo, Tai-Ting / Chao, Ju-Lan / Chen, Chiung-Ya / Hu, Hisao-Tang / Hsueh, Yi-Ping / Wang, Ting-Fang

eLife

2024 Volume 12

Abstract: Serine(S)/threonine(T)-glutamine(Q) cluster domains (SCDs), polyglutamine (polyQ) tracts and polyglutamine/asparagine (polyQ/N) tracts are Q-rich motifs found in many proteins. SCDs often are intrinsically disordered regions that mediate protein ... ...

Abstract	Serine(S)/threonine(T)-glutamine(Q) cluster domains (SCDs), polyglutamine (polyQ) tracts and polyglutamine/asparagine (polyQ/N) tracts are Q-rich motifs found in many proteins. SCDs often are intrinsically disordered regions that mediate protein phosphorylation and protein-protein interactions. PolyQ and polyQ/N tracts are structurally flexible sequences that trigger protein aggregation. We report that due to their high percentages of STQ or STQN amino acid content, four SCDs and three prion-causing Q/N-rich motifs of yeast proteins possess autonomous protein expression-enhancing activities. Since these Q-rich motifs can endow proteins with structural and functional plasticity, we suggest that they represent useful toolkits for evolutionary novelty. Comparative Gene Ontology (GO) analyses of the near-complete proteomes of 26 representative model eukaryotes reveal that Q-rich motifs prevail in proteins involved in specialized biological processes, including
MeSH term(s)	Animals ; Mice ; Codon, Terminator/metabolism ; Drosophila melanogaster/genetics ; Drosophila melanogaster/metabolism ; Dictyostelium/genetics ; Fungal Proteins/metabolism ; Glutamine/metabolism
Chemical Substances	Codon, Terminator ; Fungal Proteins ; Glutamine (0RH81L854J)
Language	English
Publishing date	2024-02-23
Publishing country	England
Document type	Journal Article
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.91405
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Article ; Online: The involvement of endoplasmic reticulum formation and protein synthesis efficiency in VCP- and ATL1-related neurological disorders.

Shih, Yu-Tzu / Hsueh, Yi-Ping

Journal of biomedical science

2018 Volume 25, Issue 1, Page(s) 2

Abstract: The endoplasmic reticulum (ER) is the biggest organelle in cells and is involved in versatile cellular processes. Formation and maintenance of ER morphology are regulated by a series of proteins controlling membrane fusion and curvature. At least six ... ...

Abstract	The endoplasmic reticulum (ER) is the biggest organelle in cells and is involved in versatile cellular processes. Formation and maintenance of ER morphology are regulated by a series of proteins controlling membrane fusion and curvature. At least six different ER morphology regulators have been demonstrated to be involved in neurological disorders-including Valosin-containing protein (VCP), Atlastin-1 (ATL1), Spastin (SPAST), Reticulon 2 (RTN2), Receptor expression enhancing protein 1 (REEP1) and RAB10-suggesting a critical role of ER formation in neuronal activity and function. Among these genes, mutations in VCP gene involve in inclusion body myopathy with Paget disease of bone and frontotemporal dementia (IBMPFD), familial amyotrophic lateral sclerosis (ALS), autism spectrum disorders (ASD), and hereditary spastic paraplegia (HSP). ATL1 is also one of causative genes of HSP. RAB10 is associated with Parkinson's disease (PD). A recent study showed that VCP and ATL1 work together to regulate dendritic spine formation by controlling ER formation and consequent protein synthesis efficiency. RAB10 shares the same function with VCP and ATL1 to control ER formation and protein synthesis efficiency but acts independently. Increased protein synthesis by adding extra leucine to cultured neurons ameliorated dendritic spine deficits caused by VCP and ATL1 deficiencies, strengthening the significance of protein synthesis in VCP- and ATL1-regulated dendritic spine formation. These findings provide new insight into the roles of ER and protein synthesis in controlling dendritic spine formation and suggest a potential etiology of neurodegenerative disorders caused by mutations in VCP, ATL1 and other genes encoding proteins regulating ER formation and morphogenesis.
MeSH term(s)	Endoplasmic Reticulum/metabolism ; GTP-Binding Proteins/genetics ; GTP-Binding Proteins/metabolism ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Nervous System Diseases/genetics ; Nervous System Diseases/physiopathology ; Protein Biosynthesis ; Valosin Containing Protein/genetics ; Valosin Containing Protein/metabolism
Chemical Substances	Membrane Proteins ; ATL1 protein, human (EC 3.6.1.-) ; GTP-Binding Proteins (EC 3.6.1.-) ; VCP protein, human (EC 3.6.4.6) ; Valosin Containing Protein (EC 3.6.4.6)
Language	English
Publishing date	2018-01-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-017-0403-3
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Article: Anterior Commissure Regulates Neuronal Activity of Amygdalae and Influences Locomotor Activity, Social Interaction and Fear Memory in Mice.

Hsu, Tsan-Ting / Huang, Tzyy-Nan / Hsueh, Yi-Ping

Frontiers in molecular neuroscience

2020 Volume 13, Page(s) 47

Abstract: The two hemispheres of the vertebrate brain are connected through several commissures. Although the anterior commissure (AC) is the most conserved white matter structure in the brains of different vertebrates, its complete physiological functionality ... ...

Abstract	The two hemispheres of the vertebrate brain are connected through several commissures. Although the anterior commissure (AC) is the most conserved white matter structure in the brains of different vertebrates, its complete physiological functionality remains elusive. Since the AC is involved in the connection between two amygdalae and because amygdalae are critical for emotional behaviors and social interaction, we assessed amygdalar activity and function to investigate the physiological role of the AC. We first performed
Language	English
Publishing date	2020-03-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2020.00047
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