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Book ; Online: Protein Interaction Networks in Health and Disease

Petrakis, Spyros / Andrade-Navarro, Miguel A.

2016

Abstract: The identification and mapping of protein-protein interactions (PPIs) is a major goal in systems biology. Experimental data are currently produced in large scale using a variety of high-throughput assays in yeast or mammalian systems. Analysis of these ... ...

Abstract	The identification and mapping of protein-protein interactions (PPIs) is a major goal in systems biology. Experimental data are currently produced in large scale using a variety of high-throughput assays in yeast or mammalian systems. Analysis of these data using computational tools leads to the construction of large protein interaction networks, which help researchers identify novel protein functions.However, our current view of protein interaction networks is still limited and there is an active field of research trying to further develop this concept to include important processes: the topology of interactions and their changes in real time, the effects of competition for binding to the same protein region, PPI variation due to alternative splicing or post-translational modifications, etc.In particular, a clinically relevant topic for development of the concept of protein interactions networks is the consideration of mutant isoforms, which may be responsible for a pathological condition. Mutations in proteins may result in loss of normal interactions and appearance of novel abnormal interactions that may affect a protein's function and biological cycle.This Research Topic presents novel findings and recent achievements in the field of protein interaction networks with a focus on disease. Authors describe methods for the identification and quantification of PPIs, the annotation and analysis of networks, considering PPIs and protein complexes formed by mutant proteins associated with pathological conditions or genetic diseases
Keywords	Science (General) ; Genetics
Size	1 electronic resource (89 p.)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT020090698
ISBN	9782889199822 ; 2889199827
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article: Omics Analyses in a Neural Stem Cell Model of Familial Parkinson's Disease.

Notopoulou, Sofia / Gkekas, Ioannis / Petrakis, Spyros

Advances in experimental medicine and biology

2023 Volume 1423, Page(s) 149–160

Abstract: Parkinson's disease (PD) is the second most common neurodegenerative disorder, affecting millions of people worldwide. Despite considerable efforts, the underlying pathological mechanisms remain elusive, and yet, no treatment has been developed to ... ...

Abstract	Parkinson's disease (PD) is the second most common neurodegenerative disorder, affecting millions of people worldwide. Despite considerable efforts, the underlying pathological mechanisms remain elusive, and yet, no treatment has been developed to efficiently reverse or modify disease progression. Thus, new experimental models are required to provide insights into the pathology of PD. Small-molecule neural precursor cells (smNPCs) are ideal for the study of neurodegenerative disorders due to their neural identity and stem cell properties. Cytoplasmic aggregates of α-synuclein (αSyn) are considered a hallmark of PD and a point mutation in the gene encoding p.A53T is responsible for a familial PD form with earlier and robust symptom onset. In order to study the cellular pathology of PD, we genetically modified smNPCs to inducibly overexpress EYFP-SNCA A53T. This cellular model was biochemically characterized, while dysregulated biological pathways and key regulators of PD pathology were identified by computational analyses. Our study indicates three novel genes, UBA52, PIP5K1A, and RPS2, which may mediate PD cellular pathology.
MeSH term(s)	Humans ; Parkinson Disease/metabolism ; Neural Stem Cells/metabolism ; alpha-Synuclein/genetics ; alpha-Synuclein/metabolism ; Neurodegenerative Diseases ; Neurons/metabolism
Chemical Substances	alpha-Synuclein
Language	English
Publishing date	2023-07-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	410187-X
ISSN	0065-2598
ISSN	0065-2598
DOI	10.1007/978-3-031-31978-5_12
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Editorial: Mental health: cell models to mechanisms.

Harwood, Adrian J / Petrakis, Spyros / Oktay, Yavuz / Pasterkamp, R Jeroen

Frontiers in cell and developmental biology

2023 Volume 11, Page(s) 1244425

Language	English
Publishing date	2023-07-25
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2023.1244425
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Analysis of Huntington's Disease Modifiers Using the Hyperbolic Mapping of the Protein Interaction Network.

Vagiona, Aimilia-Christina / Mier, Pablo / Petrakis, Spyros / Andrade-Navarro, Miguel A

International journal of molecular sciences

2022 Volume 23, Issue 10

Abstract: Huntington's disease (HD) is caused by the production of a mutant huntingtin (HTT) with an abnormally long poly-glutamine (polyQ) tract, forming aggregates and inclusions in neurons. Previous work by us and others has shown that an increase or decrease ... ...

Abstract	Huntington's disease (HD) is caused by the production of a mutant huntingtin (HTT) with an abnormally long poly-glutamine (polyQ) tract, forming aggregates and inclusions in neurons. Previous work by us and others has shown that an increase or decrease in polyQ-triggered aggregates can be passive simply due to the interaction of proteins with the aggregates. To search for proteins with active (functional) effects, which might be more effective in finding therapies and mechanisms of HD, we selected among the proteins that interact with HTT a total of 49 pairs of proteins that, while being paralogous to each other (and thus expected to have similar passive interaction with HTT), are located in different regions of the protein interaction network (suggesting participation in different pathways or complexes). Three of these 49 pairs contained members with opposite effects on HD, according to the literature. The negative members of the three pairs, MID1, IKBKG, and IKBKB, interact with PPP2CA and TUBB, which are known negative factors in HD, as well as with HSP90AA1 and RPS3. The positive members of the three pairs interact with HSPA9. Our results provide potential HD modifiers of functional relevance and reveal the dynamic aspect of paralog evolution within the interaction network.
MeSH term(s)	Humans ; Huntington Disease/metabolism ; I-kappa B Kinase/metabolism ; Inclusion Bodies/metabolism ; Neurons/metabolism ; Protein Interaction Maps
Chemical Substances	IKBKG protein, human ; I-kappa B Kinase (EC 2.7.11.10)
Language	English
Publishing date	2022-05-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23105853
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Fabrication and Optimization of 3D-Printed Silica Scaffolds for Neural Precursor Cell Cultivation.

Kastrinaki, Georgia / Pechlivani, Eleftheria-Maria / Gkekas, Ioannis / Kladovasilakis, Nikolaos / Gkagkari, Evdokia / Petrakis, Spyros / Asimakopoulou, Akrivi

Journal of functional biomaterials

2023 Volume 14, Issue 9

Abstract: The latest developments in tissue engineering scaffolds have sparked a growing interest in the creation of controlled 3D cellular structures that emulate the intricate biophysical and biochemical elements found within versatile in vivo microenvironments. ...

Abstract	The latest developments in tissue engineering scaffolds have sparked a growing interest in the creation of controlled 3D cellular structures that emulate the intricate biophysical and biochemical elements found within versatile in vivo microenvironments. The objective of this study was to 3D-print a monolithic silica scaffold specifically designed for the cultivation of neural precursor cells. Initially, a preliminary investigation was conducted to identify the critical parameters pertaining to calcination. This investigation aimed to produce sturdy and uniform scaffolds with a minimal wall-thickness of 0.5 mm in order to mitigate the formation of cracks. Four cubic specimens, with different wall-thicknesses of 0.5, 1, 2, and 4 mm, were 3D-printed and subjected to two distinct calcination profiles. Thermogravimetric analysis was employed to examine the freshly printed material, revealing critical temperatures associated with increased mass loss. Isothermal steps were subsequently introduced to facilitate controlled phase transitions and reduce crack formation even at the minimum wall thickness of 0.5 mm. The optimized structure stability was obtained for the slow calcination profile (160 min) then the fast calcination profile (60 min) for temperatures up to 900 °C. In situ X-ray diffraction analysis was also employed to assess the crystal phases of the silicate based material throughout various temperature profiles up to 1200 °C, while scanning electron microscopy was utilized to observe micro-scale crack formation. Then, ceramic scaffolds were 3D-printed, adopting a hexagonal and spherical channel structures with channel opening of 2 mm, and subsequently calcined using the optimized slow profile. Finally, the scaffolds were evaluated in terms of biocompatibility, cell proliferation, and differentiation using neural precursor cells (NPCs). These experiments indicated proliferation of NPCs (for 13 days) and differentiation into neurons which remained viable (up to 50 days in culture). In parallel, functionality was verified by expression of pre- (SYN1) and post-synaptic (GRIP1) markers, suggesting that 3D-printed scaffolds are a promising system for biotechnological applications using NPCs.
Language	English
Publishing date	2023-09-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2648525-4
ISSN	2079-4983
ISSN	2079-4983
DOI	10.3390/jfb14090465
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Enhanced Growth of Bacterial Cells in a Smart 3D Printed Bioreactor.

Pechlivani, Eleftheria Maria / Pemas, Sotirios / Kanlis, Alexandros / Pechlivani, Paraskevi / Petrakis, Spyros / Papadimitriou, Athanasios / Tzovaras, Dimitrios / Hatzistergos, Konstantinos E

Micromachines

2023 Volume 14, Issue 10

Abstract: In the last decade, there has been a notable advancement in diverse bioreactor types catering to various applications. However, conventional bioreactors often exhibit bulkiness and high costs, making them less accessible to many researchers and ... ...

Abstract	In the last decade, there has been a notable advancement in diverse bioreactor types catering to various applications. However, conventional bioreactors often exhibit bulkiness and high costs, making them less accessible to many researchers and laboratory facilities. In light of these challenges, this article aims to introduce and evaluate the development of a do-it-yourself (DIY) 3D printed smart bioreactor, offering a cost-effective and user-friendly solution for the proliferation of various bioentities, including bacteria and human organoids, among others. The customized bioreactor was fabricated under an ergonomic design and assembled with 3D printed mechanical parts combined with electronic components, under 3D printed housing. The 3D printed parts were designed using SOLIDWORKS
Language	English
Publishing date	2023-09-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2620864-7
ISSN	2072-666X
ISSN	2072-666X
DOI	10.3390/mi14101829
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases

Gkekas, Ioannis / Gioran, Anna / Boziki, Marina Kleopatra / Grigoriadis, Nikolaos / Chondrogianni, Niki / Petrakis, Spyros

Antioxidants. 2021 Sept. 13, v. 10, no. 9

2021

Abstract: Neurodegenerative polyglutamine (polyQ) disorders are caused by trinucleotide repeat expansions within the coding region of disease-causing genes. PolyQ-expanded proteins undergo conformational changes leading to the formation of protein inclusions which ...

Abstract	Neurodegenerative polyglutamine (polyQ) disorders are caused by trinucleotide repeat expansions within the coding region of disease-causing genes. PolyQ-expanded proteins undergo conformational changes leading to the formation of protein inclusions which are associated with selective neuronal degeneration. Several lines of evidence indicate that these mutant proteins are associated with oxidative stress, proteasome impairment and microglia activation. These events may correlate with the induction of inflammation in the nervous system and disease progression. Here, we review the effect of polyQ-induced oxidative stress in cellular and animal models of polyQ diseases. Furthermore, we discuss the interplay between oxidative stress, neurodegeneration and neuroinflammation using as an example the well-known neuroinflammatory disease, Multiple Sclerosis. Finally, we review some of the pharmaceutical interventions which may delay the onset and progression of polyQ disorders by targeting disease-associated mechanisms.
Keywords	animals ; disease progression ; inflammation ; microsatellite repeats ; mutants ; neurodegenerative diseases ; neuroglia ; oxidative stress ; proteasome endopeptidase complex ; sclerosis
Language	English
Dates of publication	2021-0913
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10091450
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Dynamics of a Protein Interaction Network Associated to the Aggregation of polyQ-Expanded Ataxin-1.

Vagiona, Aimilia-Christina / Andrade-Navarro, Miguel A / Psomopoulos, Fotis / Petrakis, Spyros

Genes

2020 Volume 11, Issue 10

Abstract: Background: Several experimental models of polyglutamine (polyQ) diseases have been previously developed that are useful for studying disease progression in the primarily affected central nervous system. However, there is a missing link between cellular ...

Abstract	Background: Several experimental models of polyglutamine (polyQ) diseases have been previously developed that are useful for studying disease progression in the primarily affected central nervous system. However, there is a missing link between cellular and animal models that would indicate the molecular defects occurring in neurons and are responsible for the disease phenotype in vivo. Methods: Here, we used a computational approach to identify dysregulated pathways shared by an in vitro and an in vivo model of ATXN1(Q82) protein aggregation, the mutant protein that causes the neurodegenerative polyQ disease spinocerebellar ataxia type-1 (SCA1). Results: A set of common dysregulated pathways were identified, which were utilized to construct cerebellum-specific protein-protein interaction (PPI) networks at various time-points of protein aggregation. Analysis of a SCA1 network indicated important nodes which regulate its function and might represent potential pharmacological targets. Furthermore, a set of drugs interacting with these nodes and predicted to enter the blood-brain barrier (BBB) was identified. Conclusions: Our study points to molecular mechanisms of SCA1 linked from both cellular and animal models and suggests drugs that could be tested to determine whether they affect the aggregation of pathogenic ATXN1 and SCA1 disease progression.
MeSH term(s)	Animals ; Ataxin-1/genetics ; Ataxin-1/metabolism ; Cerebellum/metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Regulatory Networks ; Mice, Transgenic ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neurons/metabolism ; Peptides/genetics ; Peptides/metabolism ; Protein Interaction Maps
Chemical Substances	Ataxin-1 ; Atxn1 protein, mouse ; Nerve Tissue Proteins ; Peptides ; polyglutamine (26700-71-0)
Language	English
Publishing date	2020-09-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes11101129
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases.

Gkekas, Ioannis / Gioran, Anna / Boziki, Marina Kleopatra / Grigoriadis, Nikolaos / Chondrogianni, Niki / Petrakis, Spyros

Antioxidants (Basel, Switzerland)

2021 Volume 10, Issue 9

Abstract	Neurodegenerative polyglutamine (polyQ) disorders are caused by trinucleotide repeat expansions within the coding region of disease-causing genes. PolyQ-expanded proteins undergo conformational changes leading to the formation of protein inclusions which are associated with selective neuronal degeneration. Several lines of evidence indicate that these mutant proteins are associated with oxidative stress, proteasome impairment and microglia activation. These events may correlate with the induction of inflammation in the nervous system and disease progression. Here, we review the effect of polyQ-induced oxidative stress in cellular and animal models of polyQ diseases. Furthermore, we discuss the interplay between oxidative stress, neurodegeneration and neuroinflammation using as an example the well-known neuroinflammatory disease, Multiple Sclerosis. Finally, we review some of the pharmaceutical interventions which may delay the onset and progression of polyQ disorders by targeting disease-associated mechanisms.
Language	English
Publishing date	2021-09-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10091450
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Dynamics of a Protein Interaction Network Associated to the Aggregation of polyQ-Expanded Ataxin-1

Vagiona, Aimilia-Christina / Andrade-Navarro, Miguel A / Psomopoulos, Fotis / Petrakis, Spyros

Genes. 2020 Sept. 25, v. 11, no. 10

2020

Abstract	Background: Several experimental models of polyglutamine (polyQ) diseases have been previously developed that are useful for studying disease progression in the primarily affected central nervous system. However, there is a missing link between cellular and animal models that would indicate the molecular defects occurring in neurons and are responsible for the disease phenotype in vivo. Methods: Here, we used a computational approach to identify dysregulated pathways shared by an in vitro and an in vivo model of ATXN1(Q82) protein aggregation, the mutant protein that causes the neurodegenerative polyQ disease spinocerebellar ataxia type-1 (SCA1). Results: A set of common dysregulated pathways were identified, which were utilized to construct cerebellum-specific protein-protein interaction (PPI) networks at various time-points of protein aggregation. Analysis of a SCA1 network indicated important nodes which regulate its function and might represent potential pharmacological targets. Furthermore, a set of drugs interacting with these nodes and predicted to enter the blood–brain barrier (BBB) was identified. Conclusions: Our study points to molecular mechanisms of SCA1 linked from both cellular and animal models and suggests drugs that could be tested to determine whether they affect the aggregation of pathogenic ATXN1 and SCA1 disease progression.
Keywords	animal models ; ataxia (disorder) ; blood-brain barrier ; central nervous system ; disease progression ; drugs ; mutants ; neurons ; phenotype ; protein-protein interactions
Language	English
Dates of publication	2020-0925
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes11101129
Database	NAL-Catalogue (AGRICOLA)

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