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Artikel ; Online: Mechanisms and Therapeutic Implications of GSK-3 in Treating Neurodegeneration.

Rippin, Ido / Eldar-Finkelman, Hagit

2021 Band 10, Heft 2

Abstract: Neurodegenerative disorders are spreading worldwide and are one of the greatest threats to public health. There is currently no adequate therapy for these disorders, and therefore there is an urgent need to accelerate the discovery and development of ... ...

Abstract	Neurodegenerative disorders are spreading worldwide and are one of the greatest threats to public health. There is currently no adequate therapy for these disorders, and therefore there is an urgent need to accelerate the discovery and development of effective treatments. Although neurodegenerative disorders are broad ranging and highly complex, they may share overlapping mechanisms, and thus potentially manifest common targets for therapeutic interventions. Glycogen synthase kinase-3 (GSK-3) is now acknowledged to be a central player in regulating mood behavior, cognitive functions, and neuron viability. Indeed, many targets controlled by GSK-3 are critically involved in progressing neuron deterioration and disease pathogenesis. In this review, we focus on three pathways that represent prominent mechanisms linking GSK-3 with neurodegenerative disorders: cytoskeleton organization, the mammalian target of rapamycin (mTOR)/autophagy axis, and mitochondria. We also consider the challenges and opportunities in the development of GSK-3 inhibitors for treating neurodegeneration.
Mesh-Begriff(e)	Autophagy ; Axonal Transport ; Energy Metabolism ; Glycogen Synthase Kinase 3/antagonists & inhibitors ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Microtubules/metabolism ; Neurodegenerative Diseases/drug therapy
Chemische Substanzen	Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Sprache	Englisch
Erscheinungsdatum	2021-01-29
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10020262
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Prospects in GSK-3 Signaling: From Cellular Regulation to Disease Therapy.

Arciniegas Ruiz, Sara / Rippin, Ido / Eldar-Finkelman, Hagit

Cells

2022 Band 11, Heft 10

Abstract: Over the last decade, there has been continuous progress in our understanding of the biology of the protein kinase GSK-3 [ ... ]. ...

Abstract	Over the last decade, there has been continuous progress in our understanding of the biology of the protein kinase GSK-3 [...].
Mesh-Begriff(e)	Cell Cycle ; Glycogen Synthase Kinase 3 ; Signal Transduction/physiology
Chemische Substanzen	Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Sprache	Englisch
Erscheinungsdatum	2022-05-12
Erscheinungsland	Switzerland
Dokumenttyp	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11101618
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Correction: Nonsense mutation suppression is enhanced by targeting different stages of the protein synthesis process.

Wittenstein, Amnon / Caspi, Michal / Rippin, Ido / Elroy-Stein, Orna / Eldar-Finkelman, Hagit / Thoms, Sven / Rosin-Arbesfeld, Rina

PLoS biology

2024 Band 22, Heft 2, Seite(n) e3002524

Abstract: This corrects the article DOI: 10.1371/journal.pbio.3002355.]. ...

Abstract	[This corrects the article DOI: 10.1371/journal.pbio.3002355.].
Sprache	Englisch
Erscheinungsdatum	2024-02-14
Erscheinungsland	United States
Dokumenttyp	Published Erratum
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3002524
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Modulating Gene Expression within a Microbiome Based on Computational Models

Chitayat Levi, Liyam / Rippin, Ido / Ben Tulila, Moran / Galron, Rotem / Tuller, Tamir

Biology. 2022 Aug. 31, v. 11, no. 9

2022

Abstract: Recent research in the field of bioinformatics and molecular biology has revealed the immense complexity and uniqueness of microbiomes, while also showcasing the impact of the symbiosis between a microbiome and its host or environment. A core property ... ...

Abstract	Recent research in the field of bioinformatics and molecular biology has revealed the immense complexity and uniqueness of microbiomes, while also showcasing the impact of the symbiosis between a microbiome and its host or environment. A core property influencing this process is horizontal gene transfer between members of the bacterial community used to maintain genetic variation. The essential effect of this mechanism is the exposure of genetic information to a wide array of members of the community, creating an additional “layer” of information in the microbiome named the “plasmidome”. From an engineering perspective, introduction of genetic information to an environment must be facilitated into chosen species which will be able to carry out the desired effect instead of competing and inhibiting it. Moreover, this process of information transfer imposes concerns for the biosafety of genetic engineering of microbiomes as exposure of genetic information into unwanted hosts can have unprecedented ecological impacts. Current technologies are usually experimentally developed for a specific host/environment, and only deal with the transformation process itself at best, ignoring the impact of horizontal gene transfer and gene-microbiome interactions that occur over larger periods of time in uncontrolled environments. The goal of this research was to design new microbiome-specific versions of engineered genetic information, providing an additional layer of compatibility to existing engineering techniques. The engineering framework is entirely computational and is agnostic to the selected microbiome or gene by reducing the problem into the following set up: microbiome species can be defined as wanted or unwanted hosts of the modification. Then, every element related to gene expression (e.g., promoters, coding regions, etc.) and regulation is individually examined and engineered by novel algorithms to provide the defined expression preferences. Additionally, the synergistic effect of the combination of engineered gene blocks facilitates robustness to random mutations that might occur over time. This method has been validated using both computational and experimental tools, stemming from the research done in the iGEM 2021 competition, by the TAU group.
Schlagwörter	bacterial communities ; bioinformatics ; biosafety ; gene expression ; genes ; genetic variation ; horizontal gene transfer ; information exchange ; microbiome ; molecular biology ; symbiosis ; synergism
Sprache	Englisch
Erscheinungsverlauf	2022-0831
Erscheinungsort	Multidisciplinary Digital Publishing Institute
Dokumenttyp	Artikel
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology11091301
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel: Modulating Gene Expression within a Microbiome Based on Computational Models.

Chitayat Levi, Liyam / Rippin, Ido / Ben Tulila, Moran / Galron, Rotem / Tuller, Tamir

Biology

2022 Band 11, Heft 9

Abstract	Recent research in the field of bioinformatics and molecular biology has revealed the immense complexity and uniqueness of microbiomes, while also showcasing the impact of the symbiosis between a microbiome and its host or environment. A core property influencing this process is horizontal gene transfer between members of the bacterial community used to maintain genetic variation. The essential effect of this mechanism is the exposure of genetic information to a wide array of members of the community, creating an additional "layer" of information in the microbiome named the "plasmidome". From an engineering perspective, introduction of genetic information to an environment must be facilitated into chosen species which will be able to carry out the desired effect instead of competing and inhibiting it. Moreover, this process of information transfer imposes concerns for the biosafety of genetic engineering of microbiomes as exposure of genetic information into unwanted hosts can have unprecedented ecological impacts. Current technologies are usually experimentally developed for a specific host/environment, and only deal with the transformation process itself at best, ignoring the impact of horizontal gene transfer and gene-microbiome interactions that occur over larger periods of time in uncontrolled environments. The goal of this research was to design new microbiome-specific versions of engineered genetic information, providing an additional layer of compatibility to existing engineering techniques. The engineering framework is entirely computational and is agnostic to the selected microbiome or gene by reducing the problem into the following set up: microbiome species can be defined as wanted or unwanted hosts of the modification. Then, every element related to gene expression (e.g., promoters, coding regions, etc.) and regulation is individually examined and engineered by novel algorithms to provide the defined expression preferences. Additionally, the synergistic effect of the combination of engineered gene blocks facilitates robustness to random mutations that might occur over time. This method has been validated using both computational and experimental tools, stemming from the research done in the iGEM 2021 competition, by the TAU group.
Sprache	Englisch
Erscheinungsdatum	2022-08-31
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology11091301
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: GSK-3β Inhibition in Birds Affects Social Behavior and Increases Motor Activity.

Moaraf, Stan / Rippin, Ido / Terkel, Joseph / Eldar-Finkelman, Hagit / Barnea, Anat

Frontiers in physiology

2022 Band 13, Seite(n) 881174

Abstract: Glycogen synthase kinase-3 (GSK-3) is a highly conserved serine/threonine protein kinase that plays a central role in a wide variety of cellular processes, cognition and behaviour. In a previous study we showed that its α and β isozymes are highly ... ...

Abstract	Glycogen synthase kinase-3 (GSK-3) is a highly conserved serine/threonine protein kinase that plays a central role in a wide variety of cellular processes, cognition and behaviour. In a previous study we showed that its α and β isozymes are highly conserved in vertebrates, however the α gene is missing in birds. This selective loss offers a unique opportunity to study the role of GSK-3β independently. Accordingly, in the present study we aimed to investigate the role of GSK-3β in social behaviour, motivation, and motor activity in zebra finches (
Sprache	Englisch
Erscheinungsdatum	2022-04-28
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2022.881174
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Nonsense mutation suppression is enhanced by targeting different stages of the protein synthesis process.

Wittenstein, Amnon / Caspi, Michal / Rippin, Ido / Elroy-Stein, Orna / Eldar-Finkelman, Hagit / Thoms, Sven / Rosin-Arbesfeld, Rina

PLoS biology

2023 Band 21, Heft 11, Seite(n) e3002355

Abstract: The introduction of premature termination codons (PTCs), as a result of splicing defects, insertions, deletions, or point mutations (also termed nonsense mutations), lead to numerous genetic diseases, ranging from rare neuro-metabolic disorders to ... ...

Abstract	The introduction of premature termination codons (PTCs), as a result of splicing defects, insertions, deletions, or point mutations (also termed nonsense mutations), lead to numerous genetic diseases, ranging from rare neuro-metabolic disorders to relatively common inheritable cancer syndromes and muscular dystrophies. Over the years, a large number of studies have demonstrated that certain antibiotics and other synthetic molecules can act as PTC suppressors by inducing readthrough of nonsense mutations, thereby restoring the expression of full-length proteins. Unfortunately, most PTC readthrough-inducing agents are toxic, have limited effects, and cannot be used for therapeutic purposes. Thus, further efforts are required to improve the clinical outcome of nonsense mutation suppressors. Here, by focusing on enhancing readthrough of pathogenic nonsense mutations in the adenomatous polyposis coli (APC) tumor suppressor gene, we show that disturbing the protein translation initiation complex, as well as targeting other stages of the protein translation machinery, enhances both antibiotic and non-antibiotic-mediated readthrough of nonsense mutations. These findings strongly increase our understanding of the mechanisms involved in nonsense mutation readthrough and facilitate the development of novel therapeutic targets for nonsense suppression to restore protein expression from a large variety of disease-causing mutated transcripts.
Mesh-Begriff(e)	Humans ; Codon, Nonsense/genetics ; Protein Biosynthesis/genetics ; Anti-Bacterial Agents/pharmacology ; Neoplasms
Chemische Substanzen	Codon, Nonsense ; Anti-Bacterial Agents
Sprache	Englisch
Erscheinungsdatum	2023-11-09
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3002355
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Inhibition of GSK-3 ameliorates the pathogenesis of Huntington's disease.

Rippin, Ido / Bonder, Katherina / Joseph, Shirley / Sarsor, Ammar / Vaks, Lilach / Eldar-Finkelman, Hagit

Neurobiology of disease

2021 Band 154, Seite(n) 105336

Abstract: In Huntington's disease (HD), the mutant huntingtin (mHtt) accumulates as toxic aggregates in the striatum tissue, with deleterious effects on motor-coordination and cognitive functions. Reducing the levels of mHtt is therefore a promising therapeutic ... ...

Abstract	In Huntington's disease (HD), the mutant huntingtin (mHtt) accumulates as toxic aggregates in the striatum tissue, with deleterious effects on motor-coordination and cognitive functions. Reducing the levels of mHtt is therefore a promising therapeutic strategy. We have previously reported that GSK-3 is a negative regulator of the autophagy/lysosome pathway, which is responsible for intracellular degradation, and is critically important for maintaining neuronal vitality. Thus, we hypothesized that inhibition of GSK-3 may trigger mHtt clearance thereby reducing mHtt cytotoxicity and improving HD symptoms. Here, we demonstrate that depletion or suppression of autophagy results in a massive accumulation of mHtt aggregates. Accordingly, mHtt aggregates were localized in lysosomes, but, mostly mislocalized from lysosomes in the absence of functional autophagy. Overexpression of GSK-3, particularly the α isozyme, increased the number of mHtt aggregates, while silencing GSK-3α/β, or treatment with a selective GSK-3 inhibitor, L807mts, previously described by us, reduced the amounts of mHtt aggregates. This effect was mediated by increased autophagic and lysosomal activity. Treating R6/2 mouse model of HD with L807mts, reduced striatal mHtt aggregates and elevated autophagic and lysosomal markers. The L807mts treatment also reduced hyperglycemia and improved motor-coordination functions in these mice. In addition, L807mts restored the expression levels of Sirt1, a critical neuroprotective factor in the HD striatum, along with its targets BDNF, DRPP-32, and active Akt, all provide neurotrophic/pro-survival support and typically decline in the HD brain. Our results provide strong evidence for a role for GSK-3 in the regulation of mHtt dynamics, and demonstrate the benefits of GSK-3 inhibition in reducing mHtt toxicity, providing neuroprotective support, and improving HD symptoms.
Mesh-Begriff(e)	Animals ; Cell Line, Tumor ; Glycogen Synthase Kinase 3/antagonists & inhibitors ; Glycogen Synthase Kinase 3/genetics ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Huntington Disease/pathology ; Lysosomes/metabolism ; Male ; Mice ; Mice, Inbred CBA ; Mice, Transgenic
Chemische Substanzen	HTT protein, human ; Huntingtin Protein ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Sprache	Englisch
Erscheinungsdatum	2021-03-19
Erscheinungsland	United States
Dokumenttyp	Journal Article ; 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.2021.105336
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Discovery and Design of Novel Small Molecule GSK-3 Inhibitors Targeting the Substrate Binding Site.

Rippin, Ido / Khazanov, Netaly / Shirley Ben Joseph / Kudinov, Tania / Berent, Eva / Arciniegas Ruiz, Sara Melisa / Marciano, Daniele / Levy, Laura / Gruzman, Arie / Senderowitz, Hanoch / Eldar-Finkelman, Hagit

International journal of molecular sciences

2020 Band 21, Heft 22

Abstract: The serine/threonine kinase, GSK-3, is a promising drug discovery target for treating multiple pathological disorders. Most GSK-3 inhibitors that were developed function as ATP competitive inhibitors, with typical limitations in specificity, safety and ... ...

Abstract	The serine/threonine kinase, GSK-3, is a promising drug discovery target for treating multiple pathological disorders. Most GSK-3 inhibitors that were developed function as ATP competitive inhibitors, with typical limitations in specificity, safety and drug-induced resistance. In contrast, substrate competitive inhibitors (SCIs), are considered highly selective, and more suitable for clinical practice. The development of SCIs has been largely neglected in the past because the ambiguous, undefined nature of the substrate-binding site makes them difficult to design. In this study, we used our previously described structural models of GSK-3 bound to SCI peptides, to design a pharmacophore model and to virtually screen the "drug-like" Zinc database (~6.3 million compounds). We identified leading hits that interact with critical binding elements in the GSK-3 substrate binding site and are chemically distinct from known GSK-3 inhibitors. Accordingly, novel GSK-3 SCI compounds were designed and synthesized with IC
Mesh-Begriff(e)	Animals ; Binding Sites ; Cell Line, Tumor ; Cells, Cultured ; Drug Design ; Drug Discovery/methods ; Glycogen Synthase Kinase 3/antagonists & inhibitors ; Glycogen Synthase Kinase 3/chemistry ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Kinetics ; Mice, Inbred C57BL ; Molecular Docking Simulation ; Molecular Structure ; Protein Binding ; Protein Domains ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/metabolism ; Protein Kinase Inhibitors/pharmacology ; Small Molecule Libraries/chemistry ; Small Molecule Libraries/metabolism ; Small Molecule Libraries/pharmacology ; Substrate Specificity
Chemische Substanzen	Protein Kinase Inhibitors ; Small Molecule Libraries ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Sprache	Englisch
Erscheinungsdatum	2020-11-18
Erscheinungsland	Switzerland
Dokumenttyp	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/ijms21228709
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Ataxia Telangiectasia Mutated Signaling Delays Skin Pigmentation upon UV Exposure by Mediating MITF Function toward DNA Repair Mode.

Elkoshi, Nadav / Parikh, Shivang / Malcov-Brog, Hagar / Parikh, Roma / Manich, Paulee / Netti, Francesca / Maliah, Avishai / Elkoshi, Hana / Haj, Majd / Rippin, Ido / Frand, Jacob / Perluk, Tomer / Haiat-Factor, Rivi / Golan, Tamar / Regev-Rudzki, Neta / Kiper, Edo / Brenner, Ronen / Gonen, Pinchas / Dror, Iris /

Levi, Hagai / Hameiri, Ofir / Cohen-Gulkar, Mazal / Eldar-Finkelman, Hagit / Ast, Gil / Nizri, Eran / Ziv, Yael / Elkon, Rani / Khaled, Mehdi / Ebenstein, Yuval / Shiloh, Yosef / Levy, Carmit

The Journal of investigative dermatology

2023 Band 143, Heft 12, Seite(n) 2494–2506.e4

Abstract: Skin pigmentation is paused after sun exposure; however, the mechanism behind this pausing is unknown. In this study, we found that the UVB-induced DNA repair system, led by the ataxia telangiectasia mutated (ATM) protein kinase, represses MITF ... ...

Abstract	Skin pigmentation is paused after sun exposure; however, the mechanism behind this pausing is unknown. In this study, we found that the UVB-induced DNA repair system, led by the ataxia telangiectasia mutated (ATM) protein kinase, represses MITF transcriptional activity of pigmentation genes while placing MITF in DNA repair mode, thus directly inhibiting pigment production. Phosphoproteomics analysis revealed ATM to be the most significantly enriched pathway among all UVB-induced DNA repair systems. ATM inhibition in mouse or human skin, either genetically or chemically, induces pigmentation. Upon UVB exposure, MITF transcriptional activation is blocked owing to ATM-dependent phosphorylation of MITF on S414, which modifies MITF activity and interactome toward DNA repair, including binding to TRIM28 and RBBP4. Accordingly, MITF genome occupancy is enriched in sites of high DNA damage that are likely repaired. This suggests that ATM harnesses the pigmentation key activator for the necessary rapid, efficient DNA repair, thus optimizing the chances of the cell surviving. Data are available from ProteomeXchange with the identifier PXD041121.
Mesh-Begriff(e)	Humans ; Animals ; Mice ; Ataxia Telangiectasia ; Skin Pigmentation/genetics ; DNA Repair ; Ataxia Telangiectasia Mutated Proteins/genetics ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Signal Transduction ; DNA Damage ; Phosphorylation ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Microphthalmia-Associated Transcription Factor/genetics ; Microphthalmia-Associated Transcription Factor/metabolism
Chemische Substanzen	Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Cell Cycle Proteins ; MITF protein, human ; Microphthalmia-Associated Transcription Factor
Sprache	Englisch
Erscheinungsdatum	2023-05-25
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2023.03.1686
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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