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  1. Article ; Online: Epigenetic Regulation in Neurodegeneration Disease.

    Bodai, László

    International journal of molecular sciences

    2022  Volume 23, Issue 11

    Abstract: Due to their often age-dependent nature, neurodegenerative diseases impact an increasing portion of modern societies [ ... ]. ...

    Abstract Due to their often age-dependent nature, neurodegenerative diseases impact an increasing portion of modern societies [...].
    MeSH term(s) Epigenesis, Genetic ; Humans ; Neurodegenerative Diseases/genetics
    Language English
    Publishing date 2022-05-31
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23116185
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Dysregulated miRNA and mRNA Expression Affect Overlapping Pathways in a Huntington's Disease Model.

    Zsindely, Nóra / Nagy, Gábor / Siági, Fruzsina / Farkas, Anita / Bodai, László

    International journal of molecular sciences

    2023  Volume 24, Issue 15

    Abstract: Huntington's disease (HD) is a fatal neurodegenerative disorder caused by the expansion of a CAG trinucleotide repeat in the Huntingtin gene. Transcriptional dysregulation is one of the main cellular processes affected by mutant Huntingtin (mHtt). In ... ...

    Abstract Huntington's disease (HD) is a fatal neurodegenerative disorder caused by the expansion of a CAG trinucleotide repeat in the Huntingtin gene. Transcriptional dysregulation is one of the main cellular processes affected by mutant Huntingtin (mHtt). In this study, we investigate the alterations in miRNA and mRNA expression levels in a
    MeSH term(s) Animals ; Huntington Disease/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Trinucleotide Repeats ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Huntingtin Protein/genetics ; Disease Models, Animal
    Chemical Substances MicroRNAs ; RNA, Messenger ; Huntingtin Protein
    Language English
    Publishing date 2023-07-26
    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/ijms241511942
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The ubiquitin thioesterase YOD1 ameliorates mutant Huntingtin induced pathology in Drosophila.

    Farkas, Anita / Zsindely, Nóra / Nagy, Gábor / Kovács, Levente / Deák, Péter / Bodai, László

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 21951

    Abstract: Huntington's disease (HD) is a neurodegenerative disorder caused by a dominant gain-of-function mutation in the huntingtin gene, resulting in an elongated polyglutamine repeat in the mutant Huntingtin (mHtt) that mediates aberrant protein interactions. ... ...

    Abstract Huntington's disease (HD) is a neurodegenerative disorder caused by a dominant gain-of-function mutation in the huntingtin gene, resulting in an elongated polyglutamine repeat in the mutant Huntingtin (mHtt) that mediates aberrant protein interactions. Previous studies implicated the ubiquitin-proteasome system in HD, suggesting that restoring cellular proteostasis might be a key element in suppressing pathology. We applied genetic interaction tests in a Drosophila model to ask whether modulating the levels of deubiquitinase enzymes affect HD pathology. By testing 32 deubiquitinase genes we found that overexpression of Yod1 ameliorated all analyzed phenotypes, including neurodegeneration, motor activity, viability, and longevity. Yod1 did not have a similar effect in amyloid beta overexpressing flies, suggesting that the observed effects might be specific to mHtt. Yod1 overexpression did not alter the number of mHtt aggregates but moderately increased the ratio of larger aggregates. Transcriptome analysis showed that Yod1 suppressed the transcriptional effects of mHtt and restored the expression of genes involved in neuronal plasticity, vesicular transport, antimicrobial defense, and protein synthesis, modifications, and clearance. Furthermore, Yod1 overexpression in HD flies leads to the upregulation of genes involved in transcriptional regulation and synaptic transmission, which might be part of a response mechanism to mHtt-induced stress.
    MeSH term(s) Animals ; Amyloid beta-Peptides/genetics ; Deubiquitinating Enzymes/genetics ; Disease Models, Animal ; Drosophila/genetics ; Drosophila/metabolism ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism ; Huntington Disease/metabolism ; Mutation ; Ubiquitin/genetics
    Chemical Substances Amyloid beta-Peptides ; Deubiquitinating Enzymes (EC 3.4.19.12) ; Huntingtin Protein ; Ubiquitin ; Htt protein, Drosophila
    Language English
    Publishing date 2023-12-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-49241-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: DNA Methylation in Huntington's Disease.

    Zsindely, Nóra / Siági, Fruzsina / Bodai, László

    International journal of molecular sciences

    2021  Volume 22, Issue 23

    Abstract: Methylation of cytosine in CpG dinucleotides is the major DNA modification in mammalian cells that is a key component of stable epigenetic marks. This modification, which on the one hand is reversible, while on the other hand, can be maintained through ... ...

    Abstract Methylation of cytosine in CpG dinucleotides is the major DNA modification in mammalian cells that is a key component of stable epigenetic marks. This modification, which on the one hand is reversible, while on the other hand, can be maintained through successive rounds of replication plays roles in gene regulation, genome maintenance, transgenerational epigenetic inheritance, and imprinting. Disturbed DNA methylation contributes to a wide array of human diseases from single-gene disorders to sporadic metabolic diseases or cancer. DNA methylation was also shown to affect several neurodegenerative disorders, including Huntington's disease (HD), a fatal, monogenic inherited disease. HD is caused by a polyglutamine repeat expansion in the Huntingtin protein that brings about a multifaceted pathogenesis affecting several cellular processes. Research of the last decade found complex, genome-wide DNA methylation changes in HD pathogenesis that modulate transcriptional activity and genome stability. This article reviews current evidence that sheds light on the role of DNA methylation in HD.
    MeSH term(s) Animals ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Regulation ; Humans ; Huntingtin Protein/genetics ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Huntington Disease/pathology ; Protein Processing, Post-Translational
    Chemical Substances Huntingtin Protein
    Language English
    Publishing date 2021-11-25
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms222312736
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The histone replacement gene His4r is involved in heat stress induced chromatin rearrangement.

    Faragó, Anikó / Ürmösi, Adél / Farkas, Anita / Bodai, László

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 4878

    Abstract: His4r is the only known variant of histone H4 in Drosophila. It is encoded by the His4r single-copy gene that is located outside of the histone gene cluster and expressed in a different pattern than H4, although the encoded polypeptides are identical. We ...

    Abstract His4r is the only known variant of histone H4 in Drosophila. It is encoded by the His4r single-copy gene that is located outside of the histone gene cluster and expressed in a different pattern than H4, although the encoded polypeptides are identical. We generated a null mutant (His4r
    MeSH term(s) Animals ; Chromatin/genetics ; Chromatin/metabolism ; Chromatin Assembly and Disassembly ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Drosophila melanogaster ; HSP70 Heat-Shock Proteins/genetics ; HSP70 Heat-Shock Proteins/metabolism ; Heat-Shock Proteins/genetics ; Heat-Shock Proteins/metabolism ; Heat-Shock Response ; Histones/genetics ; Histones/metabolism
    Chemical Substances Chromatin ; Drosophila Proteins ; HSP70 Heat-Shock Proteins ; Heat-Shock Proteins ; His4r protein, Drosophila ; Histones ; Hsp26 protein, Drosophila ; Hsp68 protein, Drosophila
    Language English
    Publishing date 2021-03-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-84413-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Histone methylation in Huntington's disease: are bivalent promoters the critical targets?

    Zsindely, Nóra / Bodai, László

    Neural regeneration research

    2018  Volume 13, Issue 7, Page(s) 1191–1192

    Language English
    Publishing date 2018-07-20
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.235029
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Mutant huntingtin disturbs circadian clock gene expression and sleep patterns in Drosophila.

    Faragó, Anikó / Zsindely, Nóra / Bodai, László

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 7174

    Abstract: Deficiency of the sleep-wake cycle can accelerate the progression of Huntington's disease (HD) and exacerbate symptoms making it a target of investigation to better understand the molecular pathology of the disorder. In this study we analyzed sleep ... ...

    Abstract Deficiency of the sleep-wake cycle can accelerate the progression of Huntington's disease (HD) and exacerbate symptoms making it a target of investigation to better understand the molecular pathology of the disorder. In this study we analyzed sleep defects in a Drosophila model of HD and investigated whether disturbed sleep coincides with alterations in the molecular mechanism controlling circadian rhythm. To analyze sleep defects we recorded the daily activity of flies in 12:12 hours light:dark entrainment and in regard to the underlying molecular mechanism measured circadian "clock" gene expression. In HD flies we observed reduced amount of sleep, sleep fragmentation and prolonged sleep latency. We found changes in gene expression patterns of both transcriptional feedback loops of circadian regulation. We detected prolonged expression of the core feedback loop components period and timeless, whilst the secondary feedback loop member vrille had lower expression rates in general. Our results show that the Drosophila HD model recapitulates most of the sleep related symptoms reported in patients therefore it can be a potential tool to study the molecular background of sleep defects in HD. Altered expression of circadian "clock" genes suggests that disturbed sleep pattern in HD might be the consequence of disturbed circadian regulation.
    MeSH term(s) Animals ; Basic-Leucine Zipper Transcription Factors/genetics ; Basic-Leucine Zipper Transcription Factors/metabolism ; Circadian Clocks/genetics ; Disease Models, Animal ; Drosophila/genetics ; Drosophila/physiology ; Drosophila Proteins/deficiency ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Gene Expression Regulation ; Huntingtin Protein/deficiency ; Huntingtin Protein/genetics ; Huntington Disease/metabolism ; Huntington Disease/pathology ; Phenotype ; Sleep/genetics ; Sleep/physiology ; Transcriptome
    Chemical Substances Basic-Leucine Zipper Transcription Factors ; Drosophila Proteins ; Huntingtin Protein ; PDP1 protein, Drosophila ; tim protein, Drosophila
    Language English
    Publishing date 2019-05-09
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-43612-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Differential Gene Expression of

    Homa, Mónika / Ibragimova, Sandugash / Szebenyi, Csilla / Nagy, Gábor / Zsindely, Nóra / Bodai, László / Vágvölgyi, Csaba / Papp, Tamás

    Journal of fungi (Basel, Switzerland)

    2022  Volume 8, Issue 4

    Abstract: Mucor lusitanicus and some other members of the fungal order Mucorales display the phenomenon of morphological dimorphism. This means that these fungi aerobically produce filamentous hyphae, developing a coenocytic mycelium, but they grow in a multipolar ...

    Abstract Mucor lusitanicus and some other members of the fungal order Mucorales display the phenomenon of morphological dimorphism. This means that these fungi aerobically produce filamentous hyphae, developing a coenocytic mycelium, but they grow in a multipolar yeast-like form under anaerobiosis. Revealing the molecular mechanism of the reversible yeast-hyphal transition can be interesting for both the biotechnological application and in the understanding of the pathomechanism of mucormycosis. In the present study, transcriptomic analyses were carried out after cultivating the fungus either aerobically or anaerobically revealing significant changes in gene expression under the two conditions. In total, 539 differentially expressed genes (FDR < 0.05, |log2FC| ≥ 3) were identified, including 190 upregulated and 349 downregulated transcripts. Within the metabolism-related genes, carbohydrate metabolism was proven to be especially affected. Anaerobiosis also affected the transcription of transporters: among the 14 up- and 42 downregulated transporters, several putative sugar transporters were detected. Moreover, a considerable number of transcripts related to amino acid transport and metabolism, lipid transport and metabolism, and energy production and conversion were proven to be downregulated when the culture had been transferred into an anaerobic atmosphere.
    Language English
    Publishing date 2022-04-15
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2784229-0
    ISSN 2309-608X ; 2309-608X
    ISSN (online) 2309-608X
    ISSN 2309-608X
    DOI 10.3390/jof8040404
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Acetylation State of Lysine 14 of Histone H3.3 Affects Mutant Huntingtin Induced Pathogenesis.

    Faragó, Anikó / Zsindely, Nóra / Farkas, Anita / Neller, Alexandra / Siági, Fruzsina / Szabó, Márton Richárd / Csont, Tamás / Bodai, László

    International journal of molecular sciences

    2022  Volume 23, Issue 23

    Abstract: Huntington's Disease (HD) is a fatal neurodegenerative disorder caused by the expansion of a polyglutamine-coding CAG repeat in ... ...

    Abstract Huntington's Disease (HD) is a fatal neurodegenerative disorder caused by the expansion of a polyglutamine-coding CAG repeat in the
    Language English
    Publishing date 2022-12-02
    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/ijms232315173
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Despite its sequence identity with canonical H4, Drosophila H4r product is enriched at specific chromatin regions.

    Ábrahám, Andrea / Villányi, Zoltán / Zsindely, Nóra / Nagy, Gábor / Szabó, Áron / Bodai, László / Henn, László / Boros, Imre M

    Scientific reports

    2022  Volume 12, Issue 1, Page(s) 5007

    Abstract: Histone variants are different from their canonical counterparts in structure and are encoded by solitary genes with unique regulation to fulfill tissue or differentiation specific functions. A single H4 variant gene (His4r or H4r) that is located ... ...

    Abstract Histone variants are different from their canonical counterparts in structure and are encoded by solitary genes with unique regulation to fulfill tissue or differentiation specific functions. A single H4 variant gene (His4r or H4r) that is located outside of the histone cluster and gives rise to a polyA tailed messenger RNA via replication-independent expression is preserved in Drosophila strains despite that its protein product is identical with canonical H4. In order to reveal information on the possible role of this alternative H4 we epitope tagged endogenous H4r and studied its spatial and temporal expression, and revealed its genome-wide localization to chromatin at the nucleosomal level. RNA and immunohistochemistry analysis of H4r expressed under its cognate regulation indicate expression of the gene throughout zygotic and larval development and presence of the protein product is evident already in the pronuclei of fertilized eggs. In the developing nervous system a slight disequibrium in H4r distribution is observable, cholinergic neurons are the most abundant among H4r-expressing cells. ChIP-seq experiments revealed H4r association with regulatory regions of genes involved in cellular stress response. The data presented here indicate that H4r has a variant histone function.
    MeSH term(s) Animals ; Chromatin/genetics ; Drosophila/genetics ; Histones/genetics ; Nucleosomes ; Receptors, Histamine H4/genetics
    Chemical Substances Chromatin ; Histones ; Nucleosomes ; Receptors, Histamine H4
    Language English
    Publishing date 2022-03-23
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-09026-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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