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  1. Article ; Online: The CST complex facilitates cell survival under oxidative genotoxic stress.

    Hara, Tomohiko / Nakaoka, Hidenori / Miyoshi, Tomoicihiro / Ishikawa, Fuyuki

    PloS one

    2023  Volume 18, Issue 8, Page(s) e0289304

    Abstract: Genomic DNA is constantly exposed to a variety of genotoxic stresses, and it is crucial for organisms to be equipped with mechanisms for repairing the damaged genome. Previously, it was demonstrated that the mammalian CST (CTC1-STN1-TEN1) complex, which ... ...

    Abstract Genomic DNA is constantly exposed to a variety of genotoxic stresses, and it is crucial for organisms to be equipped with mechanisms for repairing the damaged genome. Previously, it was demonstrated that the mammalian CST (CTC1-STN1-TEN1) complex, which was originally identified as a single-stranded DNA-binding trimeric protein complex essential for telomere maintenance, is required for survival in response to hydroxyurea (HU), which induces DNA replication fork stalling. It is still unclear, however, how the CST complex is involved in the repair of diverse types of DNA damage induced by oxidizing agents such as H2O2. STN1 knockdown (KD) sensitized HeLa cells to high doses of H2O2. While H2O2 induced DNA strand breaks throughout the cell cycle, STN1 KD cells were as resistant as control cells to H2O2 treatment when challenged in the G1 phase of the cell cycle, but they were sensitive when exposed to H2O2 in S/G2/M phase. STN1 KD cells showed a failure of DNA synthesis and RAD51 foci formation upon H2O2 treatment. Chemical inhibition of RAD51 in shSTN1 cells did not exacerbate the sensitivity to H2O2, implying that the CST complex and RAD51 act in the same pathway. Collectively, our results suggest that the CST complex is required for maintaining genomic stability in response to oxidative DNA damage, possibly through RAD51-dependent DNA repair/protection mechanisms.
    MeSH term(s) Humans ; Animals ; Shelterin Complex ; Cell Survival ; HeLa Cells ; Hydrogen Peroxide/pharmacology ; Telomere ; DNA Damage ; Mammals
    Chemical Substances Shelterin Complex ; Hydrogen Peroxide (BBX060AN9V)
    Language English
    Publishing date 2023-08-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0289304
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  2. Book ; Online: Formal Modelling of Safety Architecture for Responsibility-Aware Autonomous Vehicle via Event-B Refinement

    Kobayashi, Tsutomu / Bondu, Martin / Ishikawa, Fuyuki

    2024  

    Abstract: Ensuring the safety of autonomous vehicles (AVs) is the key requisite for their acceptance in society. This complexity is the core challenge in formally proving their safety conditions with AI-based black-box controllers and surrounding objects under ... ...

    Abstract Ensuring the safety of autonomous vehicles (AVs) is the key requisite for their acceptance in society. This complexity is the core challenge in formally proving their safety conditions with AI-based black-box controllers and surrounding objects under various traffic scenarios. This paper describes our strategy and experience in modelling, deriving, and proving the safety conditions of AVs with the Event-B refinement mechanism to reduce complexity. Our case study targets the state-of-the-art model of goal-aware responsibility-sensitive safety to argue over interactions with surrounding vehicles. We also employ the Simplex architecture to involve advanced black-box AI controllers. Our experience has demonstrated that the refinement mechanism can be effectively used to gradually develop the complex system over scenario variations.

    Comment: 18 pages, 10 figures, author version of the manuscript of the same name published in the proceedings of the 25th International Symposium on Formal Methods (FM 2023)
    Keywords Computer Science - Software Engineering
    Subject code 629
    Publishing date 2024-01-09
    Publishing country us
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Book ; Online: SCAPE

    Lim, Soo Ling / Bentley, Peter J / Ishikawa, Fuyuki

    Searching Conceptual Architecture Prompts using Evolution

    2024  

    Abstract: Conceptual architecture involves a highly creative exploration of novel ideas, often taken from other disciplines as architects consider radical new forms, materials, textures and colors for buildings. While today's generative AI systems can produce ... ...

    Abstract Conceptual architecture involves a highly creative exploration of novel ideas, often taken from other disciplines as architects consider radical new forms, materials, textures and colors for buildings. While today's generative AI systems can produce remarkable results, they lack the creativity demonstrated for decades by evolutionary algorithms. SCAPE, our proposed tool, combines evolutionary search with generative AI, enabling users to explore creative and good quality designs inspired by their initial input through a simple point and click interface. SCAPE injects randomness into generative AI, and enables memory, making use of the built-in language skills of GPT-4 to vary prompts via text-based mutation and crossover. We demonstrate that compared to DALL-E 3, SCAPE enables a 67% improvement in image novelty, plus improvements in quality and effectiveness of use; we show that in just 3 iterations SCAPE has a 24% image novelty increase enabling effective exploration, plus optimization of images by users. We use more than 20 independent architects to assess SCAPE, who provide markedly positive feedback.

    Comment: 8 pages
    Keywords Computer Science - Neural and Evolutionary Computing ; Computer Science - Artificial Intelligence ; 68W50 ; 68T07 ; G.1.6 ; I.2.10
    Subject code 720
    Publishing date 2024-01-31
    Publishing country us
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Author Correction: The interferon stimulated gene-encoded protein HELZ2 inhibits human LINE-1 retrotransposition and LINE-1 RNA-mediated type I interferon induction.

    Luqman-Fatah, Ahmad / Watanabe, Yuzo / Uno, Kazuko / Ishikawa, Fuyuki / Moran, John V / Miyoshi, Tomoichiro

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 493

    Language English
    Publishing date 2023-01-30
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-36226-4
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  5. Article ; Online: Author Correction

    Ahmad Luqman-Fatah / Yuzo Watanabe / Kazuko Uno / Fuyuki Ishikawa / John V. Moran / Tomoichiro Miyoshi

    Nature Communications, Vol 14, Iss 1, Pp 1-

    The interferon stimulated gene-encoded protein HELZ2 inhibits human LINE-1 retrotransposition and LINE-1 RNA-mediated type I interferon induction

    2023  Volume 1

    Keywords Science ; Q
    Language English
    Publishing date 2023-01-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Proteostasis failure and cellular senescence in long-term cultured postmitotic rat neurons.

    Ishikawa, Shoma / Ishikawa, Fuyuki

    Aging cell

    2019  Volume 19, Issue 1, Page(s) e13071

    Abstract: Cellular senescence, a stress-induced irreversible cell cycle arrest, has been defined for mitotic cells and is implicated in aging of replicative tissues. Age-related functional decline in the brain is often attributed to a failure of protein ... ...

    Abstract Cellular senescence, a stress-induced irreversible cell cycle arrest, has been defined for mitotic cells and is implicated in aging of replicative tissues. Age-related functional decline in the brain is often attributed to a failure of protein homeostasis (proteostasis), largely in postmitotic neurons, which accordingly is a process distinct by definition from senescence. It is nevertheless possible that proteostasis failure and cellular senescence have overlapping molecular mechanisms. Here, we identify postmitotic cellular senescence as an adaptive stress response to proteostasis failure. Primary rat hippocampal neurons in long-term cultures show molecular changes indicative of both senescence (senescence-associated β-galactosidase, p16, and loss of lamin B1) and proteostasis failure relevant to Alzheimer's disease. In addition, we demonstrate that the senescent neurons exhibit resistance to stress. Importantly, treatment of the cultures with an mTOR antagonist, protein synthesis inhibitor, or chemical compound that reduces the amount of protein aggregates relieved the proteotoxic stresses as well as the appearance of senescence markers. Our data propose mechanistic insights into the pathophysiological brain aging by establishing senescence as a primary cell-autonomous neuroprotective response.
    MeSH term(s) Aging/genetics ; Animals ; Cells, Cultured ; Cellular Senescence ; Humans ; Neurons/metabolism ; Proteostasis/physiology ; Rats
    Language English
    Publishing date 2019-11-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2113083-8
    ISSN 1474-9726 ; 1474-9718
    ISSN (online) 1474-9726
    ISSN 1474-9718
    DOI 10.1111/acel.13071
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    Zs.A 6581: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: DHX36 maintains genomic integrity by unwinding G-quadruplexes.

    Mizumoto, Ayaka / Yokoyama, Yuta / Miyoshi, Tomoichiro / Takikawa, Masahiro / Ishikawa, Fuyuki / Sadaie, Mahito

    Genes to cells : devoted to molecular & cellular mechanisms

    2023  Volume 28, Issue 10, Page(s) 694–708

    Abstract: The guanine-rich stretch of single-stranded DNA (ssDNA) forms a G-quadruplex (G4) in a fraction of genic and intergenic chromosomal regions. The probability of G4 formation increases during events causing ssDNA generation, such as transcription and ... ...

    Abstract The guanine-rich stretch of single-stranded DNA (ssDNA) forms a G-quadruplex (G4) in a fraction of genic and intergenic chromosomal regions. The probability of G4 formation increases during events causing ssDNA generation, such as transcription and replication. In turn, G4 abrogates these events, leading to DNA damage. DHX36 unwinds G4-DNA in vitro and in human cells. However, its spatial correlation with G4-DNA in vivo and its role in genome maintenance remain unclear. Here, we demonstrate a connection between DHX36 and G4-DNA and its implications for genomic integrity. The nuclear localization of DHX36 overlapped with that of G4-DNA, RNA polymerase II, and a splicing-related factor. Depletion of DHX36 resulted in accumulated DNA damage, slower cell growth, and enhanced cell growth inhibition upon treatment with a G4-stabilizing compound; DHX36 expression reversed these defects. In contrast, the reversal upon expression of DHX36 mutants that could not bind G4 was imperfect. Thus, DHX36 may suppress DNA damage by promoting the clearance of G4-DNA for cell growth and survival. Our findings deepen the understanding of G4 resolution in the maintenance of genomic integrity.
    Language English
    Publishing date 2023-08-26
    Publishing country England
    Document type Journal Article
    ZDB-ID 1330000-3
    ISSN 1365-2443 ; 1356-9597
    ISSN (online) 1365-2443
    ISSN 1356-9597
    DOI 10.1111/gtc.13061
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    Zs.A 4539: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
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  8. Article ; Online: The interferon stimulated gene-encoded protein HELZ2 inhibits human LINE-1 retrotransposition and LINE-1 RNA-mediated type I interferon induction.

    Luqman-Fatah, Ahmad / Watanabe, Yuzo / Uno, Kazuko / Ishikawa, Fuyuki / Moran, John V / Miyoshi, Tomoichiro

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 203

    Abstract: Some interferon stimulated genes (ISGs) encode proteins that inhibit LINE-1 (L1) retrotransposition. Here, we use immunoprecipitation followed by liquid chromatography-tandem mass spectrometry to identify proteins that associate with the L1 ORF1-encoded ... ...

    Abstract Some interferon stimulated genes (ISGs) encode proteins that inhibit LINE-1 (L1) retrotransposition. Here, we use immunoprecipitation followed by liquid chromatography-tandem mass spectrometry to identify proteins that associate with the L1 ORF1-encoded protein (ORF1p) in ribonucleoprotein particles. Three ISG proteins that interact with ORF1p inhibit retrotransposition: HECT and RLD domain containing E3 ubiquitin-protein ligase 5 (HERC5); 2'-5'-oligoadenylate synthetase-like (OASL); and helicase with zinc finger 2 (HELZ2). HERC5 destabilizes ORF1p, but does not affect its cellular localization. OASL impairs ORF1p cytoplasmic foci formation. HELZ2 recognizes sequences and/or structures within the L1 5'UTR to reduce L1 RNA, ORF1p, and ORF1p cytoplasmic foci levels. Overexpression of WT or reverse transcriptase-deficient L1s lead to a modest induction of IFN-α expression, which is abrogated upon HELZ2 overexpression. Notably, IFN-α expression is enhanced upon overexpression of an ORF1p RNA binding mutant, suggesting ORF1p binding might protect L1 RNA from "triggering" IFN-α induction. Thus, ISG proteins can inhibit retrotransposition by different mechanisms.
    MeSH term(s) Humans ; Interferon Type I/genetics ; Long Interspersed Nucleotide Elements/genetics ; Proteins/genetics ; RNA/genetics ; RNA Helicases/genetics ; RNA-Directed DNA Polymerase/genetics
    Chemical Substances Interferon Type I ; Proteins ; RNA (63231-63-0) ; RNA Helicases (EC 3.6.4.13) ; RNA-Directed DNA Polymerase (EC 2.7.7.49) ; HELZ2 protein, human (EC 3.6.4.13)
    Language English
    Publishing date 2023-01-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-35757-6
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  9. Article ; Online: Timeless tunes: replicating happy endings.

    Ishikawa, Fuyuki

    Cell cycle (Georgetown, Tex.)

    2012  Volume 11, Issue 16, Page(s) 2977–2978

    MeSH term(s) Cell Cycle Proteins/metabolism ; DNA Replication ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Telomere/metabolism
    Chemical Substances Cell Cycle Proteins ; Intracellular Signaling Peptides and Proteins
    Language English
    Publishing date 2012-08-09
    Publishing country United States
    Document type News ; Comment
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.21530
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5881: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  10. Article ; Online: Portrait of replication stress viewed from telomeres.

    Ishikawa, Fuyuki

    Cancer science

    2013  Volume 104, Issue 7, Page(s) 790–794

    Abstract: Genetic instability is the driving force of the malignant progression of cancer cells. Recently, replication stress has attracted much attention as a source of genetic instability that gives rise to an accumulation of mutations during the lifespan of ... ...

    Abstract Genetic instability is the driving force of the malignant progression of cancer cells. Recently, replication stress has attracted much attention as a source of genetic instability that gives rise to an accumulation of mutations during the lifespan of individuals. However, the molecular details of the process are not fully understood. Here, recent progress in understanding how genetic alterations accumulate at telomeres will be reviewed. In particular, two aspects of telomere replication will be discussed in this context, covering conventional semi-conservative replication, and DNA synthesis by telomerase plus the C-strand fill-in reactions. Although these processes are seemingly telomere-specific, I will emphasize the possibility that the molecular understanding of the telomere events may shed light on genetic instability at other genetic loci in general.
    MeSH term(s) Animals ; DNA Replication/genetics ; DNA, Neoplasm/biosynthesis ; DNA, Neoplasm/genetics ; Genomic Instability ; Humans ; Mutation ; Neoplasms/genetics ; Neoplasms/pathology ; Telomere/genetics
    Chemical Substances DNA, Neoplasm
    Language English
    Publishing date 2013-05-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2115647-5
    ISSN 1349-7006 ; 1347-9032
    ISSN (online) 1349-7006
    ISSN 1347-9032
    DOI 10.1111/cas.12165
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