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  1. Article ; Online: SIRT7 and p53 interaction in embryonic development and tumorigenesis

    Berta N. Vazquez / Irene Fernández-Duran / Yurdiana Hernandez / Shahriar Tarighi / Joshua K. Thackray / Maria Espinosa-Alcantud / Poonam Kumari / Alessandro Ianni / Lionel Cesaire / Thomas Braun / Manel Esteller / Jay Tischfield / Alejandro Vaquero / Lourdes Serrano

    Frontiers in Cell and Developmental Biology, Vol

    2024  Volume 11

    Abstract: p53 is a hallmark tumor suppressor due in part to its role in cell cycle progression, DNA damage repair, and cellular apoptosis; its protein activity interrelates with the Sirtuin family of proteins, major regulators of the cellular response to metabolic, ...

    Abstract p53 is a hallmark tumor suppressor due in part to its role in cell cycle progression, DNA damage repair, and cellular apoptosis; its protein activity interrelates with the Sirtuin family of proteins, major regulators of the cellular response to metabolic, oxidative, and genotoxic stress. In the recent years, mammalian Sirtuin 7 (SIRT7) has emerged as a pivotal regulator of p53, fine-tuning its activity in a context dependent manner. SIRT7 is frequently overexpressed in human cancer, yet its precise role in tumorigenesis and whether it involves p53 regulation is insufficiently understood. Depletion of SIRT7 in mice results in impaired embryo development and premature aging. While p53 activity has been suggested to contribute to tissue specific dysfunction in adult Sirt7−/− mice, whether this also applies during development is currently unknown. By generating SIRT7 and p53 double-knockout mice, here we show that the demise of SIRT7-deficient embryos is not the result of p53 activity. Notably, although SIRT7 is commonly considered an oncogene, SIRT7 haploinsufficiency increases tumorigenesis in p53 knockout mice. Remarkably, in specific human tumors harboring p53 mutation, we identified that SIRT7 low expression correlates with poor patient prognosis. Transcriptomic analysis unveils a previously unrecognized interplay between SIRT7 and p53 in epithelial-to-mesenchymal transition (EMT) and extracellular matrix regulation with major implications for our understanding of embryonic development and tumor progression.
    Keywords p53 ; SIRTUIN ; Sirt7 ; embryonic development ; tumor suppressor ; gene expression ; Biology (General) ; QH301-705.5
    Subject code 572
    Language English
    Publishing date 2024-01-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: A complex interplay between H2A.Z and HP1 isoforms regulates pericentric heterochromatin

    Jessica González / Laia Bosch-Presegué / Anna Marazuela-Duque / Anna Guitart-Solanes / María Espinosa-Alcantud / Agustín F. Fernandez / Jeremy P. Brown / Juan Ausió / Berta N. Vazquez / Prim B. Singh / Mario F. Fraga / Alejandro Vaquero

    Frontiers in Cell and Developmental Biology, Vol

    2023  Volume 11

    Abstract: Pericentric heterochromatin (PCH) plays an essential role in the maintenance of genome integrity and alterations in PCH have been linked to cancer and aging. HP1 α, β, and γ, are hallmarks of constitutive heterochromatin that are thought to promote PCH ... ...

    Abstract Pericentric heterochromatin (PCH) plays an essential role in the maintenance of genome integrity and alterations in PCH have been linked to cancer and aging. HP1 α, β, and γ, are hallmarks of constitutive heterochromatin that are thought to promote PCH structure through binding to heterochromatin-specific histone modifications and interaction with a wide range of factors. Among the less understood components of PCH is the histone H2A variant H2A.Z, whose role in the organization and maintenance of PCH is poorly defined. Here we show that there is a complex interplay between H2A.Z and HP1 isoforms in PCH. While the loss of HP1α results in the accumulation of H2A.Z.1 in PCH, which is associated with a significant decrease in its mobile fraction, H2A.Z.1 binds preferentially to HP1β in these regions. Of note, H2A.Z.1 downregulation results in increased heterochromatinization and instability of PCH, reflected by accumulation of the major epigenetic hallmarks of heterochromatin in these regions and increased frequency of chromosome aberrations related to centromeric/pericentromeric defects. Our studies support a role for H2A.Z in genome stability and unveil a key role of H2A.Z in the regulation of heterochromatin-specific epigenetic modifications through a complex interplay with the HP1 isoforms.
    Keywords HP1α,β,γ ; heterochromatin ; H2A.Z ; epigenetics ; genome stability ; H3K9me3 ; Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2023-11-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: SIRT6-dependent cysteine monoubiquitination in the PRE-SET domain of Suv39h1 regulates the NF-κB pathway

    Irene Santos-Barriopedro / Laia Bosch-Presegué / Anna Marazuela-Duque / Carolina de la Torre / Carlota Colomer / Berta N. Vazquez / Thomas Fuhrmann / Bárbara Martínez-Pastor / Wenfu Lu / Thomas Braun / Eva Bober / Thomas Jenuwein / Lourdes Serrano / Manel Esteller / Zhenbang Chen / Silvia Barceló-Batllori / Raúl Mostoslavsky / Lluis Espinosa / Alejandro Vaquero

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 15

    Abstract: Sirtuins are involved in the regulation of responses to diverse types of cellular stress. Here the authors describe the SirT6-dependent cysteine monoubiquitination of the histone methyltransferase Suv39h1 as part of a regulatory circuit for the NF-κB ... ...

    Abstract Sirtuins are involved in the regulation of responses to diverse types of cellular stress. Here the authors describe the SirT6-dependent cysteine monoubiquitination of the histone methyltransferase Suv39h1 as part of a regulatory circuit for the NF-κB pathway.
    Keywords Science ; Q
    Language English
    Publishing date 2018-01-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: SIRT6-dependent cysteine monoubiquitination in the PRE-SET domain of Suv39h1 regulates the NF-κB pathway

    Irene Santos-Barriopedro / Laia Bosch-Presegué / Anna Marazuela-Duque / Carolina de la Torre / Carlota Colomer / Berta N. Vazquez / Thomas Fuhrmann / Bárbara Martínez-Pastor / Wenfu Lu / Thomas Braun / Eva Bober / Thomas Jenuwein / Lourdes Serrano / Manel Esteller / Zhenbang Chen / Silvia Barceló-Batllori / Raúl Mostoslavsky / Lluis Espinosa / Alejandro Vaquero

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 15

    Abstract: Sirtuins are involved in the regulation of responses to diverse types of cellular stress. Here the authors describe the SirT6-dependent cysteine monoubiquitination of the histone methyltransferase Suv39h1 as part of a regulatory circuit for the NF-κB ... ...

    Abstract Sirtuins are involved in the regulation of responses to diverse types of cellular stress. Here the authors describe the SirT6-dependent cysteine monoubiquitination of the histone methyltransferase Suv39h1 as part of a regulatory circuit for the NF-κB pathway.
    Keywords Science ; Q
    Language English
    Publishing date 2018-01-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: New insights on the transcriptional regulation of CD69 gene through a potent enhancer located in the conserved non-coding sequence 2

    Laguna, Teresa / Ángel L. Corbí / Berta N. Vázquez / Laura Notario / María D. Odero / Miguel G. Fontela / Miren Maicas / Noemí Aguilera-Montilla / Pilar Lauzurica / Raffaella Pippa

    Molecular Immunology. 2015 Aug., v. 66

    2015  

    Abstract: The CD69 type II C-type lectin is one of the earliest indicators of leukocyte activation acting in lymphocyte migration and cytokine secretion. CD69 expression in hematopoietic lineage undergoes rapid changes depending on the cell-lineage, the activation ...

    Abstract The CD69 type II C-type lectin is one of the earliest indicators of leukocyte activation acting in lymphocyte migration and cytokine secretion. CD69 expression in hematopoietic lineage undergoes rapid changes depending on the cell-lineage, the activation state or the localization of the cell where it is expressed, suggesting a complex and tightly controlled regulation. Here we provide new insights on the transcriptional regulation of CD69 gene in mammal species. Through in silico studies, we analyzed several regulatory features of the 4 upstream conserved non-coding sequences (CNS 1–4) previously described, confirming a major function of CNS2 in the transcriptional regulation of CD69. In addition, multiple transcription binding sites are identified in the CNS2 region by DNA cross-species conservation analysis. By functional approaches we defined a core region of 226bp located within CNS2 as the main enhancer element of CD69 transcription in the hematopoietic cells analyzed. By chromatin immunoprecipitation, binding of RUNX1 to the core-CNS2 was shown in a T cell line. In addition, we found an activating but not essential role of RUNX1 in CD69 gene transcription by site-directed mutagenesis and RNA silencing, probably through the interaction with this potent enhancer specifically in the hematopoietic lineage. In summary, in this study we contribute with new evidences to the landscape of the transcriptional regulation of the CD69 gene.
    Keywords binding sites ; chromatin ; cytokines ; DNA ; enhancer elements ; genes ; hematopoietic stem cells ; lectins ; mammals ; precipitin tests ; RNA interference ; secretion ; site-directed mutagenesis ; T-lymphocytes ; transcription (genetics)
    Language English
    Dates of publication 2015-08
    Size p. 171-179.
    Publishing place Elsevier Ltd
    Document type Article
    ZDB-ID 424427-8
    ISSN 1872-9142 ; 0161-5890
    ISSN (online) 1872-9142
    ISSN 0161-5890
    DOI 10.1016/j.molimm.2015.02.031
    Database NAL-Catalogue (AGRICOLA)

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  6. Article ; Online: MiR-93 Controls Adiposity via Inhibition of Sirt7 and Tbx3

    Michele Cioffi / Mireia Vallespinos-Serrano / Sara M. Trabulo / Pablo Jose Fernandez-Marcos / Ashley N. Firment / Berta N. Vazquez / Catarina R. Vieira / Francesca Mulero / Juan A. Camara / Ultan P. Cronin / Manuel Perez / Joaquim Soriano / Beatriz G. Galvez / Alvaro Castells-Garcia / Verena Haage / Deepak Raj / Diego Megias / Stephan Hahn / Lourdes Serrano /
    Anne Moon / Alexandra Aicher / Christopher Heeschen

    Cell Reports, Vol 12, Iss 10, Pp 1594-

    2015  Volume 1605

    Abstract: Conquering obesity has become a major socioeconomic challenge. Here, we show that reduced expression of the miR-25-93-106b cluster, or miR-93 alone, increases fat mass and, subsequently, insulin resistance. Mechanistically, we discovered an intricate ... ...

    Abstract Conquering obesity has become a major socioeconomic challenge. Here, we show that reduced expression of the miR-25-93-106b cluster, or miR-93 alone, increases fat mass and, subsequently, insulin resistance. Mechanistically, we discovered an intricate interplay between enhanced adipocyte precursor turnover and increased adipogenesis. First, miR-93 controls Tbx3, thereby limiting self-renewal in early adipocyte precursors. Second, miR-93 inhibits the metabolic target Sirt7, which we identified as a major driver of in vivo adipogenesis via induction of differentiation and maturation of early adipocyte precursors. Using mouse parabiosis, obesity in mir-25-93-106b–/– mice could be rescued by restoring levels of circulating miRNA and subsequent inhibition of Tbx3 and Sirt7. Downregulation of miR-93 also occurred in obese ob/ob mice, and this phenocopy of mir-25-93-106b–/– was partially reversible with injection of miR-93 mimics. Our data establish miR-93 as a negative regulator of adipogenesis and a potential therapeutic option for obesity and the metabolic syndrome.
    Keywords Biology (General) ; QH301-705.5
    Subject code 500
    Language English
    Publishing date 2015-09-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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