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  1. Article ; Online: Keep quiet: the HUSH complex in transcriptional silencing and disease.

    Müller, Iris / Helin, Kristian

    Nature structural & molecular biology

    2024  Volume 31, Issue 1, Page(s) 11–22

    Abstract: The human silencing hub (HUSH) complex is an epigenetic repressor complex whose role has emerged as an important guardian of genome integrity. It protects the genome from exogenous DNA invasion and regulates endogenous retroelements by recruiting histone ...

    Abstract The human silencing hub (HUSH) complex is an epigenetic repressor complex whose role has emerged as an important guardian of genome integrity. It protects the genome from exogenous DNA invasion and regulates endogenous retroelements by recruiting histone methyltransferases catalyzing histone 3 lysine 9 trimethylation (H3K9me3) and additional proteins involved in chromatin compaction. In particular, its regulation of transcriptionally active LINE1 retroelements, by binding to and neutralizing LINE1 transcripts, has been well characterized. HUSH is required for mouse embryogenesis and is associated with disease, in particular cancer. Here we provide insights into the structural and biochemical features of the HUSH complex. Furthermore, we discuss the molecular mechanisms by which the HUSH complex is recruited to specific genomic regions and how it silences transcription. Finally, we discuss the role of HUSH complex members in mammalian development, antiretroviral immunity, and diseases such as cancer.
    MeSH term(s) Humans ; Animals ; Mice ; Histones/genetics ; Histones/metabolism ; Nuclear Proteins/metabolism ; Gene Silencing ; Retroelements ; Neoplasms/genetics ; Mammals/genetics
    Chemical Substances Histones ; Nuclear Proteins ; Retroelements
    Language English
    Publishing date 2024-01-12
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2126708-X
    ISSN 1545-9985 ; 1545-9993
    ISSN (online) 1545-9985
    ISSN 1545-9993
    DOI 10.1038/s41594-023-01173-7
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  2. Article ; Online: EZH2i unlocks PDAC immune surveillance.

    Damhofer, Helene / Helin, Kristian

    Nature cancer

    2023  Volume 4, Issue 6, Page(s) 781–783

    MeSH term(s) Humans ; Pancreatic Neoplasms ; Carcinoma, Pancreatic Ductal
    Language English
    Publishing date 2023-06-27
    Publishing country England
    Document type Journal Article ; Comment
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-023-00562-7
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  3. Article ; Online: Catching active enhancers via H2B N-terminal acetylation.

    Huang, Chang / Helin, Kristian

    Nature genetics

    2023  Volume 55, Issue 4, Page(s) 525–526

    MeSH term(s) Acetylation ; Histones/genetics ; Histones/metabolism ; Chromatin ; Regulatory Sequences, Nucleic Acid
    Chemical Substances Histones ; Chromatin
    Language English
    Publishing date 2023-04-07
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/s41588-023-01347-5
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  4. Article ; Online: ChIP-Sequencing of TET Proteins.

    Rasmussen, Kasper D / Helin, Kristian

    Methods in molecular biology (Clifton, N.J.)

    2021  Volume 2272, Page(s) 251–262

    Abstract: TET proteins are methylcytosine dioxygenases that interact directly with chromatin to shape the DNA methylation landscape. To increase the understanding of TET protein function in a specific cellular context, it is important to be able to map the ... ...

    Abstract TET proteins are methylcytosine dioxygenases that interact directly with chromatin to shape the DNA methylation landscape. To increase the understanding of TET protein function in a specific cellular context, it is important to be able to map the interactions between TET proteins and DNA. This ChIP-seq protocol details our procedure to analyze TET2 bound DNA in disuccinimidyl glutarate (DSG) and formaldehyde-crosslinked chromatin but can also be adapted to study other TET enzymes.
    MeSH term(s) Chromatin Immunoprecipitation Sequencing/methods ; DNA Methylation ; Humans ; Mixed Function Oxygenases/classification ; Mixed Function Oxygenases/genetics ; Mixed Function Oxygenases/metabolism ; Proto-Oncogene Proteins/classification ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Sequence Analysis, DNA/methods
    Chemical Substances Proto-Oncogene Proteins ; Mixed Function Oxygenases (EC 1.-) ; TET1 protein, human (EC 1.-)
    Language English
    Publishing date 2021-05-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-1294-1_15
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  5. Article ; Online: Author Correction: EZH2 is downstream of the pRB-E2F pathway, essential for proliferation and amplified in cancer.

    Bracken, Adrian P / Pasini, Diego / Capra, Maria / Prosperini, Elena / Colli, Elena / Helin, Kristian

    The EMBO journal

    2024  Volume 43, Issue 5, Page(s) 886

    Language English
    Publishing date 2024-02-12
    Publishing country England
    Document type Published Erratum
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.1038/s44318-024-00033-4
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  6. Article ; Online: RIO-kinase 2 is essential for hematopoiesis.

    Messling, Jan-Erik / Peña-Rømer, Isabel / Moroni, Ann Sophie / Bruestl, Sarah / Helin, Kristian

    PloS one

    2024  Volume 19, Issue 4, Page(s) e0300623

    Abstract: Regulation of protein synthesis is a key factor in hematopoietic stem cell maintenance and differentiation. Rio-kinase 2 (RIOK2) is a ribosome biogenesis factor that has recently been described an important regulator of human blood cell development. ... ...

    Abstract Regulation of protein synthesis is a key factor in hematopoietic stem cell maintenance and differentiation. Rio-kinase 2 (RIOK2) is a ribosome biogenesis factor that has recently been described an important regulator of human blood cell development. Additionally, we have previously identified RIOK2 as a regulator of protein synthesis and a potential target for the treatment of acute myeloid leukemia (AML). However, its functional relevance in several organ systems, including normal hematopoiesis, is not well understood. Here, we investigate the consequences of RIOK2 loss on normal hematopoiesis using two different conditional knockout mouse models. Using competitive and non-competitive bone marrow transplantations, we demonstrate that RIOK2 is essential for the differentiation of hematopoietic stem and progenitor cells (HSPCs) as well as for the maintenance of fully differentiated blood cells in vivo as well as in vitro. Loss of RIOK2 leads to rapid death in full-body knockout mice as well as mice with RIOK2 loss specific to the hematopoietic system. Taken together, our results indicate that regulation of protein synthesis and ribosome biogenesis by RIOK2 is essential for the function of the hematopoietic system.
    MeSH term(s) Animals ; Humans ; Mice ; Bone Marrow Transplantation ; Cell Differentiation/physiology ; Hematopoiesis/genetics ; Hematopoietic Stem Cells/metabolism ; Leukemia, Myeloid, Acute/metabolism ; Mice, Knockout
    Chemical Substances Rio-kinase 2, mouse
    Language English
    Publishing date 2024-04-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0300623
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  7. Article ; Online: Generation of locus-specific degradable tag knock-ins in mouse and human cell lines.

    Damhofer, Helene / Radzisheuskaya, Aliaksandra / Helin, Kristian

    STAR protocols

    2021  Volume 2, Issue 2, Page(s) 100575

    Abstract: Protein degradation technologies represent a powerful functional genomics tool, allowing fast and controllable target protein depletion. Establishing these systems requires a knock-in of the degradation tag into both endogenous target gene alleles. Here, ...

    Abstract Protein degradation technologies represent a powerful functional genomics tool, allowing fast and controllable target protein depletion. Establishing these systems requires a knock-in of the degradation tag into both endogenous target gene alleles. Here, we provide a step-by-step protocol for the efficient generation of biallelic degradation tag knock-ins in mouse and human cell lines using CRISPR-Cas9. We use knockin of an endogenous
    MeSH term(s) Animals ; Cell Line ; Chromosome Mapping ; Gene Knock-In Techniques ; Genetic Vectors ; Humans ; Mice ; Mouse Embryonic Stem Cells/metabolism ; Plasmids
    Language English
    Publishing date 2021-06-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2021.100575
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  8. Article ; Online: Oncohistones: drivers of pediatric cancers.

    Mohammad, Faizaan / Helin, Kristian

    Genes & development

    2017  Volume 31, Issue 23-24, Page(s) 2313–2324

    Abstract: One of the most striking results in the area of chromatin and cancer in recent years has been the identification of recurrent mutations in histone genes in pediatric cancers. These mutations occur at high frequency and lead to the expression of mutant ... ...

    Abstract One of the most striking results in the area of chromatin and cancer in recent years has been the identification of recurrent mutations in histone genes in pediatric cancers. These mutations occur at high frequency and lead to the expression of mutant histones that exhibit oncogenic features. Thus, they are termed oncohistones. Thus far, mutations have been found in the genes encoding histone H3 and its variants. The expression of the oncohistones affects the global chromatin landscape through mechanisms that have just begun to be unraveled. In this review, we provide an overview of histone mutations that have been identified and discuss the possible mechanisms by which they contribute to tumor development. We further discuss the targeted therapies that have been proposed to treat cancers expressing oncohistones.
    MeSH term(s) Carcinogenesis/genetics ; Chondroblastoma/genetics ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic/genetics ; Genetic Therapy ; Histones/genetics ; Humans ; Mutation ; Neoplasms/genetics ; Neoplasms/therapy
    Chemical Substances Histones
    Language English
    Publishing date 2017-12-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.309013.117
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  9. Article ; Online: Author Correction: H3K4me3 regulates RNA polymerase II promoter-proximal pause-release.

    Wang, Hua / Fan, Zheng / Shliaha, Pavel V / Miele, Matthew / Hendrickson, Ronald C / Jiang, Xuejun / Helin, Kristian

    Nature

    2023  Volume 623, Issue 7987, Page(s) E8

    Language English
    Publishing date 2023-11-16
    Publishing country England
    Document type Published Erratum
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-023-06778-y
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  10. Article ; Online: H3K4me3 regulates RNA polymerase II promoter-proximal pause-release.

    Wang, Hua / Fan, Zheng / Shliaha, Pavel V / Miele, Matthew / Hendrickson, Ronald C / Jiang, Xuejun / Helin, Kristian

    Nature

    2023  Volume 615, Issue 7951, Page(s) 339–348

    Abstract: Trimethylation of histone H3 lysine 4 (H3K4me3) is associated with transcriptional start sites and has been proposed to regulate transcription ... ...

    Abstract Trimethylation of histone H3 lysine 4 (H3K4me3) is associated with transcriptional start sites and has been proposed to regulate transcription initiation
    MeSH term(s) Animals ; Mice ; Gene Expression Regulation ; Histone Demethylases/metabolism ; Histones/chemistry ; Histones/metabolism ; Methylation ; Mouse Embryonic Stem Cells/metabolism ; Promoter Regions, Genetic/genetics ; RNA Polymerase II/metabolism ; Transcription Elongation, Genetic ; Transcription Termination, Genetic
    Chemical Substances Histone Demethylases (EC 1.14.11.-) ; histone H3 trimethyl Lys4 ; Histones ; RNA Polymerase II (EC 2.7.7.-) ; Ints11 protein, mouse (EC 3.1.27.-)
    Language English
    Publishing date 2023-03-01
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-023-05780-8
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