LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Zurück zur letzten Suche Suchhistorie
Erweiterte Suche

Ihre letzten Suchen

  1. AU="Petsalaki, Eleni"
  2. AU="Yu, Weichao"
  3. AU="Mertens, Anne Wiebke"
  4. AU="Roitershtein, Alexander"
  5. AU="Deppen, Stephen"
  6. AU="Goliath, Rene"
  7. AU="Emons, Günter"
  8. AU="Sarah S. Barnett"

Suchergebnis

Treffer 1 - 10 von insgesamt 19

Suchoptionen

  1. Artikel ; Online: Activating the abscission checkpoint: Top2α senses chromatin bridges in cytokinesis: Top2α binds to DNA knots on chromatin bridges to activate the abscission checkpoint in human cells.

    Petsalaki, Eleni / Zachos, George

    BioEssays : news and reviews in molecular, cellular and developmental biology

    2024  Band 46, Heft 5, Seite(n) e2400011

    Abstract: How chromatin bridges are detected by the abscission checkpoint during mammalian cell division is unknown. Here, we discuss recent findings from our lab showing that the DNA topoisomerase IIα (Top2α) enzyme binds to catenated ("knotted") DNA next to the ... ...

    Abstract How chromatin bridges are detected by the abscission checkpoint during mammalian cell division is unknown. Here, we discuss recent findings from our lab showing that the DNA topoisomerase IIα (Top2α) enzyme binds to catenated ("knotted") DNA next to the midbody and forms abortive Top2-DNA cleavage complexes (Top2ccs) on chromatin bridges. Top2ccs are then processed by the proteasome to promote localization of the DNA damage sensor protein Rad17 to Top2-generated double-strand DNA ends on DNA knots. In turn, Rad17 promotes local recruitment of the MRN protein complex and downstream ATM-Chk2-INCENP signaling to delay abscission and prevent chromatin bridge breakage in cytokinesis.
    Mesh-Begriff(e) Humans ; DNA Topoisomerases, Type II/metabolism ; Cytokinesis/physiology ; Chromatin/metabolism ; DNA-Binding Proteins/metabolism ; Poly-ADP-Ribose Binding Proteins/metabolism ; DNA/metabolism ; Signal Transduction
    Chemische Substanzen DNA Topoisomerases, Type II (EC 5.99.1.3) ; Chromatin ; DNA-Binding Proteins ; Poly-ADP-Ribose Binding Proteins ; TOP2A protein, human (EC 5.99.1.3) ; DNA (9007-49-2)
    Sprache Englisch
    Erscheinungsdatum 2024-02-25
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 50140-2
    ISSN 1521-1878 ; 0265-9247
    ISSN (online) 1521-1878
    ISSN 0265-9247
    DOI 10.1002/bies.202400011
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 2024: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  2. Artikel: An ATM-CHK2-INCENP pathway prevents chromatin breakage by regulating the abscission checkpoint.

    Petsalaki, Eleni / Zachos, George

    Molecular & cellular oncology

    2021  Band 8, Heft 2, Seite(n) 1877999

    Abstract: In response to chromatin bridges, the chromosomal passenger complex (CPC) delays completion of cytokinesis (abscission) to prevent chromosome breakage. Here, we discuss recent findings from our lab showing that an ATM-CHK2-INCENP pathway imposes the ... ...

    Abstract In response to chromatin bridges, the chromosomal passenger complex (CPC) delays completion of cytokinesis (abscission) to prevent chromosome breakage. Here, we discuss recent findings from our lab showing that an ATM-CHK2-INCENP pathway imposes the abscission checkpoint in human cells by regulating CPC midbody-localization.
    Sprache Englisch
    Erscheinungsdatum 2021-02-08
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2021.1877999
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  3. Artikel ; Online: The Abscission Checkpoint: A Guardian of Chromosomal Stability.

    Petsalaki, Eleni / Zachos, George

    Cells

    2021  Band 10, Heft 12

    Abstract: The abscission checkpoint contributes to the fidelity of chromosome segregation by delaying completion of cytokinesis (abscission) when there is chromatin lagging in the intercellular bridge between dividing cells. Although additional triggers of an ... ...

    Abstract The abscission checkpoint contributes to the fidelity of chromosome segregation by delaying completion of cytokinesis (abscission) when there is chromatin lagging in the intercellular bridge between dividing cells. Although additional triggers of an abscission checkpoint-delay have been described, including nuclear pore defects, replication stress or high intercellular bridge tension, this review will focus only on chromatin bridges. In the presence of such abnormal chromosomal tethers in mammalian cells, the abscission checkpoint requires proper localization and optimal kinase activity of the Chromosomal Passenger Complex (CPC)-catalytic subunit Aurora B at the midbody and culminates in the inhibition of Endosomal Sorting Complex Required for Transport-III (ESCRT-III) components at the abscission site to delay the final cut. Furthermore, cells with an active checkpoint stabilize the narrow cytoplasmic canal that connects the two daughter cells until the chromatin bridges are resolved. Unsuccessful resolution of chromatin bridges in checkpoint-deficient cells or in cells with unstable intercellular canals can lead to chromatin bridge breakage or tetraploidization by regression of the cleavage furrow. In turn, these outcomes can lead to accumulation of DNA damage, chromothripsis, generation of hypermutation clusters and chromosomal instability, which are associated with cancer formation or progression. Recently, many important questions regarding the mechanisms of the abscission checkpoint have been investigated, such as how the presence of chromatin bridges is signaled to the CPC, how Aurora B localization and kinase activity is regulated in late midbodies, the signaling pathways by which Aurora B implements the abscission delay, and how the actin cytoskeleton is remodeled to stabilize intercellular canals with DNA bridges. Here, we review recent progress toward understanding the mechanisms of the abscission checkpoint and its role in guarding genome integrity at the chromosome level, and consider its potential implications for cancer therapy.
    Mesh-Begriff(e) Animals ; Cell Cycle Checkpoints ; Chromatin/metabolism ; Chromosomal Instability ; Cytokinesis ; Humans ; Models, Biological ; Signal Transduction
    Chemische Substanzen Chromatin
    Sprache Englisch
    Erscheinungsdatum 2021-11-29
    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/cells10123350
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  4. Artikel ; Online: The abscission checkpoint senses chromatin bridges through Top2α recruitment to DNA knots.

    Petsalaki, Eleni / Balafouti, Sofia / Kyriazi, Athina A / Zachos, George

    The Journal of cell biology

    2023  Band 222, Heft 11

    Abstract: In response to chromatin bridges, the abscission checkpoint delays completion of cytokinesis to prevent chromosome breakage or tetraploidization. Here, we show that spontaneous or replication stress-induced chromatin bridges exhibit "knots" of catenated ... ...

    Abstract In response to chromatin bridges, the abscission checkpoint delays completion of cytokinesis to prevent chromosome breakage or tetraploidization. Here, we show that spontaneous or replication stress-induced chromatin bridges exhibit "knots" of catenated and overtwisted DNA next to the midbody. Topoisomerase IIα (Top2α) forms abortive Top2-DNA cleavage complexes (Top2ccs) on DNA knots; furthermore, impaired Top2α-DNA cleavage activity correlates with chromatin bridge breakage in cytokinesis. Proteasomal degradation of Top2ccs is required for Rad17 localization to Top2-generated double-strand DNA ends on DNA knots; in turn, Rad17 promotes local recruitment of the MRN complex and downstream ATM-Chk2-INCENP signaling to delay abscission and prevent chromatin breakage. In contrast, dicentric chromosomes that do not exhibit knotted DNA fail to activate the abscission checkpoint in human cells. These findings are the first to describe a mechanism by which the abscission checkpoint detects chromatin bridges, through generation of abortive Top2ccs on DNA knots, to preserve genome integrity.
    Mesh-Begriff(e) Humans ; Cell Cycle Proteins/genetics ; Cell Nucleus ; Chromatin/genetics ; Chromosome Breakage ; Cytokinesis ; DNA/genetics ; Cell Cycle Checkpoints ; DNA Topoisomerases, Type II/genetics
    Chemische Substanzen Cell Cycle Proteins ; Chromatin ; DNA (9007-49-2) ; Rad17 protein, human ; TOP2A protein, human (EC 5.99.1.3) ; DNA Topoisomerases, Type II (EC 5.99.1.3)
    Sprache Englisch
    Erscheinungsdatum 2023-08-28
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202303123
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Ub I Zs.190: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  5. Artikel ; Online: An ATM-Chk2-INCENP pathway activates the abscission checkpoint.

    Petsalaki, Eleni / Zachos, George

    The Journal of cell biology

    2020  Band 220, Heft 2

    Abstract: During cell division, in response to chromatin bridges, the chromosomal passenger complex (CPC) delays abscission to prevent chromosome breakage or tetraploidization. Here, we show that inhibition of ATM or Chk2 kinases impairs CPC localization to the ... ...

    Abstract During cell division, in response to chromatin bridges, the chromosomal passenger complex (CPC) delays abscission to prevent chromosome breakage or tetraploidization. Here, we show that inhibition of ATM or Chk2 kinases impairs CPC localization to the midbody center, accelerates midbody resolution in normally segregating cells, and correlates with premature abscission and chromatin breakage in cytokinesis with trapped chromatin. In cultured human cells, ATM activates Chk2 at late midbodies. In turn, Chk2 phosphorylates human INCENP-Ser91 to promote INCENP binding to Mklp2 kinesin and CPC localization to the midbody center through Mklp2 association with Cep55. Expression of truncated Mklp2 that does not bind to Cep55 or nonphosphorylatable INCENP-Ser91A impairs CPC midbody localization and accelerates abscission. In contrast, expression of phosphomimetic INCENP-Ser91D or a chimeric INCENP protein that is targeted to the midbody center rescues the abscission delay in Chk2-deficient or ATM-deficient cells. Furthermore, the Mre11-Rad50-Nbs1 complex is required for ATM activation at the midbody in cytokinesis with chromatin bridges. These results identify an ATM-Chk2-INCENP pathway that imposes the abscission checkpoint by regulating CPC midbody localization.
    Mesh-Begriff(e) Ataxia Telangiectasia Mutated Proteins/metabolism ; Aurora Kinase B/metabolism ; Cell Cycle Checkpoints ; Cell Proliferation ; Checkpoint Kinase 2/antagonists & inhibitors ; Checkpoint Kinase 2/metabolism ; Chromatin/metabolism ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosome Segregation ; Cytokinesis ; Green Fluorescent Proteins/metabolism ; HeLa Cells ; Humans ; Kinesin/metabolism ; MRE11 Homologue Protein/metabolism ; Multiprotein Complexes/metabolism ; Mutation/genetics ; Phosphorylation ; Signal Transduction
    Chemische Substanzen Chromatin ; Chromosomal Proteins, Non-Histone ; INCENP protein, human ; KIF20A protein, human ; MRE11 protein, human ; Multiprotein Complexes ; Green Fluorescent Proteins (147336-22-9) ; Checkpoint Kinase 2 (EC 2.7.1.11) ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Aurora Kinase B (EC 2.7.11.1) ; CHEK2 protein, human (EC 2.7.11.1) ; MRE11 Homologue Protein (EC 3.1.-) ; Kinesin (EC 3.6.4.4)
    Sprache Englisch
    Erscheinungsdatum 2020-12-18
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202008029
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Ub I Zs.190: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  6. Artikel ; Online: DNA damage response proteins regulating mitotic cell division: double agents preserving genome stability.

    Petsalaki, Eleni / Zachos, George

    The FEBS journal

    2020  Band 287, Heft 9, Seite(n) 1700–1721

    Abstract: The DNA damage response recognizes DNA lesions and coordinates a cell cycle arrest with the repair of the damaged DNA, or removal of the affected cells to prevent the passage of genetic alterations to the next generation. The mitotic cell division, on ... ...

    Abstract The DNA damage response recognizes DNA lesions and coordinates a cell cycle arrest with the repair of the damaged DNA, or removal of the affected cells to prevent the passage of genetic alterations to the next generation. The mitotic cell division, on the other hand, is a series of processes that aims to accurately segregate the genomic material from the maternal to the two daughter cells. Despite their great importance in safeguarding genomic integrity, the DNA damage response and the mitotic cell division were long viewed as unrelated processes, mainly because animal cells that are irradiated during mitosis continue cell division without repairing the broken chromosomes. However, recent studies have demonstrated that DNA damage proteins play an important role in mitotic cell division. This is performed through regulation of the onset of mitosis, mitotic spindle formation, correction of misattached kinetochore-microtubules, spindle checkpoint signaling, or completion of cytokinesis (abscission), in the absence of DNA damage. In this review, we summarize the roles of DNA damage proteins in unperturbed mitosis, analyze the molecular mechanisms involved, and discuss the potential implications of these findings in cancer therapy.
    Mesh-Begriff(e) Animals ; Cell Cycle Proteins/metabolism ; Cell Division ; DNA Damage ; Genomic Instability ; Humans ; Mitosis/genetics
    Chemische Substanzen Cell Cycle Proteins
    Sprache Englisch
    Erscheinungsdatum 2020-02-18
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.15240
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 260: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  7. Artikel: DNA damage response proteins regulating mitotic cell division: double agents preserving genome stability

    Petsalaki, Eleni / Zachos, George

    FEBS journal. 2020 May, v. 287, no. 9

    2020  

    Abstract: The DNA damage response recognizes DNA lesions and coordinates a cell cycle arrest with the repair of the damaged DNA, or removal of the affected cells to prevent the passage of genetic alterations to the next generation. The mitotic cell division, on ... ...

    Abstract The DNA damage response recognizes DNA lesions and coordinates a cell cycle arrest with the repair of the damaged DNA, or removal of the affected cells to prevent the passage of genetic alterations to the next generation. The mitotic cell division, on the other hand, is a series of processes that aims to accurately segregate the genomic material from the maternal to the two daughter cells. Despite their great importance in safeguarding genomic integrity, the DNA damage response and the mitotic cell division were long viewed as unrelated processes, mainly because animal cells that are irradiated during mitosis continue cell division without repairing the broken chromosomes. However, recent studies have demonstrated that DNA damage proteins play an important role in mitotic cell division. This is performed through regulation of the onset of mitosis, mitotic spindle formation, correction of misattached kinetochore–microtubules, spindle checkpoint signaling, or completion of cytokinesis (abscission), in the absence of DNA damage. In this review, we summarize the roles of DNA damage proteins in unperturbed mitosis, analyze the molecular mechanisms involved, and discuss the potential implications of these findings in cancer therapy.
    Schlagwörter DNA ; DNA damage ; abscission ; cancer therapy ; cell cycle checkpoints ; cytokinesis ; genome ; genomics ; mitosis ; mitotic spindle apparatus
    Sprache Englisch
    Erscheinungsverlauf 2020-05
    Umfang p. 1700-1721.
    Erscheinungsort John Wiley & Sons, Ltd
    Dokumenttyp Artikel
    Anmerkung NAL-AP-2-clean ; REVIEW
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.15240
    Datenquelle NAL Katalog (AGRICOLA)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Bonn

    Z 2006/704: Hefte anzeigen

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  8. Artikel ; Online: Building bridges between chromosomes: novel insights into the abscission checkpoint.

    Petsalaki, Eleni / Zachos, George

    Cellular and molecular life sciences : CMLS

    2019  Band 76, Heft 21, Seite(n) 4291–4307

    Abstract: In the presence of chromatin bridges, mammalian cells delay completion of cytokinesis (abscission) to prevent chromatin breakage or tetraploidization by regression of the cleavage furrow. This abscission delay is called "the abscission checkpoint" and is ...

    Abstract In the presence of chromatin bridges, mammalian cells delay completion of cytokinesis (abscission) to prevent chromatin breakage or tetraploidization by regression of the cleavage furrow. This abscission delay is called "the abscission checkpoint" and is dependent on Aurora B kinase. Furthermore, cells stabilize the narrow cytoplasmic canal between the two daughter cells until the DNA bridges are resolved. Impaired abscission checkpoint signaling or unstable intercellular canals can lead to accumulation of DNA damage, aneuploidy, or generation of polyploid cells which are associated with tumourigenesis. However, the molecular mechanisms involved have only recently started to emerge. In this review, we focus on the molecular pathways of the abscission checkpoint and describe newly identified triggers, Aurora B-regulators and effector proteins in abscission checkpoint signaling. We also describe mechanisms that control intercellular bridge stabilization, DNA bridge resolution, or abscission checkpoint silencing upon satisfaction, and discuss how abscission checkpoint proteins can be targeted to potentially improve cancer therapy.
    Mesh-Begriff(e) Animals ; Aurora Kinase B/metabolism ; Aurora Kinase B/physiology ; Chromatin/metabolism ; Chromosomes/metabolism ; Cytokinesis/physiology ; Genes, cdc/physiology ; Humans ; Signal Transduction
    Chemische Substanzen Chromatin ; AURKB protein, human (EC 2.7.11.1) ; Aurora Kinase B (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2019-07-13
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-019-03224-z
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 195: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  9. Artikel: Building bridges between chromosomes: novel insights into the abscission checkpoint

    Petsalaki, Eleni / Zachos, George

    Cellular and molecular life sciences. 2019 Nov., v. 76, no. 21

    2019  

    Abstract: In the presence of chromatin bridges, mammalian cells delay completion of cytokinesis (abscission) to prevent chromatin breakage or tetraploidization by regression of the cleavage furrow. This abscission delay is called “the abscission checkpoint” and is ...

    Abstract In the presence of chromatin bridges, mammalian cells delay completion of cytokinesis (abscission) to prevent chromatin breakage or tetraploidization by regression of the cleavage furrow. This abscission delay is called “the abscission checkpoint” and is dependent on Aurora B kinase. Furthermore, cells stabilize the narrow cytoplasmic canal between the two daughter cells until the DNA bridges are resolved. Impaired abscission checkpoint signaling or unstable intercellular canals can lead to accumulation of DNA damage, aneuploidy, or generation of polyploid cells which are associated with tumourigenesis. However, the molecular mechanisms involved have only recently started to emerge. In this review, we focus on the molecular pathways of the abscission checkpoint and describe newly identified triggers, Aurora B-regulators and effector proteins in abscission checkpoint signaling. We also describe mechanisms that control intercellular bridge stabilization, DNA bridge resolution, or abscission checkpoint silencing upon satisfaction, and discuss how abscission checkpoint proteins can be targeted to potentially improve cancer therapy.
    Schlagwörter abscission ; aneuploidy ; cancer therapy ; carcinogenesis ; chromatin ; cytokinesis ; DNA ; DNA damage ; IKappaB kinase ; mammals ; neoplasms ; non-specific serine/threonine protein kinase ; polyploidy
    Sprache Englisch
    Erscheinungsverlauf 2019-11
    Umfang p. 4291-4307.
    Erscheinungsort Springer International Publishing
    Dokumenttyp Artikel
    Anmerkung Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-019-03224-z
    Datenquelle NAL Katalog (AGRICOLA)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Bonn

    Z 4' 47/14: Hefte anzeigen

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  10. Artikel ; Online: Novel ESCRT functions at kinetochores.

    Petsalaki, Eleni / Zachos, George

    Aging

    2018  Band 10, Heft 3, Seite(n) 299–300

    Mesh-Begriff(e) Cell Cycle Checkpoints/physiology ; Endosomal Sorting Complexes Required for Transport/genetics ; Endosomal Sorting Complexes Required for Transport/metabolism ; Gene Expression Regulation/physiology ; Humans ; Kinetochores/physiology
    Chemische Substanzen CHMP4C protein, human ; Endosomal Sorting Complexes Required for Transport
    Sprache Englisch
    Erscheinungsdatum 2018-03-21
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 1945-4589
    ISSN (online) 1945-4589
    DOI 10.18632/aging.101399
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

Zum Seitenanfang