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  • 1
    Online Resource
    Online Resource
    DNA Damage Mediated S and G2 Checkpoints in Human Embryonal Carcinoma Cells
    Oxford University Press (OUP) ; 2009
    In:  Stem Cells Vol. 27, No. 3 ( 2009-03-01), p. 568-576
    Details
    In: Stem Cells, Oxford University Press (OUP), Vol. 27, No. 3 ( 2009-03-01), p. 568-576
    Abstract: For mouse embryonic stem (ES) cells, the importance of the S and G2 cell cycle checkpoints for genomic integrity is increased by the absence of the G1 checkpoint. We have investigated ionizing radiation (IR)-mediated cell cycle checkpoints in undifferentiated and retinoic acid-differentiated human embryonal carcinoma (EC) cells. Like mouse ES cells, human EC cells did not undergo G1 arrest after IR but displayed a prominent S-phase delay followed by a G2-phase delay. In contrast, although differentiated EC cells also failed to arrest at G1-phase after IR, they quickly exited S-phase and arrested in G2-phase. In differentiated EC cells, the G2-M-phase cyclin B1/CDC2 complex was upregulated after IR, but the G1-S-phase cyclin E and the cyclin E/CDK2 complex were expressed at constitutively low levels, which could be an important factor distinguishing DNA damage responses between undifferentiated and differentiated EC cells. S-phase arrest and expression of p21 could be inhibited by 7-hydroxystaurosporine, suggesting that the ataxia-telangiectasia and Rad-3-related-checkpoint kinase 1 (ATR-CHK1), and p21 pathways might play a role in the IR-mediated S-phase checkpoint in EC cells. IR-mediated phosphorylation of ataxia-telangiectasia mutated, (CHK1), and checkpoint kinase 2 were distinctly higher in undifferentiated EC cells compared with differentiated EC cells. Combined with the prominent S and G2 checkpoints and a more efficient DNA damage repair system, these mechanisms operate together in the maintenance of genome stability for EC cells.
    Type of Medium: Online Resource
    ISSN: 1066-5099 , 1549-4918
    URL: Article
    DOI: 10.1634/stemcells.2008-0690
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2009
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  • 2
    Online Resource
    Online Resource
    Label-free enumeration of colorectal cancer cells from lymphocytes performed at a high cell-loading density by using interdigitated ring-array microelectrodes
    Elsevier BV ; 2014
    In:  Biosensors and Bioelectronics Vol. 61 ( 2014-11), p. 434-442
    Details
    In: Biosensors and Bioelectronics, Elsevier BV, Vol. 61 ( 2014-11), p. 434-442
    Type of Medium: Online Resource
    ISSN: 0956-5663
    URL: Article
    DOI: 10.1016/j.bios.2014.05.054
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 1496379-6
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  • 3
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    Online Resource
    Genome reduplication: Redeployment of cyclin-CDK complexes and spontaneous oscillation of APC/C
    Informa UK Limited ; 2010
    In:  Cell Cycle Vol. 9, No. 3 ( 2010-02), p. 431-432
    Details
    In: Cell Cycle, Informa UK Limited, Vol. 9, No. 3 ( 2010-02), p. 431-432
    Type of Medium: Online Resource
    ISSN: 1538-4101 , 1551-4005
    URL: Article
    DOI: 10.4161/cc.9.3.10734
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2010
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  • 4
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    Cyclin-Dependent Kinases and S Phase Control in Mammalian Cells
    Informa UK Limited ; 2003
    In:  Cell Cycle Vol. 2, No. 4 ( 2003-07), p. 315-323
    Details
    In: Cell Cycle, Informa UK Limited, Vol. 2, No. 4 ( 2003-07), p. 315-323
    Type of Medium: Online Resource
    ISSN: 1538-4101 , 1551-4005
    URL: Article
    DOI: 10.4161/cc.2.4.468
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2003
    detail.hit.zdb_id: 2102687-7
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  • 5
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    TRIP13 Functions in the Establishment of the Spindle Assembly Checkpoint by Replenishing O-MAD2
    Elsevier BV ; 2018
    In:  Cell Reports Vol. 22, No. 6 ( 2018-02), p. 1439-1450
    Details
    In: Cell Reports, Elsevier BV, Vol. 22, No. 6 ( 2018-02), p. 1439-1450
    Type of Medium: Online Resource
    ISSN: 2211-1247
    URL: Article
    DOI: 10.1016/j.celrep.2018.01.027
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
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  • 6
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    Timeless Interacts with PARP-1 to Promote Homologous Recombination Repair
    Elsevier BV ; 2015
    In:  Molecular Cell Vol. 60, No. 1 ( 2015-10), p. 163-176
    Details
    In: Molecular Cell, Elsevier BV, Vol. 60, No. 1 ( 2015-10), p. 163-176
    Type of Medium: Online Resource
    ISSN: 1097-2765
    URL: Article
    DOI: 10.1016/j.molcel.2015.07.031
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2015
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  • 7
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    Activated oncogenes promote and cooperate with chromosomal instability for neoplastic transformation
    Cold Spring Harbor Laboratory ; 2004
    In:  Genes & Development Vol. 18, No. 11 ( 2004-06-01), p. 1317-1330
    Details
    In: Genes & Development, Cold Spring Harbor Laboratory, Vol. 18, No. 11 ( 2004-06-01), p. 1317-1330
    Abstract: Most cancer cells are aneuploid. The chromosomal instability hypothesis contends that aneuploidy is the catalyst for transformation, whereas the gene mutation hypothesis asserts that cancer is driven by mutations to proto-oncogenes and tumor-suppressor genes, with the aneuploidy a side effect of tumorigenesis. Because genotoxic stress induced by “culture shock” can obscure the transforming potential of exogenous genes, we cultured wild-type and p53 -/- mouse embryo fibroblasts in a more physiological (serum-free) environment. Under these conditions, the cells were immortal and, more importantly, chromosomally stable. Expression of oncogenic H-RasV12 did not induce senescence, but sensitized these cells to p53-dependent apoptosis. In addition, H-RasV12 induced chromosomal instability, as well as accumulation and phosphorylation of p53. Significantly, whereas cells grown under standard conditions could be transformed by coexpression of H-RasV12 and E1A, the chromosomally stable cells were refractory to transformation, as measured by anchorage-independent growth and tumor formation in nude mice. These oncogenes required a third genetic alteration that abolished the p53 pathway to create a permissive environment that promotes rapid chromosomal instability and transformation. Oncogene-induced chromosomal instability and transformation was attenuated by antioxidants. These data indicate that chromosomal instability could be a catalyst for oncogenic transformation, and bring together aspects of the chromosomal instability hypothesis and the gene mutation hypothesis for tumorigenesis.
    Type of Medium: Online Resource
    ISSN: 0890-9369 , 1549-5477
    URL: Article
    DOI: 10.1101/gad.1165204
    RVK:
    WA 15000
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2004
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  • 8
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    Dovitinib induces mitotic defects and activates the G 2 DNA damage checkpoint
    Wiley ; 2014
    In:  Journal of Cellular and Molecular Medicine Vol. 18, No. 1 ( 2014-01), p. 143-155
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 18, No. 1 ( 2014-01), p. 143-155
    Abstract: D ovitinib ( TKI 258; formerly CHIR ‐258) is an orally bioavailable inhibitor of multiple receptor tyrosine kinases. Interestingly, D ovitinib triggered a G 2 /M arrest in cancer cell lines from diverse origins including HeLa, nasopharyngeal carcinoma, and hepatocellular carcinoma. Single‐cell analysis revealed that D ovitinib promoted a delay in mitotic exit in a subset of cells, causing the cells to undergo mitotic slippage. Higher concentrations of D ovitinib induced a G 2 arrest similar to the G 2 DNA damage checkpoint. In support of this, DNA damage was triggered by D ovitinib as revealed by γ‐H2 AX and comet assays. The mitotic kinase CDK 1 was found to be inactivated by phosphorylation in the presence of D ovitinib. Furthermore, the G 2 arrest could be overcome by abrogation of the G 2 DNA damage checkpoint using small molecule inhibitors of CHK 1 and WEE 1. Finally, D ovitinib‐mediated G 2 cell cycle arrest and subsequent cell death could be promoted after DNA damage repair was disrupted by inhibitors of poly( ADP ‐ribose) polymerases. These results are consistent with the recent finding that D ovitinib can also target topoisomerases. Collectively, these results suggest additional directions for use of D ovitinib, in particular with agents that target the DNA damage checkpoint.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.2013.18.issue-1
    DOI: 10.1111/jcmm.12176
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 2076114-4
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  • 9
    Online Resource
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    MDM2 and MDMX can interact differently with ARF and members of the p53 family
    Wiley ; 2001
    In:  FEBS Letters Vol. 490, No. 3 ( 2001-02-16), p. 202-208
    Details
    In: FEBS Letters, Wiley, Vol. 490, No. 3 ( 2001-02-16), p. 202-208
    Abstract: Members of the p53 family of transcription factors have essential roles in tumor suppression and in development. MDM2 is an essential regulator of p53 that can inhibit the transcriptional activity of p53, shuttle p53 out of the nucleus, and target p53 for ubiquitination‐mediated degradation. Little is known about the interaction and selectivity of different members of the p53 family (p53, p63, and p73) and the MDM2 family (MDM2 and MDMX). Here we show that the transcriptional activities of p53 and p73, but not that of p63, were inhibited by both MDM2 and MDMX. Consistent with these, we found that MDMX can physically interact with p53 and p73, but not with p63. Moreover, ectopically expressed MDM2 and MDMX could induce alterations in the subcellular localization of p73, but did not affect the subcellular localization of p53 and p63. Finally, we demonstrate that while ARF can interact with MDM2 and inhibit the regulation of p53 by MDM2, no interaction was found between ARF and MDMX. These data reveal that significant differences and selectivity exist between the regulation of different members of the p53 family by MDM2 and MDMX.
    Type of Medium: Online Resource
    ISSN: 0014-5793 , 1873-3468
    URL: Article
    DOI: 10.1016/S0014-5793(01)02124-X
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2001
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  • 10
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    G1 versus G2 cell cycle arrest after adriamycin‐induced damage in mouse Swiss3T3 cells
    Wiley ; 1999
    In:  FEBS Letters Vol. 461, No. 3 ( 1999-11-19), p. 299-305
    Details
    In: FEBS Letters, Wiley, Vol. 461, No. 3 ( 1999-11-19), p. 299-305
    Abstract: Cell cycle arrest after different types of DNA damage can occur in either G1 phase or G2 phase of the cell cycle, involving the distinct mechanisms of p53/p21 Cip1/Waf1 induction, and phosphorylation of Cdc2, respectively. Treatment of asynchronously growing Swiss3T3 cells with the chemotherapeutic drug adriamycin induced a predominantly G2 cell cycle arrest. Here we investigate why Swiss3T3 cells were arrested in G2 phase and not in G1 phase after adriamycin‐induced damage. We show that adriamycin was capable of inducing a G1 cell cycle arrest, both during the G0‐G1 transition and during the G1 phase of the normal cell cycle. In G0 cells, adriamycin induced a prolonged cell cycle arrest. However, adriamycin caused only a transient cell cycle delay when added to cells at later time points during G0‐G1 transition or at the G1 phase of normal cell cycle. The G1 arrest correlated with the induction of p53 and p21 Cip1/Waf1 , and the exit from the arrest correlated with the decline of their expression. In contrast to the G1 arrest, adriamycin‐induced G2 arrest was relatively tight and correlated with the Thr‐14/Tyr‐15 phosphorylation of cyclin B‐Cdc2 complexes. The relative stringency of the G1 versus G2 cell cycle arrest may explain the predominance of G2 arrest after adriamycin treatment in mammalian cells.
    Type of Medium: Online Resource
    ISSN: 0014-5793 , 1873-3468
    URL: Article
    DOI: 10.1016/S0014-5793(99)01481-7
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 1999
    detail.hit.zdb_id: 1460391-3
    SSG: 12
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