Literature DB >> 9845341

Cell cycle arrest following exposure of EBV-immortalised B-cells to gamma irradiation correlates with inhibition of cdk2 activity.

E J Cannell1, P J Farrell, A J Sinclair.   

Abstract

The exposure of Epstein-Barr virus immortalised B cells (LCLs) to the genotoxic effects of gamma irradiation causes a decreased proliferation of the cells. The early events in this process have been investigated here. The induction of p53 expression correlates with a cell cycle arrest in the G1 and G2/M phases of the cell cycle within 24 h of exposure. The molecular mechanism governing the decreased proliferation appears to involve the induction of the cyclin dependent kinase (cdk) inhibitor p21CIP1 and its functional association with cdk2.

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Year:  1998        PMID: 9845341     DOI: 10.1016/s0014-5793(98)01391-x

Source DB:  PubMed          Journal:  FEBS Lett        ISSN: 0014-5793            Impact factor:   4.124


  3 in total

1.  Epstein-Barr virus selectively deregulates DNA damage responses in normal B cells but has no detectable effect on regulation of the tumor suppressor p53.

Authors:  Jenny O'Nions; Abigail Turner; Richard Craig; Martin J Allday
Journal:  J Virol       Date:  2006-09-20       Impact factor: 5.103

2.  Epstein-barr virus-induced resistance to drugs that activate the mitotic spindle assembly checkpoint in Burkitt's lymphoma cells.

Authors:  Maria Leao; Emma Anderton; Mark Wade; Kiran Meekings; Martin J Allday
Journal:  J Virol       Date:  2006-10-11       Impact factor: 5.103

3.  Upregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells.

Authors:  Sandra N Schlick; C David Wood; Andrea Gunnell; Helen M Webb; Sarika Khasnis; Aloys Schepers; Michelle J West
Journal:  PLoS One       Date:  2011-12-06       Impact factor: 3.240

  3 in total

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