Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
In response to DNA damage, cells need robust repair mechanisms to complete the cell cycle successfully. Severe forms of DNA damage are repaired by homologous recombination (HR), in which the XRCC2 protein plays a vital role. Cells deficient in XRCC2 also show disruption of the centrosome, a key component of the mitotic apparatus. We find that this centrosome disruption is dynamic and when it occurs during mitosis it is linked directly to the onset of mitotic catastrophe in a significant fraction of the XRCC2-deficient cells. However, we also show for the first time that XRCC2 and other HR proteins, including the key recombinase RAD51, co-localize with the centrosome. Co-localization is maintained throughout the cell cycle, except when cells are finishing mitosis when RAD51 accumulates in the midbody between the separating cells. Taken together, these data suggest a tight functional linkage between the centrosome and HR proteins, potentially to coordinate the deployment of a DNA damage response at vulnerable phases of the cell cycle.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.yexcr.2011.01.021 | DOI Listing |
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