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: 3122
Function: getPubMedXML
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
Cells have evolved a number of control pathways that delay or prevent them from entering mitosis under conditions that can compromise genome integrity. One recently appreciated and versatile control pathway involves the p38 stress activated protein kinase. During late G2 p38 is rapidly activated by diverse stresses (topoisomerase II (topo II)) and histone deacetylase inhibitors, osmotic shock, microtubule disassembly, UV light, etc) via a number of different pathways. Once activated p38 appears to delay entry into mitosis by inhibiting cdc25B phosphatase that, in turn, down-regulates cyclin A/CDK2 activity. Depending on the agent and degree of stress, this delay may be transient, or it may last until transcription mediated checkpoint pathways can take over.
Download full-text PDF |
Source |
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http://dx.doi.org/10.4161/cc.4.1.1357 | DOI Listing |
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