Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&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
To determine whether there exists an additional pathway of E6 that is independent of direct P53 degradation and whether hADA3, a transcriptional coactivator, is involved in this process. We investigated the association between E6 and hADA3, as well as E6-associated protein (E6AP) and hADA3, in SiHa cells via RNA interference technique. Our results showed that the expression of hADA3 protein was significantly increased, cellular proliferation was decreased and apoptotic rate was increased in SiHa cells treated by E6 siRNA and E6AP siRNA respectively. Our results suggested that oncoprotein E6 inhibits hADA3 in cervical cancer cells and this process is E6AP-dependent.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1080/07357900802350798 | DOI Listing |
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