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: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1057
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3175
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
The molecular mechanisms of switch/sucrose nonfermentable (SWI/SNF)-related BAF chromatin remodeling complex subunit ATPase 2 (SMARCA2) degradation remain elusive. Recently, Kotagiri et al. revealed that SMARCA2 degradation induces enhancer reprogramming in SMARCA4-mutant lung cancer cells, rendering enhancers of key cell-cycle genes inaccessible and suppressing their expression. In addition, the authors identified that transcriptional enhanced associate domain (TEAD) inhibitors synergize with SMARCA2 degraders in inhibiting SMARCA4-mutant lung cancer growth.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.trecan.2025.02.002 | DOI Listing |
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