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
The human opportunistic pathogen expresses three acyl carrier proteins (ACPs): AcpP, Acp1, and Acp3. The function of AcpP in membrane fatty acid synthesis (FAS) was confirmed recently, but the physiological roles of Acp1 and Acp3 remain unclear. To address this, we investigated the physiological role of Acp3 in . We found that expression of Acp3 dramatically increases in the log phase of cell growth and that its transcription is under the control of the QS regulators LasR and RhlR. Deletion of from PAO1 results in thicker biofilm formation, increased resistance of the strain to hydrogen peroxide, and higher persistence in a mouse infection model. Tandem affinity purification (TAP) experiments revealed several novel protein-binding partners of Acp3, including KatA, the major catalase in . Acp3 was found to repress the catalase activity of KatA and, consistent with inhibition by Acp3, less reactive oxygen species are present in the deletion strain. Overall, our study reveals that Acp3 has a distinct function from that of the canonical AcpP and may be involved in the oxidative stress response.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6158461 | PMC |
http://dx.doi.org/10.3389/fmicb.2018.02244 | DOI Listing |
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