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: 3165
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
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Nicotinamide adenine dinucleotides (NAD(H)) play a vital role in various biological processes, including keeping the cellular redox balance. In this study, we investigate the regulatory responses of D39 to NADH and characterize the role of the Rex protein as a transcriptional repressor of the , and genes. Transcriptomic analysis was used to observe the response of D39 to NADH. Our microarray studies revealed elevated expression of various genes/operons involved in transport and biosynthesis of niacin (, and ). Promoter -fusion assays and microarray studies with the mutant revealed the role of Rex as a transcriptional repressor of , and involved in niacin uptake and biosynthesis, in the presence of NADH. We predict the operator site (5'-TTGTKAWAAWWTTCACAA-3') of Rex in the regulatory regions of Rex-regulated genes that was subsequently validated by promoter mutational experiments.
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Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6018154 | PMC |
http://dx.doi.org/10.3389/fmicb.2018.01300 | DOI Listing |