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
Regulator of calcineurin 1 (RCAN1) is located close to the Down syndrome critical region (DSCR) on human chromosome 21 and is related to the Down syndrome (DS) phenotype. To identify a novel binding partner of RCAN1, we performed yeast two-hybrid screening and identified mitogen-activated protein (MAP) kinase/extracellular signal-regulated kinase (ERK) kinase 1 (MEK1) as a partner. MEK1 was able to bind and phosphorylate RCAN1 in vitro and in vivo. MEK1-dependent RCAN1 phosphorylation caused an increase in RCAN1 expression by increasing the protein half-life. Nerve growth factor (NGF)-dependent activation of the MEK1 pathway consistently induced RCAN1 expression. Moreover, we found that RCAN1 overexpression inhibited NGF-induced neurite outgrowth and expression of neuronal marker genes, such as growth cone-associated protein 43 (GAP43) and synapsin I, via inhibition of MEK1-ERK1/2 pathways. Our findings provide evidence that MEK1-dependent RCAN1 phosphorylation acts as an important molecular mechanism in the control of neuronal differentiation.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1002/jcp.30609 | DOI Listing |
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