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
There are many gene products reported to promote osteoblast differentiation and thus increase bone formation, but only the transcription factor Runx2 and members of the bone morphogenetic protein (BMP) family of growth/differentiation factors have been shown to be absolute requirements for osteogenesis. Mice lacking the transcription factor Runx2 (also known as cbfa1) develop no bone. Similarly, osteoblast differentiation and bone formation is blocked when BMP signaling is suppressed by overexpression of noggin, a selective BMP antagonist. It is therefore not unexpected that several different mechanisms have evolved to regulate the effects of BMP-induced signaling. In this session we focus on the multiple ways in which cells can modulate BMP-induced osteogenesis and mechanisms by which BMP signaling can lead to transcriptional control of gene expression.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1196/annals.1346.003 | DOI Listing |
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