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: 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
Huntington's disease is a rare neurodegenerative disorder whose complex pathophysiology exhibits system-wide changes in the body, with striking and debilitating clinical features targeting the central nervous system. Among the various molecular functions affected in this disease, mitochondrial dysfunction and transcriptional dysregulation are some of the most studied aspects of this disease. However, there is evidence of the involvement of a mutant Huntingtin protein in the processes of DNA damage, chromosome condensation and DNA repair. This review attempts to briefly recapitulate the clinical features, model systems used to study the disease, major molecular processes affected, and, more importantly, examines recent evidence for the involvement of the mutant Huntingtin protein in the processes regulating chromosome condensation, leading to DNA damage response and neuronal death.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1039/c6mb00598e | DOI Listing |
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