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
Metacaspases are distant relatives of animal caspases found in protozoa, fungi, and plants. Limited experimental data exist defining their function(s), despite their discovery by homology modeling a decade ago. We demonstrated that two type I metacaspases, AtMC1 and AtMC2, antagonistically control programmed cell death in Arabidopsis. AtMC1 is a positive regulator of cell death and requires conserved caspase-like putative catalytic residues for its function. AtMC2 negatively regulates cell death. This function is independent of the putative catalytic residues. Manipulation of the Arabidopsis type I metacaspase regulatory module can nearly eliminate the hypersensitive cell death response (HR) activated by plant intracellular immune receptors. This does not lead to enhanced pathogen proliferation, decoupling HR from restriction of pathogen growth.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1126/science.1194980 | DOI Listing |
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