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
Inter-organelle communication via the formation of membrane contact sites (MCS) is essential for cell homeostasis. Bacterial pathogens residing in membrane bound vacuoles have exploited this biological process by secreting effector proteins that establish and function at MCS between their vacuole and host organelles. In this issue of EMBO reports, Angara et al (2024) identify a effector protein, CbEPF1, that uses molecular mimicry of eukaryotic FFAT motifs to alter MCS between two host organelles: the endoplasmic reticulum and lipid droplets. The study provides the first example of a bacterial secreted effector that directly alters organelle-organelle contact away from the vacuole, identifying a novel mechanism by which bacterial vacuolar pathogens can rewire the host cell to promote infection.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11624187 | PMC |
http://dx.doi.org/10.1038/s44319-024-00312-5 | DOI Listing |
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