scholarly journals The BRCA1 Pseudogene Negatively Regulates Anti-Tumor Responses through Inhibition of Innate Immune Defense Mechanisms

2021 ◽  
pp. canres.1959.2020
Author(s):  
Yoo Jane Han ◽  
Jing Zhang ◽  
Jung-Hyun Lee ◽  
Jennifer M. Mason ◽  
Olga Karginova ◽  
...  
2020 ◽  
Vol 11 ◽  
Author(s):  
Els Lebegge ◽  
Sana M. Arnouk ◽  
Pauline M. R. Bardet ◽  
Máté Kiss ◽  
Geert Raes ◽  
...  

2012 ◽  
Vol 81 (1) ◽  
pp. 100-111 ◽  
Author(s):  
Andrea Ribeiro ◽  
Markus Wörnle ◽  
Nasim Motamedi ◽  
Hans J. Anders ◽  
Elisabeth F. Gröne ◽  
...  

Critical Care ◽  
2010 ◽  
Vol 14 (4) ◽  
pp. R160 ◽  
Author(s):  
Joëlle Rolli ◽  
Noureddine Loukili ◽  
Sandra Levrand ◽  
Nathalie Rosenblatt-Velin ◽  
Stéphanie Rignault-Clerc ◽  
...  

2020 ◽  
Vol 104 ◽  
pp. 506-516
Author(s):  
Jingguang Wei ◽  
Chen Li ◽  
Jisheng Ou ◽  
Xin Zhang ◽  
Zetian Liu ◽  
...  

2017 ◽  
Vol 70 ◽  
pp. 13-24 ◽  
Author(s):  
Liang Lu ◽  
Xu Wang ◽  
Sizhong Wu ◽  
Xuejiao Song ◽  
Ziqi Zou ◽  
...  

2016 ◽  
Vol 230 (2) ◽  
pp. 297-302 ◽  
Author(s):  
Martin N. Møller ◽  
Svend Kirkeby ◽  
Per Cayé-Thomasen

2018 ◽  
Vol 86 (4) ◽  
Author(s):  
Maarten F. de Jong ◽  
Neal M. Alto

ABSTRACT The enteric attaching and effacing (A/E) pathogens enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC) and the invasive pathogens enteroinvasive E. coli (EIEC) and Shigella encode type III secretion systems (T3SS) used to inject effector proteins into human host cells during infection. Among these are a group of effectors required for NF-κB-mediated host immune evasion. Recent studies have identified several effector proteins from A/E pathogens and EIEC/ Shigella that are involved in suppression of NF-κB and have uncovered their cellular and molecular functions. A novel mechanism among these effectors from both groups of pathogens is to coordinate effector function during infection. This cooperativity among effector proteins explains how bacterial pathogens are able to effectively suppress innate immune defense mechanisms in response to diverse classes of immune receptor signaling complexes (RSCs) stimulated during infection.


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