Cellular defence mechanism of the clam Tapes semidecussatus against infection by the protozoan Perkinsus sp.

1995 ◽  
Vol 279 (3) ◽  
pp. 529-538 ◽  
Author(s):  
Juan F. Montes ◽  
Merc� Durfort ◽  
Jos� Garc�a-Valero

2019 ◽  
Vol 650 ◽  
pp. 1752-1758 ◽  
Author(s):  
Camilla Carla Parenti ◽  
Anna Ghilardi ◽  
Camilla Della Torre ◽  
Matteo Mandelli ◽  
Stefano Magni ◽  
...  


2008 ◽  
Vol 38 (7) ◽  
pp. 1803-1806 ◽  
Author(s):  
Helen L. Collins


1991 ◽  
Vol 29 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Sanjay GUPTA ◽  
Mohammad ATHAR ◽  
Jai R. BEHARI ◽  
Ramesh C. SRIVASTAVA


Author(s):  
Jonathan Tak-Sum Chow ◽  
Leonardo Salmena

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), an RNA virus, is responsible for coronavirus disease 2019 (COVID-19) pandemic of 2020. Experimental evidence suggests that microRNA can mediate an intracellular defence mechanism against some RNA viruses. The purpose of this study was to identify microRNA with predicted binding sites in the SARS-CoV-2 genome, compare these to their microRNA expression profiles in lung epithelial tissue and make inference towards possible roles for microRNA in mitigating coronavirus infection. We hypothesize that high expression of specific coronavirus-targeting microRNA in lung epithelia may protect against infection and viral propagation, conversely low expression may confer susceptibility to infection. We have identified 128 human microRNA with potential to target the SARS-CoV-2 genome, most of which have very low expression in lung epithelia. Six of these 128 microRNA are differentially expressed upon in vitro infection of SARS-CoV-2. Twenty-eight and 23 microRNA also target the SARS-CoV and MERS-CoV, respectively. In addition, 48 and 32 microRNA are commonly identified in two other studies. Further research into identifying bona fide coronavirus targeting microRNA will be useful in understanding the importance of microRNA as cellular defence mechanism against pathogenic coronavirus infections.





1992 ◽  
Vol 6 (6) ◽  
pp. 536-541 ◽  
Author(s):  
S�ndor T�ri ◽  
Ilona N�meth ◽  
Ilona Varga ◽  
Tibor Bodrogi ◽  
B�la Matkovics


1995 ◽  
Vol 279 (3) ◽  
pp. 529-538 ◽  
Author(s):  
Juan F. Montes ◽  
Merc� Durfort ◽  
Jos� Garc�a-Valero


2021 ◽  
Vol 42 (3) ◽  
pp. 134
Author(s):  
Emma F Harding ◽  
Grace JH Yan ◽  
Peter A White

Genomic viral integrations, termed endogenous viral elements (EVEs), are fragments of viruses in host chromosomes that provide information about viral evolution and could even help protect the host from infection. In the present study we examined EVEs in thirteen different Australian marsupial species to identify trends in their integration, commonality and to investigate their possible cellular function. We found that marsupial EVEs are commonly derived from viruses of the Bornaviridae, Filoviridae and Parvoviridae families, and circulated up to 160 million years ago. We also show the EVEs are actively transcribed into both long and short RNA molecules in marsupials, and propose they are involved in a cellular defence mechanism to protect the germline from viral genomic invasion.



2010 ◽  
Vol 429 (1) ◽  
pp. 95-102 ◽  
Author(s):  
Hui Chen ◽  
Ling Qi

The UPR (unfolded protein response), a cellular defence mechanism against misfolded protein accumulation in the ER (endoplasmic reticulum), is associated with many human diseases such as aging, cancer and diabetes. XBP1 (X-box-binding protein 1), a key transcription factor of the UPR, is critical in maintaining ER homoeostasis. Nevertheless, the mechanism by which XBP1 transcriptional activity is regulated remains unexplored. In the present study we show that XBP1s, the active spliced form of XBP1 protein, is SUMOylated, mainly by PIAS2 [protein inhibitor of activated STAT (signal transducer and activator of transcription) 2] at two lysine residues located in the C-terminal transactivation domain. Ablation of these SUMOylation events significantly enhances the transcriptional activity of XBP1s towards UPR target genes. Thus our results reveal an unexpected role for SUMO (small ubiquitin-related modifier) in the regulation of UPR activation and ER homoeostasis.



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