Withholding iron as a cellular defence mechanism – friend or foe?

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

scholarly journals Environmental concentrations of triclosan activate cellular defence mechanism and generate cytotoxicity on zebrafish (Danio rerio) embryos

2019 ◽  
Vol 650 ◽  
pp. 1752-1758 ◽  
Author(s):  
Camilla Carla Parenti ◽  
Anna Ghilardi ◽  
Camilla Della Torre ◽  
Matteo Mandelli ◽  
Stefano Magni ◽  
...  
Keyword(s):  
Danio Rerio ◽  
Defence Mechanism ◽  
Environmental Concentrations ◽  
Cellular Defence ◽  
Danio Rerio Embryos

scholarly journals Cadmium-mediated induction of cellular defence mechanism: a novel example for the development of adaptive response against a toxicant.

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

scholarly journals Prediction and Analysis of SARS-CoV-2-Targeting microRNA in Human Lung Epithelium

2020 ◽  
Author(s):  
Jonathan Tak-Sum Chow ◽  
Leonardo Salmena
Keyword(s):  
Rna Virus ◽  
Expression Profiles ◽  
Epithelial Tissue ◽  
Defence Mechanism ◽  
Viral Propagation ◽  
Susceptibility To Infection ◽  
Bona Fide ◽  
Cellular Defence ◽  
Low Expression

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.

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
Keyword(s):  
Defence Mechanism ◽  
Cellular Defence

The effect of erythropoietin on the cellular defence mechanism of red blood cells in children with chronic renal failure

1992 ◽  
Vol 6 (6) ◽  
pp. 536-541 ◽  
Author(s):  
S�ndor T�ri ◽  
Ilona N�meth ◽  
Ilona Varga ◽  
Tibor Bodrogi ◽  
B�la Matkovics
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Defence Mechanism ◽  
Cellular Defence

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
Keyword(s):  
Defence Mechanism ◽  
Cellular Defence

scholarly journals Viral fossils in marsupial genomes: secret cellular guardians

2021 ◽  
Vol 42 (3) ◽  
pp. 134
Author(s):  
Emma F Harding ◽  
Grace JH Yan ◽  
Peter A White
Keyword(s):  
Viral Evolution ◽  
Cellular Function ◽  
Defence Mechanism ◽  
Rna Molecules ◽  
Marsupial Species ◽  
Endogenous Viral Elements ◽  
Cellular Defence ◽  
Australian Marsupial

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.

scholarly journals SUMO modification regulates the transcriptional activity of XBP1

2010 ◽  
Vol 429 (1) ◽  
pp. 95-102 ◽  
Author(s):  
Hui Chen ◽  
Ling Qi
Keyword(s):  
Transcriptional Activity ◽  
Target Genes ◽  
Protein Accumulation ◽  
Transactivation Domain ◽  
Signal Transducer ◽  
Defence Mechanism ◽  
Unfolded Protein ◽  
Lysine Residues ◽  
Protein Response ◽  
Cellular Defence

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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