scholarly journals New insights into the disulfide bond formation enzymes in epidithiodiketopiperazine alkaloids

2021 ◽  
Vol 12 (11) ◽  
pp. 4132-4138
Author(s):  
Huan Liu ◽  
Jie Fan ◽  
Peng Zhang ◽  
Youcai Hu ◽  
Xingzhong Liu ◽  
...  
Keyword(s):  
Disulfide Bond ◽  
Bond Formation ◽  
Disulfide Bond Formation ◽  
Disulfide Formation

A FAD-dependent oxidoreductase TdaR was responsible for α, β-disulfide formation in the biosynthesis of pretrichodermamide A. TdaR, together with its homologs AclT and GliT, catalysed not only α, α- but also α, β-disulfide formation in fungi.

scholarly journals ERO1-independent production of H2O2 within the endoplasmic reticulum fuels Prdx4-mediated oxidative protein folding

2015 ◽  
Vol 211 (2) ◽  
pp. 253-259 ◽  
Author(s):  
Tasuku Konno ◽  
Eduardo Pinho Melo ◽  
Carlos Lopes ◽  
Ilir Mehmeti ◽  
Sigurd Lenzen ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Disulfide Bond ◽  
Bond Formation ◽  
Eukaryotic Cells ◽  
Disulfide Bond Formation ◽  
Oxidative Protein Folding ◽  
Disulfide Formation ◽  
Major Producer ◽  
Cellular Compartments ◽  
In Cells

The endoplasmic reticulum (ER)–localized peroxiredoxin 4 (PRDX4) supports disulfide bond formation in eukaryotic cells lacking endoplasmic reticulum oxidase 1 (ERO1). The source of peroxide that fuels PRDX4-mediated disulfide bond formation has remained a mystery, because ERO1 is believed to be a major producer of hydrogen peroxide (H2O2) in the ER lumen. We report on a simple kinetic technique to track H2O2 equilibration between cellular compartments, suggesting that the ER is relatively isolated from cytosolic or mitochondrial H2O2 pools. Furthermore, expression of an ER-adapted catalase to degrade lumenal H2O2 attenuated PRDX4-mediated disulfide bond formation in cells lacking ERO1, whereas depletion of H2O2 in the cytosol or mitochondria had no similar effect. ER catalase did not effect the slow residual disulfide bond formation in cells lacking both ERO1 and PRDX4. These observations point to exploitation of a hitherto unrecognized lumenal source of H2O2 by PRDX4 and a parallel slow H2O2-independent pathway for disulfide formation.

scholarly journals Oxygen-independent disulfide bond formation in VEGF-A and CA9

2021 ◽  
pp. 100505
Author(s):  
Fiana Levitin ◽  
Sandy Che-Eun Serena Lee ◽  
Stephanie Hulme ◽  
Ryan A. Rumantir ◽  
Amy S. Wong ◽  
...  
Keyword(s):  
Disulfide Bond ◽  
Bond Formation ◽  
Disulfide Bond Formation

scholarly journals The Sex Differences in Uveal Melanoma: Potential Roles of EIF1AX, Immune Response and Redox Regulation

2021 ◽  
Vol 28 (4) ◽  
pp. 2801-2811
Author(s):  
Feng Liu-Smith ◽  
Chi-Yang Chiu ◽  
Daniel L. Johnson ◽  
Phillip Winston Miller ◽  
Evan S. Glazer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Sex Difference ◽  
Uveal Melanoma ◽  
Disulfide Bond ◽  
Bond Formation ◽  
Disulfide Bond Formation ◽  
Men And Women ◽  
Copy Numbers ◽  
Differential Gene

Background: Uveal melanoma (UVM) is a rare cancer that shows sex difference in incidence and survival, with little previous report for the underlying mechanism. Methods: This study used the SEER data (1974–2016) for an age-dependent analysis on sex difference in UVM, and further used the TCGA-UVM genomics dataset for analyzing the differential gene expression profiles in tumors from men and women. Results: Our results demonstrate a sex difference in older age (≥40 years) but not in younger patients, with men exhibiting a higher incidence rate than women. However, younger women have shown a continuous increasing trend since 1974. Examining the 11 major oncogenes and tumor suppressors in UVM revealed that EIF1AX showed a significant sex difference in mRNA accumulation and copy number variation, with female tumors expressing higher levels of EIF1AX and exhibiting more variations in copy numbers. EIF1AX mRNA levels were significantly inversely correlated with EIF1AX copy numbers in female tumors only, but not in male tumors. Differential gene expression analysis at the whole genomic level identified a set of 92 protein-coding and 16 RNA-coding genes which exhibited differential expression in men and women (fold of change cutoff at 1.7, adjusted p value < 0.05, FDR < 0.05). Network analysis showed significant difference in immune response and in disulfide bond formation, with EGR1/EGR2 and PDIA2 genes as regulators for immune response and disulfide bond formation, respectively. The melanocortin pathway which is linked to both melanin synthesis and obesity seems to be altered with unclear significance, as the sex difference in POMC, DCT/TYRP2, and MRAP2 was observed but with no clear direction. Conclusion: This study reveals possible mechanisms for the sex difference in tumorigenesis of UVM which has potentials for better understanding and prevention of UVM.

scholarly journals Maternal Nicotine Exposure Leads to Impaired Disulfide Bond Formation and Augmented Endoplasmic Reticulum Stress in the Rat Placenta

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0122295 ◽  
Author(s):  
Michael K. Wong ◽  
Catherine J. Nicholson ◽  
Alison C. Holloway ◽  
Daniel B. Hardy
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Disulfide Bond ◽  
Bond Formation ◽  
Disulfide Bond Formation ◽  
Nicotine Exposure

scholarly journals Modulation of Cellular Disulfide-Bond Formation and the ER Redox Environment by Feedback Regulation of Ero1

Cell ◽  
2007 ◽  
Vol 129 (2) ◽  
pp. 333-344 ◽  
Author(s):  
Carolyn S. Sevier ◽  
Hongjing Qu ◽  
Nimrod Heldman ◽  
Einav Gross ◽  
Deborah Fass ◽  
...  
Keyword(s):  
Disulfide Bond ◽  
Bond Formation ◽  
Feedback Regulation ◽  
Disulfide Bond Formation ◽  
Redox Environment
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