scholarly journals A small deletion in SERPINC1 causes type I antithrombin deficiency by promoting endoplasmic reticulum stress

Oncotarget ◽  
2016 ◽  
Vol 7 (47) ◽  
pp. 76882-76890 ◽  
Author(s):  
Jingjing Su ◽  
Liang Shu ◽  
Zhou Zhang ◽  
Lei Cai ◽  
Xin Zhang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Type I ◽  
Antithrombin Deficiency ◽  
Small Deletion

scholarly journals An essential dimer-forming subregion of the endoplasmic reticulum stress sensor Ire1

2005 ◽  
Vol 391 (1) ◽  
pp. 135-142 ◽  
Author(s):  
Daisuke Oikawa ◽  
Yukio Kimata ◽  
Masato Takeuchi ◽  
Kenji Kohno
Keyword(s):  
Endoplasmic Reticulum ◽  
Recombinant Protein ◽  
Endoplasmic Reticulum Stress ◽  
Transmembrane Protein ◽  
Type I ◽  
Unfolded Protein ◽  
The Unfolded Protein Response ◽  
Protein Response ◽  
Recombinant Fragments ◽  
Made In

The luminal domain of the type I transmembrane protein Ire1 senses endoplasmic reticulum stress by an undefined mechanism to up-regulate the signalling pathway for the unfolded protein response. Previously, we proposed that the luminal domain of yeast Ire1 is divided into five subregions, termed subregions I–V sequentially from the N-terminus. Ire1 lost activity when internal deletions of subregion II or IV were made. In the present paper, we show that partial proteolysis of a recombinant protein consisting of the Ire1 luminal domain suggests that subregions II–IV are tightly folded. We also show that a recombinant protein of subregions II–IV formed homodimers, and that this homodimer formation was impaired by an internal deletion of subregion IV. Furthermore, recombinant fragments of subregion IV exhibited a self-binding ability. Therefore, although its sequence is little conserved evolutionarily, subregion IV plays an essential role to promote Ire1 dimer formation.

scholarly journals Association of ORMDL3 with rhinovirus-induced endoplasmic reticulum stress and type I Interferon responses in human leucocytes

2017 ◽  
Vol 47 (3) ◽  
pp. 371-382 ◽  
Author(s):  
Y.-P. Liu ◽  
V. Rajamanikham ◽  
M. Baron ◽  
S. Patel ◽  
S. K. Mathur ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Type I Interferon ◽  
Type I ◽  
Interferon Responses

scholarly journals Type I photosensitizers based on phosphindole oxide for photodynamic therapy: apoptosis and autophagy induced by endoplasmic reticulum stress

2020 ◽  
Vol 11 (13) ◽  
pp. 3405-3417 ◽  
Author(s):  
Zeyan Zhuang ◽  
Jun Dai ◽  
Maoxing Yu ◽  
Jianqing Li ◽  
Pingchuan Shen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endoplasmic Reticulum ◽  
Photodynamic Therapy ◽  
Endoplasmic Reticulum Stress ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Type I ◽  
Oxygen Species

Phosphindole oxide-based photosensitizers with Type I reactive oxygen species generation ability are developed and used for endoplasmic reticulum stress-mediated photodynamic therapy of tumors.

scholarly journals H3 relaxin alleviated vascular injury  in rats with type 1 diabetes by inhibiting endoplasmic reticulum stress and inflammation

2021 ◽  
Author(s):  
Xiaohui Zhang ◽  
Kelaier Yang ◽  
Jinyu Chi ◽  
Wenjia Chen ◽  
Xiao Ma ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Type 1 Diabetes ◽  
Endoplasmic Reticulum Stress ◽  
Nlrp3 Inflammasome ◽  
Vascular Function ◽  
Diabetic Rats ◽  
Inflammasome Activation ◽  
Type I ◽  
Nlrp3 Inflammasome Activation

Abstract Human recombinant relaxin-3 (H3 relaxin ),a small molecule peptide hormone, ameliorated myocardial injury after myocardial infarction or isoprenaline injection by inhibiting apoptosis and fibrosis. However, whether H3 relaxin protects vascular function in rats with type 1 diabetes and its mechanism are unknown. In type 1 diabetes rats model induced by streptozotocin (STZ), rats were subcutaneously injected H3 relaxin (2 µg/kg/d or 0.2 µg/kg/d) for 2 weeks. At 4 or 8 weeks after STZ injection, we detected the expression of fibrosis (type I and III collagen), ERS (endoplasmic reticulum stress) and NLRP3 inflammasome activation in the aortas and inflammation markers in the plasma from rats with diabetes. Compared with the diabetic rats, H3 relaxin treatment exhibited markedly decreased plasma oxidative stress markers (TNF-a and MDA) levels. The protein expression levels of type I and III collagen in the aortas were increased in rats with diabetes, inhibited by H3 relaxin. H3 relaxin treatment inhibited ERS (GRP78 and CHOP) and NLRP3 inflammasome activation in the aortas of diabetic rats. These results suggest that H3 relaxin inhibited fibrosis, ERS and inflammation activation in the aortas of type 1 diabetic rats.

scholarly journals Cell‐autonomous cytotoxicity of type I interferon response via induction of endoplasmic reticulum stress

2017 ◽  
Vol 31 (12) ◽  
pp. 5432-5439 ◽  
Author(s):  
Chrysovalantou Mihailidou ◽  
Athanasios G. Papavassiliou ◽  
Hippokratis Kiaris
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Type I Interferon ◽  
Interferon Response ◽  
Type I

scholarly journals Involvement of Endoplasmic Reticulum Stress in Hereditary Tyrosinemia Type I

2005 ◽  
Vol 281 (9) ◽  
pp. 5329-5334 ◽  
Author(s):  
Anne Bergeron ◽  
Rossana Jorquera ◽  
Diana Orejuela ◽  
Robert M. Tanguay
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Type I ◽  
Tyrosinemia Type I ◽  
Hereditary Tyrosinemia
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