ArticleBritish journal of pharmacology2020
Inactivation of Cys
Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025Review
- PDIA3 rs2788: An Independent Risk Factor for Hypertension and Its Interaction With Antihypertensive Medications.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- Silicate ions as soluble form of bioactive ceramics alleviate aortic aneurysm and dissection.Bioactive materials · 2023Article
- G-protein-coupled receptor kinase 4 causes renal angiotensin II type 2 receptor dysfunction by increasing its phosphorylation.Clinical science (London, England : 1979) · 2022Article
- The substitution of SERCA2 redox cysteine 674 promotes pulmonary vascular remodeling by activating IRE1Acta pharmaceutica Sinica. B · 2022Article
- Profile and Functional Prediction of Plasma Exosome-Derived CircRNAs From Acute Ischemic Stroke Patients.Frontiers in genetics · 2022Article
- Cross-Talk between Mechanosensitive Ion Channels and Calcium Regulatory Proteins in Cardiovascular Health and Disease.International journal of molecular sciences · 2021Review
- Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases.Nature reviews. Cardiology · 2021Review
- Oxidative Stress and Hypertension.Circulation research · 2021Review
- Inactivation of CysBritish journal of pharmacology · 2020Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
background and purposeThe kidney is essential in regulating sodium homeostasis and BP. The irreversible oxidation of Cys EXPERIMENTAL APPROACH: We used heterozygous SERCA2 C674S knock-in (SKI) mice, where half of C674 was substituted by serine, to represent partial irreversible oxidation of C674. The BP, urine volume, and urine composition of SKI mice and their littermate wild-type (WT) mice were measured. The kidneys were collected for cell culture, Na KEY
resultsCompared with WT mice, SKI mice had higher BP, lower urine volume and sodium excretion, up-regulated endoplasmic reticulum (ER) stress markers and soluble epoxide hydrolase (sEH), and down-regulated dopamine D CONCLUSIONS AND IMPLICATIONS: The inactivation of SERCA2 C674 promotes the development of hypertension by inducing ER stress and sEH. Our study highlights the importance of C674 redox status in BP control and the contribution of SERCA2 to sodium homeostasis and BP in the kidney.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.