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Study on Interaction Between 5-(4 Methoxyphenyl)-1-Phenyl-1H-1,2,3-Triazole with High-Abundant Blood Proteins and Identification of Low-Abundant Proteins by Serum Proteomics.
J Sep Sci
January 2025
Key Laboratory of Tropical Medicinal Resource Chemistry of Ministry of Education, Hainan Normal University, Haikou, China.
A comprehensive strategy, including spectroscopic, molecular simulation, proteomics, and bioinformatics techniques, was employed to investigate a novel triazole, 5-(4-methoxyphenyl)-1-phenyl-1H-1,2,3-triazole, its interactions with high-abundance blood proteins, and identification of low-abundance proteins. The binding constants and thermodynamic parameters of the triazole to two high-abundance blood globular proteins, human serum albumin, and human immunoglobulin G (HIgG), were obtained by spectroscopic techniques and computational chemistry. The two-dimensional gel electrophoresis in combination with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry was employed to isolate and identify differentially expressed low-abundance proteins in human blood serum samples following exposure to the triazole.
View Article and Find Full Text PDFN-glycosylation in the SERPIN domain of C1-Esterase Inhibitor in hereditary angioedema.
JCI Insight
January 2025
Medicine, Washington University School of Medicine, St. Louis, United States of America.
Hereditary angioedema is an autosomal dominant disorder caused by defects in C1-esterase inhibitor (C1-INH), resulting in poorly controlled activation of the kallikrein-kinin system and bradykinin overproduction. C1-INH is a heavily glycosylated protein in the serine protease inhibitor (SERPIN) family, yet the role of these glycosylation sites remains unclear. To elucidate the functional impact of N-glycosylation in the SERPIN domain of C1-INH, we engineered four sets consisting of 26 variants at or near the N-linked sequon (NXS/T).
View Article and Find Full Text PDFSignalling pathways involved in urotensin II induced ventricular myocyte hypertrophy.
PLoS One
January 2025
Department of Cardiovascular Sciences, Anaesthesia, Critical Care and Pain Management, University of Leicester, Leicester, United Kingdom.
Sustained pathologic myocardial hypertrophy can result in heart failure(HF); a significant health issue affecting a large section of the population worldwide. In HF there is a marked elevation in circulating levels of the peptide urotensin II(UII) but it is unclear whether this is a result of hypertrophy or whether the high levels contribute to the development of hypertrophy. The aim of this study is to investigate a role of UII and its receptor UT in the development of cardiac hypertrophy and the signalling molecules involved.
View Article and Find Full Text PDF[Biological essence of blood stasis-heat syndrome in ischemic stroke and current research status of traditional Chinese medicine prevention and treatment based on thromboinflammation reaction].
Zhongguo Zhong Yao Za Zhi
December 2024
Institute of Basic Theory on Integrated Traditional Chinese and Western Medicine, College of Integrated Traditional Chinese Medicine and Western Medicine, Hunan University of Chinese Medicine Changsha 410208, China.
Blood stasis-heat syndrome is one of the common syndromes of ischemic stroke, which is manifested as syndromes of blood stasis and heat during the pathological progression of patients with ischemic stroke, but there is a lack of systematic research on its biological essence. Thromboinflammation reaction is a newly proposed pathological mechanism highly associated with thrombosis and inflammatory reaction, and it refers to the fact that under the mediation of von Willebrand factor(vWF) and the kallikrein-kinin system, thrombosis and inflammatory reaction interact with each other. Activation of T cells and neutrophils further aggravates thrombosis and worsens the pathological progression of ischemic stroke.
View Article and Find Full Text PDFKNG1 mutations (c.618 T > G and c.1165C > T) cause disruption of the Cys206-Cys218 disulfide bond and truncation of the D5 domain leading to hereditary high molecular weight kininogen deficiency.
Clin Biochem
January 2025
Key Laboratory of Clinical Laboratory Medicine of Guangxi Department of Education, Nanning, Guangxi, China; Department of Clinical Laboratory, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China; Key Laboratory of Hematology, Guangxi Medical University, Education Department of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, China. Electronic address:
Background: High molecular weight kininogen (HMWK), encoded by the kininogen-1 (KNG1) gene, is a multifunctional glycoprotein closely associated with the initiation of blood coagulation, tumor growth, and other pathological processes.
Objective: We conducted a study on the clinical phenotype, genetic mutations, and molecular pathogenesis of a female patient with uterine leiomyosarcoma, who presented with HMWK deficiency and an isolated prolonged activated partial thromboplastin time (APTT).
Methods: Clinical phenotyping was conducted through APTT mixing studies, quantitative assessments of intrinsic coagulation factor activities, antigen levels of HMWK, and thromboelastography.
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