Explore chapters and articles related to this topic
Proteinase Inhibitors: An Overview of their Structure and Possible Function in the Acute Phase
Published in Andrzej Mackiewicz, Irving Kushner, Heinz Baumann, Acute Phase Proteins, 2020
One of the acronyms of the serpin proteinase nexin-1 (PN-1) is “glial-derived neurite promoting factor”,19 which describes the ability of this serpin to promote the outgrowth of neurites in culture. This property was shown to be due to inhibition of thrombin present in neurite outgrowth media.20 Since thrombin inhibits neurite outgrowth, thrombin inhibitors will appear to stimulate it over the background, and it is not clear whether the outgrowth activity is real or a cell-culture artifact.
Spontaneous (Unexplained) Thrombosis: The Inherited Basis for the Thrombohemorrhagic Balance
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
A serine protease inhibitor (serpin) of possible importance in this context besides AT-III, HC II, a2AP, PC AI and PAI has recently been identified (Protease nexin 1 [PN-1]). It forms a stable 1:1 complex with enzymes such as thrombin and t-PA.43-44 A similar cellular serpin, a platelet surface protein, has also been isolated and characterized.45-47 Furthermore, a plasma nexin has been isolated recently, tetranexin, which is a plasminogen binding protein and thus a potential modulator of fibrinolysis.48
Inhibitors of Plasminogen Activators
Published in Cornelis Kluft, Tissue-Type Plasminogen Activator (t-PA): Physiological and Clinical Aspects, 1988
At the 1986 meeting of the International Committee on Thrombosis and Haemostasis10 the nomenclature PA-inhibitor 1, PA-inhibitor 2, and protease nexin was adopted. Scientists reporting on PA-inhibitor activity in biological material should indicate its similarity or dissimilarity with the above-cited three PA-inhibitors. (Antisera to PA-inhibitor 1,7 to PA-inhibitor 2,8 and protease nexin9 will be made available by Drs. Loskutoff, Kruithof, and Bajer, respectively, for this purpose — University Hospital, University of Lausanne Medical School, CH 1011, Lausanne, Switzerland.)
Beyond the amyloid hypothesis: how current research implicates autoimmunity in Alzheimer’s disease pathogenesis
Published in Critical Reviews in Clinical Laboratory Sciences, 2023
Miyo K. Chatanaka, Dorsa Sohaei, Eleftherios P. Diamandis, Ioannis Prassas
A study that has only focused on CSF samples is that of Lim et al. [231], where they used liquid chromatography-tandem mass spectrometry (LC-MS/MS) to perform an unbiased, untargeted shotgun analysis, to identify novel autoantibody candidates in patients with AD. They discovered 16 candidate autoantibodies. These results should be viewed with caution, since this was a pilot study with a limited number of samples [AD = 10, Parkinson’s Disease (PD) = 10, Headache control = 10], and it was primarily qualitative. The candidate autoantibodies found were not confirmed with alternative techniques or independent sets of samples. Some of the more promising autoantibody hits include glia-derived nexin (SERPINE2), fibromodulin (FMOD), and quinone oxidoreductase (CRYZ). SERPINE2 is a serine protease inhibitor, and it plays a crucial role in synaptic plasticity in the CNS [272]. Its levels are associated with tau-positive dystrophic neurites and amyloid processing [273]; so autoantibodies to it could indicate dysfunctional CNS neurons.
A Stargardt disease-like phenotype in GAS8-related primary ciliary dyskinesia
Published in Ophthalmic Genetics, 2022
In addition to GAS8, other genes responsible for the N-DRC subunit of the nexin-dynein regulatory complex include DRC1 and CCDC65 (7–9). Although most patients with primary ciliary dyskinesia have hypokinetic or immotile cilia, those with pathogenic variants in the N-DRC subunit have motile cilia with a subtle beating pattern defect. Previously-reported patients with biallelic pathogenic variants in the genes DRC1 or CCDC65 also had classic features of primary ciliary dyskinesia (recurrent sino-pulmonary infections and bronchiectasis since childhood) and the absence of situs inversus. They include a 15-year-old Turkish-Austrian boy (7), 17-year-old and 19-year-old Swedish brothers (7), a 32-year-old Swedish woman, and 4 individuals (3 families) of Ashkenazi Jewish decent (8,9). None of these patients were reported to have retinal dystrophy, but whether or not ophthalmic phenotyping was done is unclear (7–9).
Identification and Quantification of Quercetin, A Major Constituent of Artocarpus altilis by Targeting Related Genes of Apoptosis and Cell Cycle: In Vitro Cytotoxic Activity Against Human Lung Carcinoma Cell Lines
Published in Nutrition and Cancer, 2019
Tara K. Jalal, Al’aina Yuhanis Firus Khan, Hatim A. Natto, Mohammad Syaiful Bahari Abdull Rasad, Mohd. Arifin Kaderi, Mardhiah Mohammad, Muhammad Farid Johan, Muhammed Nor Omar, Ridhwan Abdul Wahab
In order to determine the level of apoptosis in cells, Guava Nexin reagent staining, a pre-made cocktail containing Annexin V-PE and 7-AAD in buffer, was prepared. All adhering and floated cells were harvested and pipetted 100 µl of each sample into appropriate well using 96-wells, then 100 µl Guava Nexin reagent was added to each well, incubated for 20 min at room temperature in the dark. Sample was acquired on Guava flow cytometry system. The results were analyzed using guava Incyte software, version 2.7, in which 2,000 cells were collected for the analysis. While for cell cycle after cells were harvested and transferred to sterile centrifuge tube, then discarded the supernatant and washed with PBS centrifuge, the supernatant was removed and the pellet resuspended with 70% cold ethanol (400 µl) and kept at –20 °C for 1–2 h. The cells were washed with PBS, centrifuged, and discarded the supernatant. Then, 200 µl of PI kit (containing 1 mg/ml RNAse) was added to the cell pellets and incubated in the dark for 30 min at room temperature. The cells were then analyzed by Guava flow cytometry, 5,000 cells were collected for analysis using guava Incyte software, version 2.7.