PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33363465-8 2020 Notably, our results identified ACE/ACE2-ATR1-Cholesterol-HDAC axis signals that also matched with some available clinical data. Cholesterol 46-57 angiotensin converting enzyme 2 Homo sapiens 36-40 34975904-5 2021 In this review, we discussed the novel evidence on the cholesterol-rich lipid rafts as a platform for SARS-CoV-2 entry, where receptors such as the angiotensin-converting enzyme-2 (ACE-2), heparan sulfate proteoglycans (HSPGs), human Toll-like receptors (TLRs), transmembrane serine proteases (TMPRSS), CD-147 and HDL-scavenger receptor B type 1 (SR-B1) are recruited for their interaction with the viral spike protein. Cholesterol 55-66 angiotensin converting enzyme 2 Homo sapiens 148-179 34522180-4 2021 In in vitro studies, membrane cholesterol increased the number of viral entry sites on the host cell membrane and the number of angiotensin-converting enzyme 2 (ACE2) receptors in the membrane fusion site. Cholesterol 30-41 angiotensin converting enzyme 2 Homo sapiens 128-159 34522180-4 2021 In in vitro studies, membrane cholesterol increased the number of viral entry sites on the host cell membrane and the number of angiotensin-converting enzyme 2 (ACE2) receptors in the membrane fusion site. Cholesterol 30-41 angiotensin converting enzyme 2 Homo sapiens 161-165 35547841-4 2022 With examples of zwitterionic dipalmitoyl phosphatidyl choline, cholesterol, and anionic sodium dodecyl sulphate, we show that surfactants form micellar aggregates that selectively adhere to the specific regions of S1 domain of the Spike protein that are responsible for binding with ACE2 receptors and virus transmission into the cells. Cholesterol 64-75 angiotensin converting enzyme 2 Homo sapiens 284-288 34983944-0 2022 SARS-CoV-2 treatment effects induced by ACE2-expressing microparticles are explained by the oxidized cholesterol-increased endosomal pH of alveolar macrophages. Cholesterol 101-112 angiotensin converting enzyme 2 Homo sapiens 40-44 8767468-0 1996 ACAT/CEH and ACEH/LAL: two key enzymes in hepatic cellular cholesterol homeostasis and their involvement in genetic disorders. Cholesterol 59-70 angiotensin converting enzyme 2 Homo sapiens 13-17 32511366-7 2021 The cholesterol concomitantly traffics angiotensinogen converting enzyme (ACE2) to the viral entry site where SARS-CoV-2 docks to properly exploit entry into the cell. Cholesterol 4-15 angiotensin converting enzyme 2 Homo sapiens 74-78 32457038-5 2020 SARS-CoV-2 shares extensive structural and functional conservation with SARS-CoV-1, including engagement of the same host cell receptor (angiotensin-converting enzyme 2) localized in cholesterol-rich microdomains. Cholesterol 183-194 angiotensin converting enzyme 2 Homo sapiens 137-168 32570882-3 2020 It has been shown that high cholesterol levels are associated with more lipid rafts, subdomains of the plasma membrane that can harbour angiotensin-converting enzyme 2 (ACE2) receptors for the S-protein of SARS-CoV-2. Cholesterol 28-39 angiotensin converting enzyme 2 Homo sapiens 136-167 32570882-3 2020 It has been shown that high cholesterol levels are associated with more lipid rafts, subdomains of the plasma membrane that can harbour angiotensin-converting enzyme 2 (ACE2) receptors for the S-protein of SARS-CoV-2. Cholesterol 28-39 angiotensin converting enzyme 2 Homo sapiens 169-173 32817933-5 2020 These same lipid domains recruit the SARS-CoV-2 surface receptor angiotensin converting enzyme 2 (ACE2) to an endocytic entry point and their disruption by cholesterol depletion decreases ACE2 recruitment and viral entry. Cholesterol 156-167 angiotensin converting enzyme 2 Homo sapiens 65-96 32817933-5 2020 These same lipid domains recruit the SARS-CoV-2 surface receptor angiotensin converting enzyme 2 (ACE2) to an endocytic entry point and their disruption by cholesterol depletion decreases ACE2 recruitment and viral entry. Cholesterol 156-167 angiotensin converting enzyme 2 Homo sapiens 188-192 18814896-0 2008 Importance of cholesterol-rich membrane microdomains in the interaction of the S protein of SARS-coronavirus with the cellular receptor angiotensin-converting enzyme 2. Cholesterol 14-25 angiotensin converting enzyme 2 Homo sapiens 136-167 22227126-4 2012 Hyperglycemia, insulin resistance, and/or specific cholesterol metabolites have been demonstrated to activate components required for the synthesis [angiotensinogen, renin, angiotensin-converting enzyme (ACE)], degradation (ACE2), or responsiveness (angiotensin II type 1 receptors, Mas receptors) to angiotensin peptides in cell types (e.g., pancreatic islet cells, adipocytes, macrophages) that mediate specific disorders of the metabolic syndrome. Cholesterol 51-62 angiotensin converting enzyme 2 Homo sapiens 224-228 18814896-5 2008 We found that ACE2 of both Vero E6 and Caco-2 cells co-purifies with marker proteins of detergent-resistant membranes supporting the notion that cholesterol-rich microdomains provide a platform facilitating the efficient interaction of the S protein with the cellular receptor ACE2. Cholesterol 145-156 angiotensin converting enzyme 2 Homo sapiens 277-281 18814896-8 2008 Depletion of cholesterol from the ACE2-expressing cells reduced the binding of S-expressing cells by 50% whereas the binding of soluble S protein was not affected. Cholesterol 13-24 angiotensin converting enzyme 2 Homo sapiens 34-38 18279660-4 2008 Depletion of plasma membrane cholesterol with MbetaCD relocalized raft-resident marker caveolin-1 as well as SARS-CoV receptor ACE2 to a nonraft environment, but did not significantly change the surface expression of ACE2. Cholesterol 29-40 angiotensin converting enzyme 2 Homo sapiens 127-131