Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple factors have been implicated in the development of osteonecrosis of the femoral head (ONFH). In particular, non-traumatic ONFH is directly or indirectly related to injury of the vascular supply to the femoral head. Thus, hypoxia in the femoral head caused by impaired blood flow may be an important risk factor for ONFH. In this study, we investigated whether genetic variations of angiogenesis- and hypoxia-related genes contribute to an increased risk for the development of ONFH. Candidate genes were selected based on known hypoxia and angiogenesis pathways. An association study was performed using an Affymetrix Targeted Genotyping 3K Chip array with 460 ONFH patients and 300 control subjects. We showed that single nucleotide polymorphisms (SNPs) in the genes TF, VEGFC, IGFBP3, and ACE were associated with an increased risk of ONFH. On the other hand, SNPs in the KDR and NRP1 genes were associated with protection against ONFH. The most important finding was that one SNP (rs2453839) in the IGFBP3 gene was significantly associated with a higher risk of ONFH (P=0.0061, OR 7.74). In subgroup analysis, most candidate gene variations that were associated with ONFH occurred in the idiopathic subgroup. Among other SNPs, ACE SNPs were associated with steroid-induced ONFH (P=0.0018-0.0037, OR>3). Collectively, our findings suggest that genetic variations in angiogenesis- and hypoxia-related genes may help to identify susceptibility factors for the development of ONFH in the Korean population.
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PMID:Genetic association of angiogenesis- and hypoxia-related gene polymorphisms with osteonecrosis of the femoral head. 2021 56

Insecticidal properties of natural products may present alternatives to the use of synthetic molecule pesticides that are of diminishing effectiveness due to resistance. Three compounds, thymoquinone, nootkatone, and carvacrol, components of Alaska yellow cedar, Chamaecyyparis nootkatensis (D. Don) Spach, and incense cedar, Calocedrus decurrens (Torr.), essential oils, have been shown to have biological activity against a variety of mosquito and tick species. Although these components act as both repellents and insecticides, how they function in either capacity is unknown. Their use as mosquito control insecticides would be greatly increased if their mode of action is not the same as that of currently used commercial products. This study compared the lethal dosages for nootkatone, carvacrol, and thymoquinone by using colony strains of Anopheles gambiae Giles with known mutations at three different target sites. The altered target sites evaluated were the sodium channel para-locus mutation (L1014 F KDR) that confers permethrin resistance, the ACE-1 gene that confers organophosphate and carbamate resistance, and a gamma-aminobutyric acid receptor mutation of the Rdl locus conferring dieldrin resistance. Significant increases in lethal dose were not observed in any of the mosquito strains for any of the compounds tested compared with the doses required of chemicals with known modes of action at the mutated sites. Although the mode of action was not determined, this screening study indicates that none of these compounds interact at the target sites represented in the test mosquito strains. These compounds represent a different mode of action than existing chemicals currently used in mosquito control.
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PMID:Mode of action for natural products isolated from essential oils of two trees is different from available mosquito adulticides. 2117 62

The metabolic syndrome (MetS) is highly prevalent and confers an increased risk of diabetes and cardiovascular disease. A key early event in atherosclerosis is endothelial dysfunction. Numerous groups have reported endothelial dysfunction in MetS. However, the measurement of endothelial function is far from optimum. There has been much interest recently in a subtype of progenitor cells, termed endothelial progenitor cells (EPCs), that can circulate, proliferate, and dfferentiate into mature endothelial cells. EPCs can be characterized by the assessment of surface markers, CD34 and vascular endothelial growth factor receptor-2, VEGFR-2 (KDR). The CD34(+)KDR(+) phenotype has been demonstrated to be an independent predictor of cardiovascular outcomes. MetS patients without diabetes or cardiovascular diseases have decreased EPC number and functionality as evidenced by decreased numbers of colony forming units, decreased adhesion and migration, and decreased tubule formation. Strategies that have been shown to upregulate and enhance EPC number and functionality include statins, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and peroxisome-proliferator-activating-receptor gamma agonists. Mechanisms by which they affect EPC number and functionality need to be studied. Thus, EPC number and/or functionality could emerge as novel cellular biomarkers of endothelial dysfunction and cardiovascular disease risk in MetS.
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PMID:Dysfunctional endothelial progenitor cells in metabolic syndrome. 2194 28