|1.||Turk, John: 23 articles (09/2012 - 04/2002)|
|2.||Bao, Shunzhong: 13 articles (02/2012 - 12/2003)|
|3.||Ramanadham, Sasanka: 12 articles (12/2012 - 04/2002)|
|4.||Song, Haowei: 11 articles (02/2012 - 12/2003)|
|5.||Zhang, Sheng: 9 articles (12/2012 - 04/2002)|
|6.||Wohltmann, Mary: 8 articles (09/2012 - 07/2006)|
|7.||McHowat, Jane: 8 articles (01/2012 - 11/2002)|
|8.||Gross, Richard W: 7 articles (11/2010 - 06/2003)|
|9.||Mancuso, David J: 7 articles (11/2010 - 06/2003)|
|10.||Bohrer, Alan: 6 articles (12/2012 - 02/2004)|
|1.||Bipolar Disorder (Mania)
09/01/2008 - "Thus, AA turnover and brain expression of AA-selective cytosolic phospholipase A(2) (cPLA(2)), but not DHA turnover or expression of DHA-selective Ca(2+)-independent iPLA(2), are reduced in rats given agents effective against bipolar disorder mania, whereas experimental excitotoxicity and neuroinflammation selectively increase brain AA metabolism. "
12/01/2008 - "Thus, AA turnover in brain phospholipids was reduced, and AA-selective cytosolic cPLA(2) or acyl-CoA synthetase, as well as cyclooxygenase (COX)-2, were downregulated in brains of rats given drugs effective against bipolar disorder, whereas DHA turnover and expression of DHA-selective calcium-independent iPLA(2) were unchanged. "
04/20/2001 - "Manipulation of iPLA(2)beta expression by molecular biologic means is an alternative approach to study iPLA(2)beta functions, and we have used a retroviral construct containing iPLA(2)beta cDNA to prepare two INS-1 insulinoma cell clonal lines that stably overexpress iPLA(2)beta. "
12/01/2012 - "Previously, we described participation of the Group VIA Ca(2+)-independent phospholipase A(2) (iPLA(2)β) in apoptosis of insulinoma cells due to ER stress. "
07/01/2010 - "Furthermore, the collapse of mitochondrial membrane potential in INS-1 insulinoma cells caused by high glucose and fatty acid levels was attenuated by overexpressing iPLA(2)beta. "
05/23/2006 - "Subjecting insulinoma cells to oxidative stress induces iPLA(2)beta oligomerization, loss of activity, and subcellular redistribution and reduces the rate of release of arachidonate from phospholipids. "
04/01/2002 - "Stimulation of insulin secretion and associated nuclear accumulation of iPLA(2)beta in INS-1 insulinoma cells."
|3.||Schizophrenia (Dementia Praecox)
02/15/2005 - "Increased activity of calcium independent phospholipase A2 (iPLA2) has repeatedly been found in the serum of unmedicated first-episode schizophrenia patients and assumed to reflect a pertubation of phospholipid metabolism. "
02/15/2005 - "Increased calcium-independent phospholipase A2 activity in first but not in multiepisode chronic schizophrenia."
08/01/1998 - "Calcium-independent phospholipase A2 and schizophrenia."
09/01/2015 - "Polymorphisms in PLA2G6 and PLA2G4C genes for calcium-independent phospholipase A2 do not contribute to attenuated niacin skin flush response in schizophrenia patients."
01/01/2010 - "In contrast, studies using a selective iPLA(2) inhibitor, bromoenol lactone, or antisense oligonucleotide indicate that iPLA(2) is an important "housekeeping" enzyme under basal conditions, whose activity is required for the prevention of vacuous chewing movements, a rodent model for tardive dyskinesia, and deficits in the prepulse inhibition of the auditory startle reflex, a common finding in schizophrenia. "
10/01/2010 - "Continued studies in this area will increase our understanding of the contribution of iPLA(2)β to the evolution of diabetes mellitus and will further our knowledge of factors that influence β-cell health in diabetes mellitus and identify potential targets for future therapeutic interventions to prevent β-cell death."
02/26/2010 - "Spontaneous development of endoplasmic reticulum stress that can lead to diabetes mellitus is associated with higher calcium-independent phospholipase A2 expression: a role for regulation by SREBP-1."
02/01/2010 - "This study provides evidence for the role of iPLA(2) in enhanced superoxide generation in neutrophils from people with diabetes mellitus and presents an alternate pathway independent of protein kinase C and phosphatidic acid phosphohydrolase-1 hydrolase signaling."
01/01/2012 - "Group VIB Phospholipase A(2) (iPLA(2)γ) is distributed in membranous organelles in which β-oxidation occurs, that is, mitochondria and peroxisomes, and is expressed by insulin-secreting pancreatic islet β-cells and INS-1 insulinoma cells, which can be injured by inflammatory cytokines, for example, IL-1β and IFN-γ, and by oxidants, for example, streptozotocin (STZ) or t-butyl-hydroperoxide (TBHP), via processes pertinent to mechanisms of β-cell loss in types 1 and 2 diabetes mellitus. "
01/01/2012 - "These findings suggest that iPLA(2)γ promotes β-cell proliferation and that its expression is increased during inflammation or oxidative stress as a mechanism to mitigate membrane injury that may enhance β-cell survival."
03/01/2011 - "Our findings highlight a novel regulatory role of VIA iPLA(2) in development of inflammation in brain. "
01/01/2012 - "In addition, iPLA(2)β is identified as a potential target for therapeutic interventions to reduce airway inflammation and the progression of chronic lung disease."
07/13/2012 - "Our studies thus illustrate that smooth muscle cell-specific iPLA(2)β participates in the initiation and early progression of vascular inflammation and neointima formation and suggest that iPLA(2)β may represent a novel therapeutic target for preventing cardiovascular diseases."
07/13/2012 - "Whether group VIA phospholipase A(2) (iPLA(2)β) is involved in vascular inflammation and neointima formation is largely unknown. "
|4.||Prostaglandin-Endoperoxide Synthases (Cyclooxygenase)
|6.||Acyl Coenzyme A (Acyl CoA)
|7.||6- (bromomethylene)tetrahydro- 3- (1- naphthaleneyl)- 2H- pyran- 2- one
|10.||Choline (Choline Chloride)
|1.||Heterologous Transplantation (Xenotransplantation)