ReviewDiabetes2004
Islet complex lipids: involvement in the actions of group VIA calcium-independent phospholipase A(2) in beta-cells.
Review in Diabetes, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Differential lipid signaling from CD4Frontiers in immunology · 2024Article
- Short Duration Alagebrium Chloride Therapy Prediabetes Does Not Inhibit Progression to Autoimmune Diabetes in an Experimental Model.Metabolites · 2021Article
- iPLACells · 2021Article
- The dual role of group V secretory phospholipase AEndocrine · 2017Article
- Calcium-independent phospholipases A2 and their roles in biological processes and diseases.Journal of lipid research · 2015Review
- Group VIA phospholipase A2 mitigates palmitate-induced β-cell mitochondrial injury and apoptosis.The Journal of biological chemistry · 2014Article
- Roles of acidic phospholipids and nucleotides in regulating membrane binding and activity of a calcium-independent phospholipase A2 isoform.The Journal of biological chemistry · 2012Article
- Mitochondrial dysfunction and β-cell failure in type 2 diabetes mellitus.Experimental diabetes research · 2012Review
- Role of lipid peroxidation and PPAR-δ in amplifying glucose-stimulated insulin secretion.Diabetes · 2011Article
- Arachidonic acid actions on functional integrity and attenuation of the negative effects of palmitic acid in a clonal pancreatic β-cell line.Clinical science (London, England : 1979) · 2011Article
- Genetic ablation of calcium-independent phospholipase A2gamma prevents obesity and insulin resistance during high fat feeding by mitochondrial uncoupling and increased adipocyte fatty acid oxidation.The Journal of biological chemistry · 2010Article
- Group VIA Ca2+-independent phospholipase A2 (iPLA2beta) and its role in beta-cell programmed cell death.Biochimie · 2010Review
- Evidence for proteolytic processing and stimulated organelle redistribution of iPLA(2)beta.Biochimica et biophysica acta · 2010Article
- Arachidonic Acid Activates K-Cl-cotransport in HepG2 Human Hepatoblastoma Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2009Article
- Phospholipid hydrolysis and insulin secretion: a step toward solving the Rubik's cube.American journal of physiology. Endocrinology and metabolism · 2008Article
- Characterization of N-terminal processing of group VIA phospholipase A2 and of potential cleavage sites of amyloid precursor protein constructs by automated identification of signature peptides in LC/MS/MS analyses of proteolytic digests.Journal of the American Society for Mass Spectrometry · 2004Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The beta-isoform of group VIA calcium-independent phospholipase A(2) (iPLA(2)beta) does not require calcium for activation, is stimulated by ATP, and is sensitive to inhibition by a bromoenol lactone suicide substrate. Several potential functions have been proposed for iPLA(2)beta. Our studies indicate that iPLA(2)beta is expressed in beta-cells and participates in glucose-stimulated insulin secretion but is not involved in membrane phospholipid remodeling. If iPLA(2)beta plays a signaling role in glucose-stimulated insulin secretion, then conditions that impair iPLA(2)beta functions might contribute to the diminished capacity of beta-cells to secrete insulin in response to glucose, which is a prominent characteristic of type 2 diabetes. Our recent studies suggest that iPLA(2)beta might also participate in beta-cell proliferation and apoptosis and that various phospholipid-derived mediators are involved in these processes. Detailed characterization of the iPLA(2)beta protein level reveals that beta-cells express multiple isoforms of the enzyme, and our studies involve the hypothesis that different isoforms have different functions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.