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The specific quantification of endogenous LPL protein correlates with mRNA expression levels and mutational IGHV status, suggesting LPL protein as a possible reliable prognostic marker in chronic lymphocytic leukaemia.
These results demonstrate that the LPL gene is the major driver of severe hypertriglyceridemia associated with hyperchylomicronemia, although this metabolic condition may not be associated with severe atherosclerosis.
Case Reports: report LPL variants in patients with type I hyperlipoproteinemia.
Triglyceride-lowering LPL variants and LDL-C-lowering LDLR variants were associated with similar lower risk of CHD per unit difference in ApoB.
placental activity, but not maternal adipose tissue activity, positively correlated with percent body fat of newborn
LPL-mediated release of essential fatty acid DHA regulates hematopoietic stem progenitor cell expansion and definitive hematopoiesis
the negatively charged IDR of GPIHBP1 traverses a vast space, facilitating capture of LPL by capillary endothelial cells and simultaneously contributing to GPIHBP1's ability to preserve LPL structure and activity.
nder optimal conditions, the electrochemical DNA biosensor exhibited desirable performance for the determination of rs1801177 (of the lipoprotein lipase )with a wide linearity ranging from 10 fM to 10nM and a relatively low detection limit of 3.33 fM (S/N=3).
A link between the expression of LPL in the tumor cells and a poor clinical outcome of patients suffering chronic lymphocytic leukemia has been established. (Review)
Pvu II restriction fragment length polymorphism associated with an elevated risk of hypertriglyceridemia [meta-analysis]
When her TG levels normalized after incidental use of prednisone, an autoimmune mechanism was suspected. Immunoblot analyses showed the presence of autoantibodies to LPL in the patient's plasma. Autoantibodies to LPL decreased by 37% while patient was on prednisone, and by 68% as she subsequently transitioned to hydroxychloroquine monotherapy
Updated LPL structural models were generated by combining disulfide mapping, computational modeling, and data derived from single-molecule Forster resonance energy transfer. New computational suggest that LPL may dimerize using an interface that is different from the dimerization interface suggested by crystal packing contacts seen in structures of pancreatic lipase.
This meta-analysis suggested that LPL HindIII variants were associated with a decreased risk of stroke in the Asian population, but not in the non-Asian population.
LPL HindIII (+/-) and PvuII (+/-), but not the Ser447Ter, might significantly reduce the risk of ischemic stroke.
apoC-III potently inhibits triglyceride hydrolysis when LPL is bound to GPIHBP1
The results of this meta-analysis suggested that the LPL S447X polymorphism is likely to be a protective factor in the development of hypertension.
Sequence variation in Kuwaiti Arabs was compared to other populations and was found to be similar with regards to the number of SNPs, InDels and distribution of the number of variants across the LPL gene locus and minor allele frequency
Regression analysis revealed significant risk for memory loss that are dependent on age and genetic variants like LPL.
The findings in this study suggest that there is a poor concordance between apo E genotyping and lipoprotein electrophoresis in diagnosing dysbetalipoproteinemia.
mutation of a conserved cysteine in GPIHBP1 abolishes the ability of GPIHBP1 to bind LPL
miR-224 regulated the adipogenic differentiation of bovine preadipocytes by targeting LPL.
isothermal titration calorimetry (ITC) can be used for quantitative measurements of LPL activity and interactions under in vivo-like conditions, for comparisons of the properties of plasma samples from patients and control subjects as substrates for LPL, as well as for testing of drug candidates developed with the aim to affect the LPL system.
miR-29b targets LPL and TDG genes and regulates apoptosis and triglyceride production in mammary epithelial cells.
apoC-I and apoC-III inhibit lipolysis by displacing LPL from lipid emulsion particles. We also propose a role for these apolipoproteins in the irreversible inactivation of LPL by factors such as angptl4.
ANGPTL4 is more accurately described as a reversible, noncompetitive inhibitor of LPL.
Our findings confirmed that three novel SNPs we identified in the LPL gene can affect fatty acid composition and carcass traits. Therefore, selection for AA and GA genotypes should be recommended to genetically improve beef quality and flavor.
Single nucleotide polymorphisms of the LPL gene might be useful genetic markers for growth traits in the bovine reproduction and breeding.
Results describe the functional role of the secondary structure in the lipoprotein lipase-binding portion of apolipoprotein CII.
regions that are responsive to activation by apoC-II
domain (192-238) is absolutely necessary for apolipoprotein AV in lipid binding and lipoprotein lipase activation
miR-182 upregulates LPL expression, promotes lipid accumulation in atherosclerotic lesions, and increases proinflammatory cytokine secretion, likely through targetingHDAC9, leading to an acceleration of atherogenesis in ApoE-KO mice.
LpL regulates peripheral leukocyte levels and affects bone marrow monocyte progenitor differentiation and aortic macrophage accumulation.
LPL in the hypothalamus is an important regulator of body weight and glucose homeostasis
These results identify LPL as an important regulator of fatty acid transport to skeletal compartments and demonstrate an intricate functional link between systemic and skeletal fatty acid and glucose metabolism.
The data suggests that ANGPTL3 is part of the machinery causing dyslipidemia majorily via LPL inhibition in mastitis mice.
Using in vitro ketosis model by glucose starvation, studied inhibition of ketosis by momilactone B. Found momilactone B could regulate the angiopoietin-like-3 (ANGPTL3)-lipoprotein lipase (LPL)pathway, and suppressed the expression of HMGCS2 through the increased expression of STAT5b.
physiological changes in adipose tissue ANGPTL4 expression during fasting and cold resulted in inverse changes in the amount of mature-glycosylated LPL in wild-type mice, but not Angptl4(-/-) mice. We conclude that ANGPTL4 promotes loss of intracellular LPL by stimulating LPL degradation after LPL processing in the endoplasmic reticulum (ER).
LPL moved quickly from heparan sulfate proteoglycans (HSPGs) on adipocytes to GPIHBP1-coated beads, thereby depleting LPL stores on the surface of adipocytes. We conclude that HSPG-bound LPL in the interstitial spaces of tissues is mobile, allowing the LPL to move to GPIHBP1 on endothelial cells
our study reveals that hepatic LPL is involved in the regulation of plasma LPL activity and lipid homeostasis.
The induction of LPL activity by fasting in core transgenic mice activated PPARalpha downstream target genes that are involved in fatty acid beta-oxidation.
This study shows that TNF-alpha, by a Foxo1 dependent pathway, increases the transcription of ANGPTL4 which is secreted by the cells and causes inactivation of LPL.
Our findings suggest that neuronal LPL is involved in the regulation of body weight and composition in response to either the change in quantity (HF feeding) or quality (n-3 PUFA-enriched) of dietary fat
An LPL structural model suggests that the LPL S447X truncation exposes residues implicated in LPL binding to lipoprotein binding uptake receptors, such as GPIHBP1.
feeding induces lipasin, activating the lipasin-Angptl3 pathway, which inhibits LPL in cardiac and skeletal muscles to direct circulating TAG to WAT for storage
MiR-590 agomir down-regulates LPL mRNA and protein expression in a mouse model of atherosclerosis.
Deficiency of Lipoprotein Lipase in Neurons Decreases AMPA Receptor Phosphorylation and Leads to Neurobehavioral Abnormalities in Mice
Systemic LPL deletion results in impaired glucose tolerance, whole-body and tissue-specific insulin resistance, which is associated with tissue lipid deposition in various insulin target tissues
LPL encodes lipoprotein lipase, which is expressed in heart, muscle, and adipose tissue. LPL functions as a homodimer, and has the dual functions of triglyceride hydrolase and ligand/bridging factor for receptor-mediated lipoprotein uptake. Severe mutations that cause LPL deficiency result in type I hyperlipoproteinemia, while less extreme mutations in LPL are linked to many disorders of lipoprotein metabolism.
, O 1-4-5
, adipose lipoprotein lipase
, triacylglycerol lipase