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ATX (show ENPP2 Proteins)-LPA (show APOA Proteins) axis facilitates estrogen-induced endometrial cancer cell proliferation via MAPK/ERK (show MAPK1 Proteins) signaling pathway.
DLD (show DLD Proteins)-C-F cells formed large-sized colonies, but not DLD (show DLD Proteins)-F-C cells, correlating with LPAR1 and LPAR6 (show LPAR6 Proteins) gene expression levels. These results suggest that LPA1 and LPA6 (show LPAR6 Proteins) may regulate the colony formation activity in DLD1 cells treated with anticancer drugs.
endogenous LPA1 receptor signaling and regulation
The increased expression of LPA (show APOA Proteins) and LPAR1 is associated with the fibrosis and hypertrophy of the ligamentum flavum in patients with Lumbar Spinal Stenosis.
myeloma cells stimulate mesenchymal stem cells (MSCs to produce autotaxin (show ENPP2 Proteins), an indispensable enzyme for the biosynthesis of lysophosphatidic acid, and LPA receptor 1 (LPA1) and 3 (LPA3 (show LPAR3 Proteins)) transduce opposite signals to MSCs to determine the fate of MSCs.
LPA1 plays a critical role in EGF (show EGF Proteins) responses and that FFA4 agonists inhibit proliferation by suppressing positive cross-talk between LPA1 and the EGF receptor (show EGFR Proteins)
ADAMTS7 and LPA single nucleotide polymorphisms are related to a 24-h ambulatory systolic-diastolic pressure regression index.
Polymorphism rs7023923 located near LPAR1 gene: the association of rs7023923 with monocytosis was confirmed among healthy blood donors (p = 0.0156) but not among patients admitted for elective coronarography (p = 0.61).
These results suggest that autotaxin-LPA-LPA receptor 1-AKT1 signaling axis is critical for maintaining Cancer stem cells(CSC) characteristics through an autocrine loop and provide a novel therapeutic target for ovarian CSCs
LPA (show APOA Proteins)-type agonist, via Carbonyl-oxygen/Lys39 interaction facilitates the formation of a hypothetical N-terminal cap tightly packed over the LPA1 heptahelical bundle.
Study shows that lysophosphatidic acid (LPA) propagates post-injury schwann cell (SC) dedifferentiation through lysophosphatidic acid 1 signaling. These data indicate that LPA may be a critical factor that shifts SCs (show TWIST1 Proteins) towards a post-injury phenotype and contributes to the onset of Wallerian degeneration.
we demonstrate that LPA1/3 antagonism mildly reduced plasma LDL cholesterol levels. Therefore, pharmacological inhibition of LPA1/3 receptors may prove a promising approach to diminish atherosclerosis development.
LPA receptor 1 signaling increased TGFbeta (show TGFB1 Proteins) expression via GSK3beta phosphorylation and SREBP1 (show SREBF1 Proteins) activation, contributing to the development of diabetic nephropathy.
Our data suggest that LPAR signaling stimulates SS development by induction of IL-17 (show IL17A Proteins) production via ROCK and p38 MAPK (show MAPK14 Proteins) pathways. Thus, LPAR inhibition could be a possible therapeutic strategy for SS.
LPA-LPA1 signaling initiates profibrotic epithelial cell fibroblast communication mediated by epithelial cell derived connective tissue growth factor (show CTGF Proteins).
Data (including data from studies conducted in cells from knockout mice) suggest that signaling via Lpar1, Cd14 (show CD14 Proteins), and Scara1 (show MSR1 Proteins) mediates uptake of oxidized LDL by macrophages leading to foam cell formation; lysophosphatidic acid (LPA) induces expression of Cd14 (show CD14 Proteins) and Scara1 (show MSR1 Proteins) in macrophages. (Lpar1 = LPA receptor 1; Cd14 (show CD14 Proteins) = monocyte differentiation antigen CD14 (show CD14 Proteins); Scara1 (show MSR1 Proteins) = scavenger receptor class A type I)
Our results suggest that LPA-enhanced foam cell formation is mediated by LPA1/3 -AKT (show AKT1 Proteins) activation and subsequent SRBI (show SCARB1 Proteins) expression.
Lysophosphatidic acid-LPA1 signaling is critically required for septation during alveolarization.
Data show that lysophosphatidic acid receptor 1 (LPA1)-green fluorescent proteins can be used to directly quantify the running-induced increase in precursor proliferation.
Results suggest a relevant role for the Lysophosphatidic acid/Lysophosphatidic acid receptor 1 signaling system in alcoholism. In addition, the LPA1-null mice emerge as a new model for genetic vulnerability to excessive alcohol drinking
Lysophosphatidic acid stimulates PGE (show LIPF Proteins)(2) production, cell viability, and intracellular calcium ion mobilization in cultured stromal endometrial cells via Ki16425-sensitive LPA1 receptors.
the ATX-LPA-LPAR axis is a critical regulator of embryonic vascular development that is conserved in vertebrates
LPA(1) is necessary for lymphatic vessel formation during embryonic development in zebrafish.
The integral membrane protein encoded by this gene is a lysophosphatidic acid (LPA) receptor from a group known as EDG receptors. These receptors are members of the G protein-coupled receptor superfamily. Utilized by LPA for cell signaling, EDG receptors mediate diverse biologic functions, including proliferation, platelet aggregation, smooth muscle contraction, inhibition of neuroblastoma cell differentiation, chemotaxis, and tumor cell invasion. Two transcript variants encoding the same protein have been identified for this gene
endothelial differentiation, lysophosphatidic acid G-protein-coupled receptor, 2
, lysophosphatidic acid receptor 1
, lysophosphatidic acid receptor 1-like
, LPA receptor 1
, lysophosphatidic acid receptor Edg-2
, ventricular zone gene 1
, G-protein coupled receptor 26
, clone 4.9
, endothelial differentiation lysophosphatidic acid G-protein-coupled receptor 2
, endothelium differentiation gene 2