Ask about this productRelated genes to: LPAR3 antibody
- Gene:
- LPAR3 NIH gene
- Name:
- lysophosphatidic acid receptor 3
- Previous symbol:
- EDG7
- Synonyms:
- LP-A3, Edg-7, RP4-678I3, HOFNH30, LPA3
- Chromosome:
- 1p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-02
- Date modifiied:
- 2014-11-19
Related products to: LPAR3 antibody
Related articles to: LPAR3 antibody
- Neutrophil extracellular traps (NETs) participate in thrombosis, inflammation, and cardiovascular remodeling, yet whether NET-related genes (NRGs) are associated with atrial fibrillation (AF) risk across multiple molecular layers remains unclear. This study used a multiomics Mendelian randomization framework to prioritize NRGs supported by methylation, expression, and protein quantitative trait loci (QTL) data. - Source: PubMed
Publication date: 2026/08/21
Zhou RuyaZhang PengzhaoZhu FeiyuLian TingtingWu Xianjun - Laccase domain containing 1 (LACC1) is an enzyme abundantly expressed in inflammatory macrophages that regulate diverse inflammatory diseases. This study aimed to investigate the role of LACC1 in lipopolysaccharide (LPS)-induced acute lung injury (ALI) and to elucidate its underlying regulatory mechanisms. - Source: PubMed
Publication date: 2026/07/23
He YiranHuang YiWang LinliHao ShengyuWang XuHan MingchenZhou KunlinXuan LizhenJu Minjie - Lysophosphatidic acid (LPA) receptor signaling contributes to the regulation of cancer cell functions. Lactic acid serves not only as an important energy source for cancer cells but also activates various signaling pathways that influence cancer cell behavior. To investigate the roles of LPA receptors in the malignant behavior of pancreatic cancer PANC-1 cells, PANC-LA1 and PANC-LA5 cells were generated by culturing PANC-1 cells with 1 or 5 mM lactic acid, respectively, for approximately 3 months. LPAR1, LPAR3, and LPAR5 expression levels expression levels were elevated, whereas LPAR2 expression was reduced in PANC-LA1 and PANC-LA5 cells compared with PANC-1 cells. PANC-1 cell growth was inhibited by LPA. Conversely, PANC-LA1 cell growth remained unchanged in response to LPA, and LPA increased PANC-LA5 cell growth. The motility of PANC-LA1 and PAN-LA5 cells was markedly elevated compared with that of PANC-1 cells. LPA further enhanced PANC-LA1 and PAN-LA5 cell motility but did not affect PANC-1 cell motility. In the presence of LPA, AM966 inhibited, whereas TC LPA5 4 stimulated PANC-LA5 cell growth and PANC-LA1 cell motility. Although GRI-977,143 increased PANC-LA5 cell growth, it reduced PANC-LA1 cell motility. (2S)-OMPT increased PANC-LA5 cell growth and PANC-LA1 cell motility. When cells were cultured in serum-free media, the viability of PANC-LA1 and PANC-LA5 cells was higher compared with that of PANC-1 cells. PANC-LA5 cell growth and PANC-LA1 cell motility were inhibited by AZD3965 and galloflavin. These findings indicate that LPA receptor signaling is involved in the regulation of PANC-1 cell behavior induced by long-term lactic acid exposure, with LPA and LPA acting as major positive regulators of proliferation and motility following long-term lactic acid exposure, whereas LPA and LPA exert distinct regulatory effects. - Source: PubMed
Publication date: 2026/08/28
Yamamoto MaoTakai MiwaShimomura NanamiIsa EikiYashiro NarumiTamura MoemiNagano ShionKusumoto YukaTsujiuchi Toshifumi - Temporomandibular disorders (TMD) pain is the most common orofacial pain with limited effective treatments. Here, we observed elevated lysophosphatidic acid (LPA), a bioactive lipid, in blood, trigeminal ganglion (TG), and peri-temporomandibular joint (TMJ) tissues in mouse models of TMD-like pain induced by TMJ inflammation or masseter muscle injury. Notably, LPA levels were also elevated in TMD patients' blood and positively correlated with their pain intensity. LPA receptors (LPAR) 1 and 3 were expressed in mouse and human TG neurons and upregulated in TMD-like pain models. Inhibition or knockout of LPAR1 or LPAR3 attenuated TMD-like pain, while LPA injection into the TMJ or masseter muscle evoked pain. Furthermore, we demonstrated that LPA/LPAR signaling upregulates and sensitizes PIEZO2, a mechanosensitive ion channel, in TG neurons via extracellular signal-regulated kinase (ERK). Specific deletion or inhibition of PIEZO2 and suppression of ERK activation in TG neurons mitigated TMD-like pain. These findings suggest that LPA/LPAR signaling drives TMD-like pain via PIEZO2, offering potential therapeutic targets. - Source: PubMed
Publication date: 2026/07/23
Zhang QiaojuanSu ShanchunLiang PengfeiChen YunKim MinseokBaldi RobertWang PengDias Fabiana CJang MinjiGonzalez Torres Maria ALim PeifengMoreira Roger W FChun JeroldGuilak FarshidYang HuangheLiedtke WolfgangNackley AndreaChen Yong - The Karan Fries (KF), a newly developed dairy cattle (Holstein Friesian × Tharparkar), after nine generations of inter se mating (mating among crossbreds) by maintaining a stable, composite breed structure, is expected to preserve some heterosis or hybrid vigour through the retention of heterozygosity and selective pressure for performance traits. Although a decline in productivity is generally seen from F1 to later inter se generations, the rate of loss of heterosis slows down, allowing the population to reach a new equilibrium. This seems to be an interesting proposition. Therefore, to assess the retained heterosis and to evaluate the current status of the KF population, the present study was conducted, which included a sizeable phenotyped and genotyped animals (n = 355). The analysis identified a stabilized genomic architecture with a mean exotic inheritance of 64.34 ± 0.74% (predominantly Holstein Friesian) and an indigenous contribution of 35.66 ± 0.95% (primarily Tharparkar). Genomic indicators of heterosis revealed a mean Genomic Retained Heterosis (RH) of 59% which accounts for 15.82% of the total observed KF average yield (4153.14 ± 167.32 kg). Genomic Retained Heterozygosity (RHET) of 0.44%. Notably, a near-perfect correlation (r = 0.98) was observed between these two metrics, indicating that RHET can be used interchangeably with RH to assess heterosis and its effects in instances where parental genotypic records were absent. Linear regression analysis demonstrated that RH was a primary driver of productivity, with Total Milk Yield (TMY) increasing by 1113.81 ± 301.91 kg per unit increase in RH (p < 0.001). The impact on TMY was significantly larger than on 305-day milk yield (339.08 ± 282.92 kg), suggesting that genomic heterosis specifically enhances lactation persistence and environmental robustness. A joint-model GWAS identified 182 SNPs with significant additive effects and 117 SNPs with significant dominance effects for TMY. Functional annotation revels candidate genes for milk synthesis (SLC25A1, PIP4K2A, LATS2), heat stress resilience (DNAJB5, DNAJC1), and immunological defence (ARHGAP15, LPAR3). Protein network analysis identified the Mitochondrial Ribosomal Protein (MRP) family, specifically hub gene MRPL22, as the central driving gene for both additive and dominance components. These findings confirm that KF cattle effectively leverage retained heterosis to integrate high production potential with robust tropical climatic adaptability. - Source: PubMed
Publication date: 2026/07/20
Kumar IshmeetVyas JayeshKhan AsadRamola GargiIlayaraja IMuansangi LalChitra AnilPal PritamSingh Ritik KumarKamboj M LRaja T VMukherjee AnupamaMukherjee Sabyasachi