LRFN3 antibody
- Known as:
- LRFN3 (anti-)
- Catalog number:
- orb75159
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- LRFN3 antibody
Related genes to: LRFN3 antibody
- Gene:
- LRFN3 NIH gene
- Name:
- leucine rich repeat and fibronectin type III domain containing 3
- Previous symbol:
- -
- Synonyms:
- MGC2656, SALM4, FIGLER1
- Chromosome:
- 19q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-02
- Date modifiied:
- 2014-11-19
Related products to: LRFN3 antibody
Related articles to: LRFN3 antibody
- Glycolytic reprogramming has been implicated in rheumatoid arthritis (RA) pathogenesis, yet the underlying causal genes and epigenetic mechanisms remain unclear. This study aimed to systematically identify glycolysis-related genes and their methylation-regulated expression that may causally influence RA susceptibility. - Source: PubMed
Publication date: 2026/01/22
A XinyuXin PengfeiZheng LinXu BoWang JianyeSun SongtaoXie JunGao ChenxinPan PeijunQiu GuoweiJin LangShen JunXu XiruiCheng YiweiPei ShaoqiangRan LeiBian YanqinXiao Lianbo - Genetic admixture of United States Hispanic individuals provides a unique opportunity to examine ancestral origins of inflammatory bowel disease (IBD) risk. In ∼7.3K Hispanic participants (1660 IBD cases; 5614 controls), we examined ancestral heterogeneity of IBD clinical phenotypes and sought to identify IBD risk loci that displayed heterogeneity of effect or were ancestry-specific. - Source: PubMed
Publication date: 2026/02/09
Beecham Ashley HMcGovern Dermot P BBrugger Steven WDavis Mary FTorres Esther AGomez LissetteLi DalinLopez-Marte PaolaDaly Mark JStevens ChristineYang ShaohongSinha SwetaMengesha EmebetLeavitt JamesDamas Oriana MQuintero Maria ATargan Stephan RRabizadeh ShervinSabic Ksenija Cho Judy HAbreu Maria TMcCauley Jacob LHaritunians Talin - The aim of this study was to identify genetic variants and pathways associated with the total number of piglets born and to investigate the potential negative consequences of the intensive selection for reproductive traits, particularly the formation of bumps on the legs of pigs. We used genome-wide association analysis and methods for identifying selection signatures. As a result, 47 SNPs were identified, localized in genes that play a significant role during sow pregnancy. These genes are involved in follicle growth and development (SGC), early embryonic development (CCDC3, LRRC8C, LRFN3, TNFRSF19), endometrial receptivity and implantation (NEBL), placentation, and embryonic development (ESRRG, GHRHR, TUSC3, NBAS). Several genes are associated with disorders of the nervous system and brain development (BCL11B, CDNF, ULK4, CC2D2A, KCNK2). Additionally, six SNPs are associated with the formation of bumps on the legs of pigs. These variants include intronic variants in the CCDC3, ULK4, and MINDY4 genes, as well as intergenic variants, regulatory region variants, and variants in the exons of non-coding transcripts. The results suggest important biological pathways and genetic variants associated with sow fertility and highlight the potential negative impacts on the health and physical condition of pigs. - Source: PubMed
Publication date: 2024/12/11
Bakoev SirojGetmantseva LyubovKolosova MariaBakoev FaridunKolosov AnatolyRomanets ElenaShevtsova VarvaraRomanets TimofeyKolosov YuryUsatov Alexander - Opioid use disorder (OUD) affects millions of people worldwide. While it is known that OUD originates from many factors, including social and environmental factors, the role of genetic variants in developing the disease has also been reported. This study aims to investigate the genetic variants associated with the risk of developing OUD upon exposure. Twenty-three subjects who had previously been given opioid-based painkillers to undergo minor surgical treatment were recruited at Prisma Health Upstate clinic and elsewhere. Eleven were considered nonpersistent opioid users (controls), and 12 were persistent opioid users (cases) at the time of sample collection after an initial surgery. The subjects were asked to provide saliva samples, which were subjected to DNA sequencing at Clemson University Center for Human Genetics, and variant calling was performed. The genome-wide association studies (GWASs) for genes known to be associated with OUD resulted in 13 variants (intronic or SNV) with genome-wide significance (raw -value < 0.01) and two missense variants, rs6265 (p.Val66Met in BNDF isoform a) and rs1799971 (p.Asn40Asp) in , previously reported in the literature. Furthermore, extending the GWASs to find all genomic variants and filtering the variants to include only variants found in cases (persistent opioid users) but not in controls (nonpersistent opioid users) resulted in 11 new variants (-value < 0.005). Considering that OUD is a complex disease and the effect might come from different variants in the same genes, we performed a co-occurrence analysis of variants on the genes. We identified eight additional genes that harbor multiple variants, including four genes: , , , and , with three or more variants in the case subjects but not in the control individuals. The performed PPI network construction, along with functional enrichment, indicated that the variants occur in calcium signaling, circadian entrainment, morphine addiction, alcoholism, and opioid signaling pathways, which are closely related to OUD or addiction in general. - Source: PubMed
Publication date: 2024/11/21
Panday Shailesh KumarShankar VijayLyman Rachel AnnAlexov Emil - Many synaptic adhesion molecules positively regulate synapse development and function, but relatively little is known about negative regulation. SALM4/Lrfn3 (synaptic adhesion-like molecule 4/leucine rich repeat and fibronectin type III domain containing 3) inhibits synapse development by suppressing other SALM family proteins, but whether SALM4 also inhibits synaptic function and specific behaviors remains unclear. Here we show that SALM4-knockout (Lrfn3) male mice display enhanced contextual fear memory consolidation (7-day post-training) but not acquisition or 1-day retention, and exhibit normal cued fear, spatial, and object-recognition memory. The Lrfn3 hippocampus show increased currents of GluN2B-containing N-methyl-D-aspartate (NMDA) receptors (GluN2B-NMDARs), but not α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors (AMPARs), which requires the presynaptic receptor tyrosine phosphatase PTPσ. Chronic treatment of Lrfn3 mice with fluoxetine, a selective serotonin reuptake inhibitor used to treat excessive fear memory that directly inhibits GluN2B-NMDARs, normalizes NMDAR function and contextual fear memory consolidation in Lrfn3 mice, although the GluN2B-specific NMDAR antagonist ifenprodil was not sufficient to reverse the enhanced fear memory consolidation. These results suggest that SALM4 suppresses excessive GluN2B-NMDAR (not AMPAR) function and fear memory consolidation (not acquisition). - Source: PubMed
Publication date: 2021/09/29
Lie EunkyungYeo YejiLee Eun-JaeShin WangyongKim KyungdeokHan Kyung AhYang EstherChoi Tae-YongBae MihyunLee SuhoUm Seung MinChoi Se-YoungKim HyunKo JaewonKim Eunjoon