Ask about this productRelated genes to: LGR6 antibody
- Gene:
- LGR6 NIH gene
- Name:
- leucine rich repeat containing G protein-coupled receptor 6
- Previous symbol:
- -
- Synonyms:
- FLJ14471
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-04
- Date modifiied:
- 2016-06-06
Related products to: LGR6 antibody
Related articles to: LGR6 antibody
- High-throughput transcriptomic technologies have advanced rapidly, enabling genome-wide gene expression profiling. Microarrays, introduced in 1995, laid the foundation for large-scale analysis but were later surpassed in 2008 by RNA sequencing (RNA-seq), which offers single-nucleotide resolution, detects low-abundance transcripts, and does not require prior sequence knowledge. Bulk RNA-seq provides robust insights into global transcriptomic changes but lacks single-cell resolution. Single-cell RNA-seq (scRNA-seq), introduced in 2009, addressed this limitation by revealing cellular heterogeneity and dynamic gene expression. However, its application in bone research is constrained due to difficulties in releasing bone cells called osteocytes from the mineralized matrix, often resulting in low yield and dissociation-induced artifacts. In order to address these challenges, single-nucleus RNA-seq (snRNA-seq), first introduced in 2016 to enable transcriptomic profiling from isolated nuclei, was used in this study. We developed a protocol for snRNA-seq on bone tissue, achieving high-yield recovery of osteocyte nuclei from snap-frozen, marrow-flushed long bones. This approach minimized dissociation bias and enhanced osteocyte representation. We applied this robust method to long bones from young adult male and female mice, generating a high-resolution map of osteocyte gene expression under physiological conditions. Compared to scRNA-seq datasets, where osteocytes represent only 0.18%-6.64% of cells, our snRNA-seq approach increased osteocyte capture and transcriptomic fidelity to 18.5%. We identified an osteocyte transcriptomic signature highlighting the top 30 genes, including , which is typically undetected or lowly-expressed in scRNA-seq. Notably, 23 of these genes have not been well-characterized in osteocytes, including , , , , , , and , which may represent novel regulators of osteocyte biology. This study represents the first application of snRNA-seq specifically for osteocyte analysis in bone tissue, providing a valuable resource for investigating osteocyte biology and skeletal disorders. - Source: PubMed
Publication date: 2026/03/26
Kitase YukikoJi JiaBonewald Lynda FPrideaux MatthewRoh Hyun CheolPeng Gang - Ankylosing spondylitis (AS) is a persistent autoimmune disorder marked by inflammation of the spine and sacroiliac joints, along with atypical bone development. In recent years, DNA methylation, a significant epigenetic modification, has become a pivotal element affecting AS pathogenesis, disease progression, and clinical diagnosis. This review summarizes what we know so far about abnormal DNA methylation patterns in AS-related genes like DKK1, ERAP1, PDCD1, FOXO1/3a, LGR6, and IRF5, as well as how these patterns affect gene expression. It examines the interaction between DNA methylation and essential pathological processes such as inflammatory responses, immune regulation, and bone metabolism. Additionally, the prospective utilization of DNA methylation as a biomarker for the diagnosis and prognosis of AS is analyzed. Finally, we talk about new ways to treat AS that focus on DNA methylation mechanisms. This review seeks to amalgamate recent methylome and transcriptome studies to establish a comprehensive theoretical framework and delineate future research directions aimed at elucidating epigenetic mechanisms in AS and promoting clinical translation. - Source: PubMed
Publication date: 2026/04/01
Xia RuiboQiu ZhihaoKong ShutingNing YuhuiZhu WenhuiYang Kepeng - Repeated morphine administration leads to analgesic tolerance, reducing its pain-relief effectiveness and increasing overdose risks. However, the changes in endogenous levels of specialized pro-resolving mediators and their relationship with the mu-opioid receptor, as well as their role in analgesic tolerance during extended morphine use, have yet to be fully understood. Our study demonstrates that chronic morphine exposure reduces maresin1 levels in mice, correlating with morphine dosage in tolerant patients. Systemic or intrathecal administration of maresin1 alleviates morphine tolerance, but intracerebroventricular administration does not. Additionally, Lgr6 expression decreases in the dorsal root ganglia of morphine-tolerant mice, and reducing Lgr6 expression in dorsal root ganglia via AAV injection negates the protective effects of maresin1. Maresin1 works by preventing β-arrestin2 recruitment and mu-opioid receptor internalization, preserving morphine's pain-relief effects. In conclusion, this study elucidates the functions of maresin1 in the modulation of morphine tolerance, suggesting it as a potential target to improve opioid effectiveness. - Source: PubMed
Publication date: 2026/04/07
Tian XinyiYe JishiShen ChenxiChen XiyuanXiao JiLian ChaohuiLi LiZeng RuifengFu XinyiFang WeiyueZhan GonghaoShangguan WangningXu YigengQian ChenGao YeJin Shengwei - Lgr6 has attracted significant attention in biomedical research in recent years. As a member of the G protein-coupled receptor family, Lgr6 plays a crucial role in the occurrence and development of various diseases, including diabetic cardiomyopathy, bone regeneration defects, and skin injury repair, where it is vitally involved in cellular signal transduction. This study endeavors to investigate the distribution and functions of Lgr6 cells across organisms, particularly during homeostasis and damage scenarios. Lgr6 expression occurs across skin, mammary glands, kidneys, and intestines, crucial for development and tissue repair. Abnormal expression of Lgr6 is also observed in the onset and progression of major systemic diseases, especially in tumors. Thus, Lgr6 has been identified as a promising therapeutic target for cancer and other diseases, influencing their onset, progression, and treatment. - Source: PubMed
Publication date: 2025/09/24
Li HanGuan XiaoqiWang YuGuo Haidong - Emerging evidence suggests a potential link between obstructive sleep apnea (OSA) and sarcopenia. OSA-induced hypoxia and sleep disturbances may promote the loss of muscle mass, thereby increasing the risk of sarcopenia. This study employed bioinformatics approaches to identify key diagnostic candidate genes underlying the interaction between OSA and sarcopenia. - Source: PubMed
Publication date: 2026/03/05
Lu KunzeLei HaiyanWu CaixingLin DanxiaLi YiDeng Yan