Ask about this productRelated genes to: LNPEP antibody
- Gene:
- LNPEP NIH gene
- Name:
- leucyl and cystinyl aminopeptidase
- Previous symbol:
- -
- Synonyms:
- CAP, PLAP, P-LAP, IRAP
- Chromosome:
- 5q15
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-11
- Date modifiied:
- 2016-07-11
Related products to: LNPEP antibody
Related articles to: LNPEP antibody
- Genome-wide association studies (GWASs) have identified multiple genetic regions that confer risk for juvenile idiopathic arthritis (JIA). However, identifying the single-nucleotide polymorphisms (SNPs) that drive disease risk has been impeded by the fact that the SNPs used to identify risk loci are in linkage disequilibrium (LD) with hundreds of other SNPs. Since the causal SNPs remain unknown, it is difficult to identify target genes and thus use genetic information to elucidate disease biology and inform patient care. We next used existing genotyping data from 3,939 children with JIA and 14,412 healthy controls to identify SNPs on JIA-risk haplotypes that present within open chromatin in multiple immune cell types and are more common in children with JIA than the controls (p < 0.05) in the genotyping datasets. We identified SNPs within cis-regulatory regions (cis-regulatory elements [CREs]) using precision run-on sequencing data and identified likely target genes using MicroC in both resting and activated CD4+ T cells. We identified 138 SNPs within the PROseq-identified CREs and n = 41 genes with which these CREs physically interacted. Data from Genotype-Tissue Expression (GTEx) and the Database of Immune Cell Expression Quantitative Trait Loci (DICE) corroborated these analyses by showing allelic effects for SNPs within the CREs in the ERAP2/LNPEP and locus. We further corroborated IRF1 allelic effects using a luciferase reporter assay. Our findings significantly reduce the genomic search space for risk-driving variants and target genes and support the roles of IRF1, ERAP2, and LNPEP in driving risk for JIA. - Source: PubMed
Publication date: 2026/04/28
Jiang KaiyuHaley Emma KBarshad GiladHe AdamRogic AnitaRice EdwardSudman MarcThompson Susan DMurphy David AFu YaoPonder LoriMunoz Maurice DavenportKolachala PrashantPrahalad SampathGaffney Patrick MDanko Charles GJarvis James N - High-grade gliomas are devastating cancers with dismal prognosis, largely because current chemotherapeutics fail to cross the blood-brain barrier and lack tumor-cell specificity. Nanotechnology aims to overcome these limitations through targeted drug delivery. Here, a quadruple-conjugated nanomodel was synthesized using carbon dots (C-dots) as biocompatible nanocarriers via a one-pot reaction that covalently links two targeting peptides and two anticancer agents. The short peptide (shPep-1) targets the tumor-restricted receptor IL13Rα2, whereas the long peptide (lnPep-1) contains a nuclear localization signal for enhanced intracellular trafficking. Therapeutic cargo consists of epirubicin and the temozolomide metabolite 5-aminoimidazole-4-carboxamide. This nanomodel displays potent cytotoxicity in multiple high-grade glioma cell lines at 50 nM while remaining relatively non-toxic to normal cells (IC₅₀ > 2 µM). Despite a lower drug-loading capacity than single-peptide formulations, it induced greater glioma cell death, underscoring the enhanced therapeutic synergy of its dual-peptide, dual-drug design. Fluorescence studies confirm superior uptake and nuclear delivery, establishing C-dots as a stable, cost-effective, modular platform for next-generation personalized cancer nanotherapies. - Source: PubMed
Publication date: 2026/01/30
Cilingir Emel KirbasHettiarachchi Sajini DRathee ParthZhou YiqunFerreira Braulio ClbWang LukunJoji AnnuGonzalez Carlos MMoreno Hollweg Maria JShiri MehrdadWang KunPrabhakar RajeevVanni StevenLeblanc Roger MGraham Regina M - GWAS have identified multiple genetic regions that confer risk for juvenile idiopathic arthritis (JIA). However, identifying the single nucleotide polymorphisms (SNPs) that drive disease risk has been impeded by the fact that the SNPs used to identify risk loci are in linkage disequilibrium (LD) with hundreds of other SNPs. Since the causal SNPs remain unknown, it is difficult to identify target genes and thus use genetic information to elucidate disease biology and inform patient care. We next used existing genotyping data from 3,939 children with JIA and 14,412 healthy controls to identify SNPs on JIA risk haplotypes that: present within open chromatin in multiple immune cell types and more common in children with JIA than the controls (p<0.05) in the genotyping data sets. We identified SNPs within cis-regulatory regions (CREs) using precision run-on sequencing data, and identified likely target genes using MicroC in both resting and activated CD4+ T cells. We identified 138 SNPs within the PROseq-identified CREs, and n=41 genes with which these CREs physically interacted. Data from GTEx corroborated these analyses by showing allelic effects for SNPs within the CREs in the and risk loci. We further corroborated allelic effects using a luciferase reporter assay. Our findings significantly reduce the genomic search space for risk-driving variants and target genes and support the roles of and in driving risk for JIA. - Source: PubMed
Publication date: 2025/12/16
Jiang KaiyuHaley Emma KBarshad GiladHe AdamRogic AnitaRice Edward JSudman MarcThompson Susan DDanko Charles GJarvis James N - Sleep disturbance is increasingly common and has been linked to adverse metabolic outcomes. This study investigated whether sleep recovery (SR) mitigates the effects of chronic sleep fragmentation (SF) on glucose metabolism, with a focus on gut microbiota and inguinal white adipose tissue (iWAT) transcriptomics. Mice were subjected to 8 weeks of SF followed by SR. After 2 weeks of SR (SF 8w-SR 2w), glucose intolerance persisted, accompanied by significant alterations in gut microbiota composition and iWAT gene expression. Key hub genes (Ncapg, Cenpe, Ttk) and glucose metabolism-related genes (Lnpep, Pten, Apoe, Cebpb, Ido1, Ahsg) were identified. Bacterial genera were significantly altered and associated with glucose metabolism. After 8 weeks of SR (SF 8w-SR 8w), glucose tolerance was restored, although alterations in gut microbiota composition persisted. Notably, Rikenellaceae_RC9_gut_group and Defluviitaleaceae_UCG-011 remained persistently altered. These findings indicate that short-term SR is insufficient to reverse SF-induced glucose intolerance, which is associated with changes in the gut microbiota and iWAT transcriptome. Although prolonged SR improves glucose metabolism, persistent microbial alterations suggest a lasting impact of SF, underscoring the potential role of gut dysbiosis in metabolic dysfunction following sleep disturbances. - Source: PubMed
Publication date: 2025/10/22
Zhang JieZhong LingYi XinghaoYao XinyueWen YibingYang JielinLi BoGao ShanLi Ming - Organisms living in desert habitats face multiple simultaneous pressures, such as high temperatures and arid, and the population dynamics and community diversity of small rodents are strongly affected by climate extremes. However, the potential mechanisms by which desert rodents adapt to arid remain largely unexplored. Here, we assembled a 3.18 Gb genome, including 25,812 protein-encoding genes, for Orientallactaga sibirica, which is widely distributed across both arid and semihumid environments in Eurasia. Orientallactaga sibirica has longer ears and hind limbs to enhance heat dissipation, which may be related to the positively selected genes, such as Fgf10, Fgf11, Hoxc4, Hoxd1, and Bmp4. The renal transcriptome revealed increased fat and carbohydrate metabolism for metabolic water production in O. sibirica residing in arid habitats. Pathways such as material metabolism, oxidative stress response, osmoregulation, and water and salt reabsorption were enriched in candidate genes, such as Avp, Ang, and Ace, under positive selection in O. sibirica. Moreover, amino acid replacement was observed in the protein sequences of seven candidate genes, including Aldh7a1, Lnpep, Wnk4, C1qc, and Awat2, and these specific amino acid replacements of genes such as Umod and Scnn1a were related to unique osmoregulation, osmotic protection, and water retention compensation mechanisms. Water deprivation under laboratory conditions induced the upregulation of Umod and Aldh7a1 expression, further supporting the results observed in the wild population. These findings demonstrate that the positively selected genes related to limb development and specific amino acid replacements in the genes Umod and Scnn1a for unique osmoregulation in the renal vascular system may contribute to arid adaptation in the desert rodent species O. sibirica. This study provides novel insights into the adaptive evolution of desert small mammals and can serve as a reference for future research on renal damage-related diseases, such as human kidney stones and salt-sensitive hypertension. - Source: PubMed
Yuan ShuaiZhang RongJin YonglingLi XinLi LinlinZhang DongLing YuZhang KaijianWu XiaodongZhang XueyingFu Heping