Ask about this productRelated genes to: EGFL8 Blocking Peptide
- Gene:
- EGFL8 NIH gene
- Name:
- EGF like domain multiple 8
- Previous symbol:
- C6orf8
- Synonyms:
- NG3
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-02
- Date modifiied:
- 2016-10-05
Related products to: EGFL8 Blocking Peptide
Related articles to: EGFL8 Blocking Peptide
- To investigate the genetic architecture of male genital lichen sclerosus (MGLSc) and to identify potential susceptibility loci, candidate genes, and biological pathways associated with disease pathogenesis by integrating genomic structural equation modeling (Genomic-SEM) with multi-omics analyses and experimental validation. - Source: PubMed
Publication date: 2026/07/16
Chen JianbaiZhang ZhimingFu QiangHou HaozhongXu GongquanLi ZhenyuLu ZhiguoQiu JianxinWu KeGao XiaopingZhang GengYang LongfeiSong RundongZhang Wei - BackgroundDifferential expression of long non-coding RNAs (lncRNAs) in brain, serum, and blood show strong potential to distinguish Alzheimer's disease (AD) from healthy controls.ObjectiveTo explore whether lncRNA signatures delineate AD pathology and map to distinct, multidimensional cognitive domains, enhancing specificity in assessing AD severity and progression.MethodsWe profiled 29,603 lncRNAs transcripts in blood samples from 15 AD patients and 15 healthy controls, alongside comprehensive neuropsychological assessments. Generalized Linear Models and Predictive Power Score analyses, with statistical prioritization, identified lncRNAs associated to AD neuropsychological architecture.ResultsSeveral lncRNAs share strongly associated with cognitive performance and AD severity, mapping to genes involved in key AD-related molecular processes, including synaptic and neurotransmitter regulation (e.g., , , ), protein homeostasis and Aβ pathology (e.g., , , ), mitochondrial function and cellular stress (e.g., , ), neuroinflammation and immune regulation (e.g., , , ), epigenetic and transcriptional control (e.g., , , ), neuronal excitability (e.g., ), and neuroprotection and synaptic plasticity (e.g., ). Novel associations included ferroptosis, DNA stability, microtubule dynamics, and dendritic orientation (e.g., , , , , , , ).ConclusionsWe identify candidate lncRNA signatures that may serve as potential biomarkers and enhance our understanding of the molecular basis of the cognitive architecture in AD, opening new avenues for biomarker identification and targeted therapeutic strategies development. Validation in larger, diverse cohorts is essential to confirm their mechanistic contributions to AD. - Source: PubMed
Publication date: 2026/07/29
Mosquera-Heredia María IVidal Oscar MBarceló ErnestoMorales Luis CSilvera-Redondo CarlosBolívar Daniel AAllegri RicardoArcos-Burgos MauricioGaravito-Galofre PilarVélez Jorge I - Triple-negative breast cancer (TNBC) remains a highly aggressive malignancy with limited therapeutic options due to the absence of well-defined molecular targets. Diet-induced obesity (DIO) promotes TNBC progression by reshaping systemic metabolism and inflammatory responses; however, the key circulating metabolites involved and their mechanisms remain largely unclear. This study aimed to identify key metabolites associated with TNBC progression and further investigate their biological functions and molecular mechanisms. Targeted metabolomics profiling was performed on serum samples from MMTV-PyMT spontaneous breast cancer mice to identify differential metabolites associated with DIO. Functional assays were conducted to evaluate the effects of hippuric acid on TNBC cell proliferation, migration, and invasion. RNA sequencing was conducted to explore downstream regulatory pathways, followed by validation of candidate targets using gain- and loss-of-function approaches as well as rescue experiments. Hippuric acid was identified as a significantly altered metabolite in DIO conditions. Functional studies demonstrated that hippuric acid markedly inhibited the proliferation, migration, and invasion of TNBC cells, with minimal effects on non-TNBC cells. Transcriptomic analysis identified EGFL8 as a potential downstream target, which was further confirmed by qPCR and functional assays. Overexpression of EGFL8 suppressed malignant phenotypes, whereas its knockdown promoted tumor progression. Rescue experiments showed that EGFL8 partially mitigated the inhibitory effects of hippuric acid on TNBC, suggesting that it functions as an important mediator in this process. Mechanistically, hippuric acid exerted its anti-tumor effects at least in part through modulation of the EGFL8-Notch signaling axis. Hippuric acid suppresses TNBC progression via the EGFL8-Notch signaling pathway. These findings highlight a previously unrecognized role of a gut microbiota-derived metabolite in TNBC and suggest its potential as a therapeutic candidate, providing new prospective targets and a theoretical basis for metabolic intervention for TNBC. - Source: PubMed
Publication date: 2026/06/21
Xu TianhanWang SaijunChen ShuaiZhou YanWang Dongmei - BACKGROUND: To investigate the genetic causality between Human blood cell (HBC) traits and sporadic lymphangioleiomyomatosis (sLAM) by mediation joint multi-omics and eQTL Mendelian randomization analysis. METHODS: Quality control processes were followed to select eligible instrumental variables strongly associated with 35 kinds of HBC traits. Independent cohort of European ancestry with sLAM and lung function genome-wide association study (GWAS) summary statistics were used separately. We utilized a two-step MR approach to explore potential mediators and evaluate the proportion of effect mediated in the associations linking HBC trait candidates to sLAM. Finally MR analysis integrating single cell expression quantitative trait loci (sc-eQTL) from 14 immune cell types with GWAS of sLAM was conducted. RESULTS: Increased level of basophil count was positively associated with higher risk of sLAM (BASO#; OR = 3.878, 95%CI:1.137–13.221, P = 0.030). No evidences of horizontal pleiotropy were observed. The multivariable MR still demonstrated that BASO# was genetically associated with the risk of sLAM after adjustment for other blood traits in the same category(OR = 5.918, 95% CI:1.275–27.468 P = 0.023) and estradiol (OR = 3.814, 95% CI:1.130-12.874, P = 0.031) respectively. No evidence for associations between basophil traits (BASO# and basophil percentage of white cells: BASO%) and lung functions containing forced vital capacity (FVC) and forced expiratory volume in 1 s/forced vital capacity(FEV1/FVC). The estimated degree of transitional B cell absolute count mediated the effect of BASO# on sLAM by 36%, while no mediating factors, including immune cells, inflammatory proteins, VEGF-related proteins were found. We identified 12 genes in 14 immune cell types that may have a putative causal relationship with sLAM by mediating through the regulation of BASO#, such as EGFL8, PAX8, KANSL1-AS and L3MBTL3. L3MBTL3 was implicated across several immune cell types. CONCLUSIONS: For the first time, this study leverages mediation analysis and multi-omics MR integrated with sc-eQTL data to elucidate the roles of HBC traits, immune cells, inflammatory proteins, VEGF-related proteins and immune cell-specific genes in the pathogenesis of sLAM among the European populations. - Source: PubMed
Publication date: 2026/01/27
Liu TianshuCai Yiting - Alzheimer's disease (AD) is a complex disorder with significant genetic contributions, yet only a limited number of risk loci have been conclusively identified. This research aimed to discover novel potential biomarkers for AD through multi-omics and brain pathology analysis. In this study, we investigated hippocampal molecular alterations in APP/PS1 mouse using transcriptomics and data-independent acquisition (DIA) proteomics. To further validate the involvement of differentially expressed genes (DEGs) and differentially expressed proteins (DEPs) in AD pathology and potential drug treatment, we performed an integrative analysis incorporating pathological data and protein-protein interaction networks. We identified 263 DEGs and 448 DEPs. Integrative transcriptomic and proteomic analyses revealed five co-upregulated DEGs/DEPs and one co-downregulated DEG/DEP. Comparison of KEGG pathway enrichment between the two datasets showed significant involvement in the complement and coagulation cascade, as well as neurodegeneration-multiple diseases. Furthermore, mRNA levels of LY86, CD180, and C1QB were strongly associated with amyloid-β plaque load in the AD mouse hippocampus. Protein-protein interaction analysis suggested that APP, LY86, CD180, and C1QB could serve as potential therapeutic targets for AD. The study identified three novel AD loci (EGFL8, ERMN, and CD180), with CD180 showing association with AD at both the expression and pathological levels, highlighting their potential roles in disease progression and therapeutic intervention. - Source: PubMed
Publication date: 2025/10/31
Zhao QingqingGou ChenLuo GuoshuaiDai ShujuanWang DanZhang ShifeiWang FengXu HuiHan YanbingWang Shitao