Ask about this productRelated genes to: CD51 antibody
- Gene:
- ITGAV NIH gene
- Name:
- integrin subunit alpha V
- Previous symbol:
- VNRA, MSK8, VTNR
- Synonyms:
- CD51
- Chromosome:
- 2q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-19
- Date modifiied:
- 2016-10-05
Related products to: CD51 antibody
Related articles to: CD51 antibody
- This study explored the genetic evidence linking triglyceride-related pathways and lipid-lowering drug targets with endometriosis risk and investigated the genetic association between TG levels and EM. Using genome-wide association study (GWAS) data, a two-sample Mendelian randomization (MR) analysis was conducted, estimating the association between genetically predicted TG levels and EM risk (OR = 1.1853, 95% CI: 1.070-1.313, p = 0.0011). Seven TG-lowering drug target genes (SLC9A1, SCN3A, VEGFA, APOA1, TNF, ITGAV, BACE1) were identified. Transcriptome analysis revealed that SCN3A, BACE1, and APOA1 were significantly upregulated in EM patients compared to healthy controls. Enrichment pathway analysis showed that these genes are involved in lipid transport, localization, cell adhesion, and blood vessel development. PPARA was predicted to act as a transcription factor for five of these genes, while estrogen receptor 1 (ESR1) was predicted to regulate the majority of the others. Among the TG inhibitors examined, fibrate-related targets showed relatively broader target coverage in the present genetic analyses. These findings suggest that TG-related pathways and lipid-lowering drug targets, particularly fibrate-related targets, may be relevant to EM biology and warrant further experimental and clinical validation. - Source: PubMed
Publication date: 2026/08/13
Li YonghongHe JiananZhang YuanqingYang MinJia ZhimaoFan YidanLiu ShuyunQi Mengsha - Microglia play a key role in the pathophysiology of Alzheimer's Disease (AD) and their increased heterogeneity likely affects disease progression. We previously identified distinct microglial signatures that were enriched in AD donors and associated with amyloid and tau, respectively. Here we generated a snRNAseq dataset from postmortem control and AD cases and analyzed alterations in cell-cell communication pathways that might be relevant to AD pathophysiology. One signaling pathway perturbed in AD cases involved SPP1, and while this pathway was also present in control samples, microglia-microglia SPP1 signaling was restricted to AD donors. Further analyses within microglia-microglia signaling predict AD-specific induction of GAS6-AXL signaling (from inflammatory and ribosomal microglia), and SPP1-ITGAV/ITGB5 signaling (from disease-associated and inflammatory microglia, among others). Together, these findings might in part explain the increased microglia phagocytic profile described in AD. RNAscope confirmed enrichment of SPP1 expressing microglia near amyloid plaques in AD brain tissue samples. These data indicate altered cellular communications between microglia in the AD brain. - Source: PubMed
Kotah Janssen MLima Marina TrombettaDragt Esmée CVoulgaroglou AsimeniaBrouwer NieskeHoltman Inge RKooistra Susanne MEggen Bart J L - BackgroundMesenchymal stem cell (MSC)-derived endothelial-like cells exhibit enhanced angiogenic potential compared with undifferentiated MSCs. However, the role of N6-methyladenosine (m6A) RNA modification in MSC endothelial differentiation remains unclear.MethodsHuman bone marrow-derived MSCs were isolated and induced toward an endothelial phenotype using cytokine-enriched medium. Endothelial differentiation was evaluated using flow cytometry, western blotting, immunofluorescence staining, tube formation assays, and Dil-Ac-LDL uptake assays. MeRIP-seq and RNA-seq were performed to profile transcriptome-wide m6A methylation and gene expression changes. Bioinformatics analyses, including GO enrichment, KEGG pathway analysis, and protein-protein interaction (PPI) network construction, were conducted to identify key regulatory genes and pathways.ResultsFollowing induction, MSCs exhibited endothelial characteristics, including increased expression of CD31 and CD34, enhanced tube formation ability, and increased Dil-Ac-LDL uptake. Transcriptome-wide analysis identified 16,355 differentially methylated peaks and 2,732 differentially expressed genes, including 1,204 differentially methylated and expressed genes (DMEGs). Functional enrichment analysis revealed that DMEGs were mainly associated with extracellular matrix organization, endothelial differentiation, and cell adhesion. PPI network analysis identified a highly interconnected module, and integrin family genes (ITGA1, ITGAV, ITGA11, ITGB5) and ADAMTS2 were identified as key hub genes.ConclusionsThis study provides a transcriptome-wide landscape of m6A methylation during endothelial differentiation of BM-MSCs and identifies key regulatory pathways and hub genes potentially involved in this process. These findings suggest that m6A-mediated epitranscriptomic regulation plays an important role in MSC endothelial differentiation and angiogenesis. - Source: PubMed
Publication date: 2026/07/25
Yao ZipingZhang BihuiZou YinghuaTong XiaoqiangYan ZiguangNiu GuochenLi YuanYang Min - Frailty is a well-established clinical risk factor for dementia, but its underlying mechanisms remain poorly defined. We aimed to investigate whether proteomic signatures and individual proteins linked to frailty could predict and characterize the association between frailty and dementia. - Source: PubMed
Publication date: 2026/07/17
Zhang XiruHuang QingmeiHuang JielinZhang PeidongFeng XinLi ZhihaoRaper Daniel M SMao Chen - Most plasma proteomic studies in Alzheimer's disease (AD) compare cases and controls cross-sectionally, leaving unresolved which AD-associated proteins mark diagnostic states and which are linked to disease progression. Using longitudinal SomaScan profiling from the Global Neurodegeneration Proteomics Consortium (13,449 participants, 17,269 samples, 7,362 aptamers), we separated baseline AD differences from AD-specific change over time. Linear mixed-effects models requiring concordant baseline and AD-by-time effects defined a 30-protein signature. We prioritized proteins across five evidence domains: clinical progression, AD biomarker alignment, cerebrospinal fluid concordance, independent prospective replication in UK Biobank and genetic support from Mendelian randomization and rare-variant burden. Thirteen proteins were supported in two or more domains and six in three. EDA2R, HPGDS, ITGAV and CLEC3B converged across clinical, biomarker and prospective evidence. Signature proteins aligned more strongly with tau and neuronal-injury markers than with A42/40. ANTXR1 showed direction-concordant plasma pQTL Mendelian randomization and nominal rare-variant burden signals, supporting its prioritization within the longitudinal AD signature. By distinguishing diagnostic-state markers from progression-linked changes, this longitudinal, multi-domain approach prioritizes proteins for validation as markers of AD progression and for mechanistic and therapeutic follow-up. - Source: PubMed
Publication date: 2026/07/10
Park JunyoungLe Guen YannPeña-Tauber AndrésGreicius Michael D