Anti-Mouse CD11b FITC 1 mg
- Known as:
- Antibody toMouse CD11b fluorecein 1 mg
- Catalog number:
- 11-0112-86
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD11b FITC 1
Related genes to: Anti-Mouse CD11b FITC 1 mg
- Gene:
- ITGAM NIH gene
- Name:
- integrin subunit alpha M
- Previous symbol:
- CR3A, CD11B
- Synonyms:
- MAC-1, CD11b
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-05
- Date modifiied:
- 2019-04-23
Related products to: Anti-Mouse CD11b FITC 1 mg
Related articles to: Anti-Mouse CD11b FITC 1 mg
- Postoperative neurocognitive disorder (PND) is a clinically important complication in older surgical patients. Microglial inflammatory activation is frequently accompanied by altered cellular metabolism, but whether esketamine-associated neuroprotection is accompanied by bioenergetic changes in hippocampal CD11b-enriched cell fractions remains incompletely understood. - Source: PubMed
Publication date: 2026/08/25
Liu DiLi GuangchunHuang HuiYang YongJiang FeiZhang Yue - The core pathological features of Alzheimer's disease (AD) include Aβ plaques and neurofibrillary tangles, which collectively drive the neurodegenerative process. Meanwhile, the phagocytic function of microglia plays a dual role in AD: it attempts to clear pathological proteins such as Aβ, but its chronic activation may also exacerbate neuroinflammation and synaptic damage. This study integrated microarray data from AD cohorts in the Gene Expression Omnibus (GEO) database. Through differential expression analysis, protein-protein interaction network construction, and three machine learning algorithms (Least Absolute Shrinkage and Selection Operator, Support Vector Machine-Recursive Feature Elimination, and Extreme Gradient Boosting), key microglial phagocytosis-related signature genes were identified. Diagnostic models were subsequently developed and validated, with further investigation of immune infiltration patterns, regulatory networks, and molecular subtypes. Based on comprehensive analysis, this study identified five core signature genes (HLA-DPA1, IL4R, ITGAM, SPP1, TNFRSF1B) that form a highly accurate diagnostic model validated in independent cohorts. Immune infiltration analysis revealed significant increases in neutrophils and M2 macrophages in AD brains, with these genes showing strong correlations with immune cell abundance. The study further identified two molecular subtypes with distinct immune features, constructed regulatory networks, and predicted potential therapeutics including Tamibarotene. By integrating transcriptomics and machine learning, this study identifies key molecular features of microglial phagocytosis in AD, providing a novel diagnostic framework and insights into the immune mechanisms of the disease. - Source: PubMed
Chang HuiminLiu YunYang XiaojunHan Yanqing - Systemic lupus erythematosus (SLE) is a complex autoimmune disease with a strong genetic component, and lupus nephritis (LN) represents one of its most common and severe organ-specific manifestations. This review synthesises current evidence on the genetic architecture of SLE and LN, with a particular focus on identifying shared and distinct genetic susceptibility loci and highlighting knowledge and data gaps in highly burdened African populations. Across studies, most risk loci, including , , , , , , , , and , converge on key immune pathways such as antigen presentation, type I IFN signalling, B-cell activation, and immune complex clearance. The findings support a substantial genomic overlap between SLE and LN, with most variants contributing to systemic immune dysregulation rather than kidney-specific susceptibility. A limited number of loci, including , , and , have been implicated in renal involvement, while G1/G2 risk variants are associated with renal disease progression and adverse kidney outcomes among individuals of African ancestry. Despite these advances, relatively few loci have been definitively linked to LN independent of SLE, reflecting both biological overlap and limitations in study design. Moreover, the existing literature is heavily skewed toward European, Asian, and admixed populations, with minimal representation of continental African cohorts. Given the high genetic diversity and disproportionate disease burden in African populations, this represents a critical knowledge gap. Improved inclusion of diverse populations, coupled with high-resolution genomic and functional studies, will be essential to refine causal variant identification and enhance understanding of disease mechanisms. Ultimately, insights into population-specific genetic risk may enable earlier identification of high-risk individuals and support the development of precision medicine strategies for SLE, specifically LN. - Source: PubMed
Publication date: 2026/08/18
Obadic Bianca GKatsukunya Jonathan NDavidson BiancaJones Erika S WHodkinson BridgetFreercks RobertDandara ColletMnika Khuthala - Atherosclerotic cardiovascular disease (ASCVD), including coronary heart disease (CHD), ischemic stroke (IS), and peripheral artery disease (PAD), represents a growing global health burden. Integrins have emerged as potential biomarkers and therapeutic targets. This study aimed to explore the role of integrins as biomarkers for ASCVD and to identify potential drug targets. A total of 33,210 UK Biobank participants were included. Cox proportional hazards models were used to assess associations between circulating integrin levels and ASCVD and its subtypes. Mendelian randomization and colocalization analyses were performed to investigate potential causal relationships and shared genetic variants underlying integrin levels and disease risk. During a median follow-up of 14.04 years, 2468 participants developed ASCVD. In subtype-specific analyses, 1541 CHD events, 1050 IS events, and 590 PAD events were identified. In observational analyses, ITGA11, ITGA2, ITGAM, ITGAV, ITGB1 and ITGB2 were associated with lower ASCVD risk, whereas ITGA5 and ITGBL1 were associated with higher risk. For ASCVD mortality, ITGA11, ITGAM, ITGAV, and ITGB2 showed protective associations, while ITGAX and ITGB6 were linked to increased risk. Sex-stratified analyses revealed distinct patterns, including male-specific risk associations for ITGAX and ITGBL1 and a female-specific protective association for ITGB2. Mendelian randomization supported causal associations for five integrins, with ITGA11 showing consistency with observational findings. Colocalization analysis suggested shared causal variants between ITGAV and both CHD and IS. This study provides both observational and genetic evidence for the critical role of integrins in ASCVD, implicating their potential for assessing disease risk and serving as candidate therapeutic targets. - Source: PubMed
Publication date: 2026/08/15
Niu MengyingFeng YuyaoShu KeqiangYang YixuanChen JunyeLai ZhichaoLiu BaoPeng Bin - Microgliosis and severe coagulation, including fibrinogen deposition, are features of both experimental and human cerebral malaria (CM), a lethal disease. Vascular-associated microglia migrate to coagulated cerebral vessels containing inflammatory monocytes and T cells in experimental CM. We previously showed that microglial depletion exacerbates coagulation and disease severity, including hypothermia, while anticoagulant treatment reduces microgliosis and prevents mortality. These data suggest an overall protective effect of microglia on eCM, and indicate a link between microgliosis, hypothermia, and coagulation. Therefore, mechanisms of migration and activation of microglia, T cells, and monocytes were studied in relation to the role of fibrin(ogen) in eCM. - Source: PubMed
Publication date: 2026/07/24
Domingo Nadia DSolomon Olivia DVillarreal PaulaAussenac FlorentinVanegas DifernandoEndrino Mark JosephMendiola Andrew SPuebla-Clark LucindaGbedande KomiCardona Astrid EAkassoglou KaterinaFlick Matthew JVargas GracieStephens Robin