CD11b (Mac-1) Antibody
- Known as:
- CD11b (Mac-1) Antibody
- Catalog number:
- MAB555C
- Product Quantity:
- 0.5 ml
- Category:
- -
- Supplier:
- INNOVEX
- Gene target:
- CD11b (Mac-1) Antibody
Related genes to: CD11b (Mac-1) Antibody
- 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: CD11b (Mac-1) Antibody
Related articles to: CD11b (Mac-1) Antibody
- Triple-negative breast cancer (TNBC) shows marked intratumoral heterogeneity and variable responses to neoadjuvant chemotherapy (NAC), but the cellular determinants of treatment response remain incompletely defined. - Source: PubMed
Publication date: 2026/08/19
Gao MenglongLiu ZhenXi LiliDuan HongliangGuo Jingjing - Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality worldwide. Although immunotherapy has improved outcomes for a subset of patients, its limited efficacy in many cases highlights the need for a more comprehensive understanding of the CRC immune microenvironment. This study aimed to characterize the molecular landscape of the CRC immune microenvironment using an integrated multi-omics approach and to identify candidate regulatory molecules associated with immune remodelling. - Source: PubMed
Zeng HongweiLin LiewenChen YumeiXia LigangTang DongeDai YongZhang Wei - 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