CD11b
- Known as:
- CD11b
- Catalog number:
- 10-211-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD11b
Related genes to: CD11b
- 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
Related articles to: CD11b
- To identify immune-related molecular targets in polycystic ovary syndrome (PCOS) and evaluate the role of integrin beta-2 (ITGB2) and the potential modulation by rutin. - Source: PubMed
Publication date: 2026/08/10
Yi PengCao YingZhou YanruMao SuqingFu Xianghong - This study aims to investigate the relationship between serum levels of integrin alpha M (ITGAM), CX3CR1, and inducible nitric oxide synthase (iNOS) (microglial activation markers) and the development and severity of postoperative cognitive dysfunction (POCD) in elderly patients undergoing cardiopulmonary bypass (CPB). This observational study included 246 patients aged 60-80 years undergoing CPB. Serum levels of ITGAM, CX3CR1, and iNOS were measured preoperatively and early postoperatively (within 6 hours after surgery). Cognitive function was assessed preoperatively and 7 days postoperatively using the Montreal Cognitive Assessment and a comprehensive battery of neuropsychological tests. Receiver operating characteristic (ROC) analysis was employed to evaluate the predictive value of the biomarkers. Among the participants, 94 patients developed POCD, while 152 did not. Patients with POCD exhibited significantly higher early postoperative serum levels of ITGAM, CX3CR1, and iNOS compared to non-POCD patients. ROC analysis indicated moderate predictive accuracy for each biomarker individually (AUC: ITGAM = 0.78, CX3CR1 = 0.72, iNOS = 0.74), with a notable improvement when biomarkers were combined (AUC = 0.87). MoCA scores at 7 days postoperatively showed significant negative correlations with biomarker levels, while positive correlations were observed between biomarker levels and serum neuron-specific enolase, a marker of neuronal injury. Elevated postoperative serum levels of ITGAM, CX3CR1, and iNOS are strongly associated with the development and severity of POCD in elderly patients undergoing CPB. These biomarkers show promise as predictive tools for early identification of at-risk patients and may represent potential therapeutic targets for mitigating POCD by modulating microglial activation. - Source: PubMed
Publication date: 2026/07/31
Du ShengyanWei JinChen Yao - Familial adenomatous polyposis (FAP) is a hereditary condition that almost invariably leads to colorectal cancer. While inactivation is well established as a late event in the adenoma-to-carcinoma sequence, its functional role during the early stage of colorectal polyp development remains unclear. - Source: PubMed
Publication date: 2026/07/13
Chan QixiaLiang WeiFlisikowska TatianaEbner FriederikeFlisikowski Krzysztof - Colorectal cancer liver metastasis (CRLM) represents the leading cause of mortality in colorectal cancer (CRC). However, the molecular mechanisms enabling metastatic adaptation within the hepatic microenvironment remain unclear. We integrated single-cell RNA sequencing, spatial transcriptomics, and bulk transcriptomic data from CRC patients to characterize the immunometabolic landscape of CRLM. Machine learning models were used to identify key regulators, and functional assays were conducted to validate their biological roles. Nine major cell populations were delineated within CRLM, revealing enrichment of myeloid-derived suppressor cells and depletion of fibroblasts in metastatic lesions. Malignant cells displayed pronounced chromosomal instability and metabolic reprogramming. Among candidate regulators, PIGT emerged as a pivotal node linking metabolic adaptation and immune suppression. PIGT expression increased progressively from primary to metastatic states and was associated with immunosuppressive MIF, SPP1, and TGFβ signaling. Spatial transcriptomics demonstrated colocalization of PIGT-high tumor cells with ITGAM⁺ and CD163⁺ macrophages. Functionally, PIGT knockdown significantly suppressed cell invasion, migration, proliferation, and wound healing in vitro. Conversely, transcriptomic and qPCR analyses showed that PIGT-low tumors exhibited higher expression of inflammatory genes enriched in the IL-17 and TNF signaling pathways. Our integrative multi-omics and experimental analyses identify PIGT as a central regulator bridging tumor metabolism and immune modulation in CRLM. These findings highlight PIGT as a promising prognostic biomarker and potential therapeutic target for metastatic colorectal cancer. - Source: PubMed
Publication date: 2026/07/28
Yan MengzhuLi YixingLiu YunPeng LilanZhou Haibo - In this study, we modeled gene expression profile data from Acute Myeloid Leukemia (AML) and healthy cases. At first, the GEO-GSE9476 dataset was processed, and a total of 341 genes were identified as differentially expressed genes (DEGs) in patients, and 599 DEGs in healthy individuals. Gene Ontology and pathway analysis on DEGs led to the identification of 5 Transcription Factors for patients and 3 for healthy cases. Analysis of the respective metabolic pathways revealed a common region in the metabolic pathway between AML and Tuberculosis (TB) that confirmed the validity of our procedure due to the consistency with similar reports. Upon PPI network analysis, Hub genes and three modules containing 41 up-regulated and down-regulated genes in AML patients were identified. Survival analysis on these genes results in reducing the number of identified effective genes into 3 upregulated (ITGAM, ITGAL and CD163) and 5 downregulated genes (MCM2, MCM3, RFC4, RFC5 and FEN1). Finally, drug sensitivity analysis was performed on these genes demonstrating complexity in drug-resistance due to the pattern of gene expression. This knowledge could potentially enable personalized treatment approaches based on individual patient responses due to the epigenetics and life style which affect gene expression pattern. - Source: PubMed
Publication date: 2026/07/27
Aghajan BehnamGhaemi Mohammad RezaMosammam Ali MHeshmati EmranKhalifeh Khosrow