Anti-Human CD11b PE 25 tests
- Known as:
- Antibody toHuman CD11b PE 25 tests
- Catalog number:
- 12-0118-41
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD11b 25 tests
Related genes to: Anti-Human CD11b PE 25 tests
- 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-Human CD11b PE 25 tests
Related articles to: Anti-Human CD11b PE 25 tests
- 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 - While the pro-inflammatory M4 macrophage phenotype contributes to cardiovascular pathogenesis, its specific involvement in chronic post myocardial infarction (MI) remodeling and responsiveness to different exercise modalities remain unexplored. We hypothesized that high-intensity interval training (HIIT) confers enhanced cardioprotection compared to moderate-intensity continuous training (MICT) by mitigating M4 macrophage polarization. - Source: PubMed
Publication date: 2026/07/24
Dun YaoshanZhang HaonanGan KeyuGao YuejiaZhao YueLong YuqiongChen ZixinYou BaiyangLiu Suixin - The Zika virus (ZIKV) infection has shown significant neurodevelopmental and neurological abnormalities. However, the molecular mechanisms of ZIKV-induced neuroinflammation are poorly understood. In the current study, an integrative approach of bioinformatics analysis was used to identify the molecular targets involved in the ZIKV infection. Microarray data sets consisting of 65 samples (35 ZIKV-positive and 30 controls) from the Gene Expression Omnibus (GEO) database were used for the study. The differentially expressed genes (DEGs) analysis revealed 1,268 differentially expressed genes, of which 505 genes were up-regulated, while 763 genes were found to be down-regulated. The analysis using the weighted gene co-expression network analysis (WGCNA) revealed two modules that showed significant correlation with the ZIKV-positive samples. A total of 535 overlapping genes were used for further analysis. The protein-protein interaction (PPI) network analysis revealed ten hub genes: ITGAM, CD86, PTPRC, FCGR3A, ITGB2, TNF, ITGAX, CSF1R, CCR5, and CD4. This study suggests that the immune response plays an important role in the ZIKV infection. The study also revealed a significant enrichment of genes associated with neurogenesis, synaptic organization, axon guidance, immune response and amyloid beta binding by performing gene ontology (GO) analysis. This data potentially indicates that ZIKV infection can modulate these key hub genes to cause neuroinflammation. In addition, the study also revealed that the ZIKV infection can regulate various transcription factors and microRNAs that regulate these hub genes, indicating the complex regulatory mechanism of the ZIKV infection. Furthermore, the study revealed that the receiver operating characteristic (ROC) curve analysis showed that these hub genes, especially CCR5, are of preliminary diagnostic potential value. The study provided new insights into the molecular mechanisms of ZIKV-induced neuroinflammation and revealed the potential biomarkers and therapeutic targets of ZIKV-induced neurological disorders. - Source: PubMed
Publication date: 2026/07/20
Zubair AkmalAli MuhammadAlkhedaide Adel Qlayel