Anti-Mouse CD11b FITC 500 ug
- Known as:
- Antibody toMouse CD11b fluorecein 500 ug
- Catalog number:
- 11-0112-85
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD11b FITC 500
Related genes to: Anti-Mouse CD11b FITC 500 ug
- 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 500 ug
Related articles to: Anti-Mouse CD11b FITC 500 ug
- Neutrophil extracellular traps (NETs) are increasingly recognized as critical mediators in vascular inflammation and remodeling, yet their molecular mechanisms in idiopathic pulmonary arterial hypertension (IPAH) pathogenesis remain largely unexplored. This study employed integrated bioinformatics approaches and experimental validation to identify NETs-related biomarkers in IPAH. We performed weighted gene co-expression network analysis (WGCNA) on merged transcriptomic datasets (GSE117261 and GSE48149, comprising 40 IPAH and 34 control samples), identifying a blue module significantly correlated with IPAH status. By intersecting module genes with 69 known NETs-related genes, we obtained 19 differentially expressed NETs-related genes (DE-NRGs) enriched in neutrophil degranulation, interleukin-6 regulation, and NETs formation pathways. Three complementary machine learning algorithms converged on five key biomarkers: CSF3R, MGAM, ITGAM, TLR8 (downregulated), and SELP (upregulated). These biomarkers demonstrated strong diagnostic performance in an independent validation cohort, with an area under the curve greater than 0.8. Immune infiltration analysis revealed significantly decreased neutrophils, macrophages, and myeloid-derived suppressor cells in IPAH patients. Single-cell RNA sequencing validated cell-type-specific expression patterns, with CSF3R predominantly in neutrophils, ITGAM/TLR8 in macrophages, and SELP in endothelial cells. Critically, monocrotaline-induced rat pulmonary arterial hypertension model confirmed significant downregulation of MGAM, CSF3R and ITGAM at protein levels. Our findings establish a NETs-related molecular signature for IPAH diagnosis and reveal impaired neutrophil function as a key pathogenic mechanism in IPAH, providing novel molecular targets for therapeutic intervention and risk stratification. - Source: PubMed
Publication date: 2026/05/04
Ma QiliangYou Shengban - Acute ischaemic stroke (AIS) remains a leading cause of death and disability. This exploratory study integrated transcriptomic and metabolomic analyses to identify candidate hub genes and metabolites associated with AIS and to provide preliminary insights into its molecular mechanisms and potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/15
Zhang JiayanZhou XinHe Dian - Microglia are increasingly recognized as key regulators of neural circuit development and putative contributors to the pathophysiology of neuropsychiatric disorders such as schizophrenia (SCZ). However, the functional impact of SCZ-associated genes in microglia remains largely unexplored. Here, we performed an arrayed CRISPR targeting screen of 30 SCZ-associated genes predicted to be differentially expressed in human microglia-like cells. Target genes were prioritized based on post-mortem transcriptomic relevance and predicted ontology-based roles in phagocytosis pathways. We quantified phagocytic activity and morphological changes following gene targeting using high-content confocal imaging. Key targets, including CYFIP1, MSR1, TREM2, SYK, ITGB2, ITGAM, and IRF8, modulated phagocytosis and altered morphological properties consistent with activation states, validating their functional roles in microglia. To elucidate transcriptional impact, we further applied a multiplexed RNA sequencing platform across gene targets. These analyses revealed gene-specific transcriptional signatures, implicating divergent pathways related to phagocytic, activation, cytoskeletal, and lysosomal function. Together, these findings demonstrate the utility of CRISPR-based functional genomics in characterizing microglia function and identifying new target genes and mechanisms that may underlie their contributions to SCZ pathophysiology. - Source: PubMed
Publication date: 2026/04/16
Horng Joy EMcCrea Liam TBatorsky Rebecca EBowen Joshua JBoschian CamillaSong YoonjaePerlis Roy HSheridan Steven D - Parenteral nutrition-associated liver disease (PNALD) is the most severe complication of long-term parenteral nutrition. It has a high incidence rate and can cause serious harm to patient health. Biomarkers and metabolites associated with PNALD are poorly characterized. This study aimed to identify biomarkers and key metabolites associated with PNALD progression. - Source: PubMed
Publication date: 2026/03/31
Huang YongYang XiuzhiLiu DandanQin SonghanCao YifanXie MingWang Jiwei - Spinal root injuries trigger longitudinal spinal cord damage, leading to motoneuron degeneration, gliosis, and synaptic loss. Glutamate excitotoxicity through NMDA and AMPA receptor overstimulation is a key driver of this pathology, highlighting NMDA receptor antagonists as potential neuroprotective agents. Here, we evaluated the effects of memantine after unilateral L4-L6 ventral root crush (VRC) in adult C57BL/6JUnib mice. Animals received daily oral gavage of vehicle or memantine (30, 45, or 60 mg/kg) for 14 days. At 28 days post-injury, histological analysis showed that memantine reduced astrogliosis and microglial activation, while enhancing motoneuron survival (most pronounced at 45 mg/kg, p < 0.001) and preserving synaptic coverage (p < 0.01), without significant changes in VGLUT-1 or GAD65 expression. Consistently, RT-qPCR analysis revealed early upregulation of inflammatory markers (Ccr2, Itgam) in vehicle-treated mice, which was attenuated by memantine at 3-7 days post-injury (p < 0.05). These findings indicate that memantine confers neuroprotection in VRC by modulating inflammatory gene expression, mitigating gliosis, and promoting motoneuron survival, supporting its therapeutic potential in spinal cord injuries. - Source: PubMed
Leão Arthur Ventura MartinsBíscaro Gabriel Gasparde Oliveira Alexandre Leite RodriguesCartarozzi Luciana Politti