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
- 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 Olivera Alexandre Leite RodriguesCartarozzi Luciana Politti - Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies because of its typically late diagnosis and limited treatment options, with surgical resection being the primary intervention. Emerging studies have consistently reported associations between PDAC and metabolic dysfunctions, including obesity, chronic inflammation, and diabetes. In this study, we investigated the molecular interplay between PDAC-associated genes and metabolic disorder pathways. - Source: PubMed
Nath DipanwitaDitchfield CaitlinPrice JoshuaSivakumar ShivanJones Simon WAcharjee Animesh - Several studies indicated that type 2 diabetes (T2D) patients have a higher risk on the development and progression of myocardial infarction (MI) than non-diabetic patients. The management of MI with T2D as comorbidity may become much more complicated compare to the management of MI alone due to several factors including conflicting therapies arises from one-drug for one-disease strategy, since some T2D-drugs may conflict with MI and vice-versa. However, so far, no researcher yet rigorously explored key molecular signatures and their mechanisms associated with both diseases for exploring candidate therapies as the common/unique treatment for both diseases during their co-existence. - Source: PubMed
Publication date: 2026/03/27
Ahmmed ReazAntu Umme SamiaNoor TasfiaFaysal Md FahimAkter Mst TahminaNesa MeherunMollah Md Nurul Haque