ICSBP EMSA Kit
- Known as:
- ICSBP EMSA Kit
- Catalog number:
- AY1198
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- ICSBP EMSA Kit
Related genes to: ICSBP EMSA Kit
- Gene:
- IRF8 NIH gene
- Name:
- interferon regulatory factor 8
- Previous symbol:
- ICSBP1
- Synonyms:
- IRF-8, ICSBP
- Chromosome:
- 16q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-09
- Date modifiied:
- 2019-04-23
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- 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 - Rodents are widely used in immunology but do not always recapitulate human immune functions. The tree shrew (Tupaia belangeri) is phylogenetically closer to primates than rodents and may help bridge this gap, yet its immune system has not been comprehensively characterised at single-cell resolution. Here, we present a single-cell transcriptomic atlas of the tree shrew immune system, profiling 39 cell types across 12 tissues. We uncover human-like tonsillar structures and two transcriptionally distinct splenic macrophage subsets: an NR1H3 immunoregulatory subset and an IRF8 pro-inflammatory subset. During acute Epstein-Barr virus infection, NR1H3 macrophages undergo pronounced inflammatory reprogramming and emerge as a major intercellular signalling hub. Cross-species integration of single-cell datasets from seven vertebrate species indicates that NR1H3 macrophage gene programmes are evolutionarily conserved. Functional analyses further support a shared anti-inflammatory programme mediated by NR1H3-dependent suppression of the non-canonical NF-κB pathway in both tree shrew and human macrophages. Together, these findings provide a reference resource for tree shrew immunology and support the tree shrew as a complementary model alongside rodent and primate systems. - Source: PubMed
Publication date: 2026/04/09
Xia WeiShi NanLai YongjingFeng YiweiLuo ZhenqiuChen FangfangHuang ZongjianXie MaoLi JingyuBin XiangYi XiangHe MinLi ChaoqianHe GuangyaoTang Anzhou - Innate immune and interferon-induced responses to in vivo nasal infection with rhinovirus (RV)16 in healthy subjects are accelerated by low-dose dietary supplementation with carrot-derived pectic polysaccharide rhamnogalacturonan-I (cRG-I), together with reduced duration and severity of symptoms. We aimed to further identify temporal mRNA responses by nasal epithelial cells (NEC) after RV16 infection, and to assess the effect of cRG-I supplementation. NECs were obtained prior to (day(d)-55) and after 8-weeks (d-1) of supplementation (0, 0.3, 1.5 g/d), and on d3, d6, d9 and d13 after exposure to 100 TCID50 RV16. Transcriptome data were generated and analysed with the R2: Genomics Analysis and Visualization platform (https://r2.amc.nl). RV16 infection reduced expression of genes related to oxidative phosphorylation (d3), induced gene expression by interferon (d6-9), and reduced expression of cilia-related genes (d13). cRG-I changed these responses. At low-dose, gene expression of important transcription factors and effector molecules (IRF4, IRF8, RFX3, IL-1B, CASP1) was enhanced markedly earlier (d3-6). At high-dose, cRG-I induced expression of inflammasome-related genes already after 8-weeks supplementation. cRG-I, in a dose-dependent manner, significantly affected the sequence and intensity of genes that regulate pathways involved in anti-viral responses and epithelial repair. This may underlie the reduced duration and severity of symptoms. - Source: PubMed
Mol JasperVolckmann RichardRavi AbilashRavanetti LaraCalame WimMcKay SueAlbers RuudKoster JanLutter René - High-density lipoproteins (HDLs) and their main protein, apolipoprotein A-I (apoA-I), are considered immunomodulators of the vascular wall. However, the precise mechanisms are incompletely understood. Using intravital microscopy, flow cytometry, experimental ex vivo models, and bulk RNA sequencing of cultured macrophages, this study reveals the immunomodulatory capacity of apoA-I, which is validated in representative inflammatory models. Intravital imaging in mice shows specific uptake of intravenously injected, lipid-free apoA-I by dermal perivascular macrophages. Supraphysiological doses of apoA-I alter key cellular pathways, involving mammalian target of rapamycin complex 1 (mTORC1) and interferon regulatory factor 8 (IRF8), in THP-1-derived macrophages. In lipopolysaccharide (LPS)-induced skin inflammation, apoA-I pretreatment dampens the inflammatory response and reduces immune cell trafficking in and out of the skin. Moreover, apoA-I inhibits joint inflammation in a mouse model of rheumatoid arthritis (RA). Overall, apoA-I acts as an integrator of vascular-immune interactions by modulating macrophage function in the vicinity of blood vessels. These findings open avenues for HDL-targeting strategies in a broad spectrum of autoimmune disorders, including RA. - Source: PubMed
Publication date: 2026/03/31
Bisoendial RadjeshKusienicka AnnaWielscher MatthiasRoediger BenJain RohitMitchell AndrewGrau Georgesvan Olden CasperStroes ErikTas SanderVan Eck MirandaYoussef PeterCavanagh Lois LRye Kerry AnneFarlik MatthiasWeninger Wolfgang - Aortic dissection (AD), a life-threatening cardiovascular emergency, poses a significant threat to global cardiovascular health. Emerging evidence implicates programmed cell death (PCD) as a critical driver of AD pathogenesis, yet the molecular mechanisms remain poorly defined. This study systematically investigates PCD-related biomarkers in AD to identify novel therapeutic targets. - Source: PubMed
Du YukuiChang DongqingYu BofengZhang LiHe LiangWang FengxiaChang Shaoyan