Ask about this productRelated genes to: SPI1 antibody
- Gene:
- SPI1 NIH gene
- Name:
- Spi-1 proto-oncogene
- Previous symbol:
- -
- Synonyms:
- PU.1, SPI-A, OF, SFPI1, SPI-1
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-04
- Date modifiied:
- 2016-10-05
Related products to: SPI1 antibody
Related articles to: SPI1 antibody
- Although the anti-inflammatory role of tumor necrosis factor alpha-induced protein 3 (TNFAIP3) in M2 macrophages has been reported, its function in subretinal fibrosis remains unclear. This study aimed to investigate the role of TNFAIP3 in M2 macrophages in subretinal fibrosis and to elucidate its mechanism. - Source: PubMed
Zhao QinGong YajunZhang LongjiChen ChiayuanLi LonghuiMa ZijianChen FeierCai ShiyinSovannkiri NeauvZhou XiaolaiLai Kunbei - In this study, we systematically analyzed the dynamic changes in chromatin accessibility and the transcriptional responses in the spleen of largemouth bass () following infection with iridovirus (LMBV) using the assay for transposase-accessible chromatin with sequencing (ATAC-seq) and transcriptome sequencing (RNA-seq). Based on post-infection survival status, largemouth bass were classified into a resistant group (SR) and a susceptible group (SS). A total of 11,317 differentially accessible regions were identified between the two groups, among which the chromatin accessibility of core promoter regions was entirely increased in the SR group, suggesting that chromatin remodeling in these regions may directly participate in the transcriptional regulation of immune-related genes. Functional enrichment analysis revealed that genes associated with differentially accessible regions were significantly enriched in immune-related pathways such as autophagy, apoptosis, Toll-like receptor signaling, and NOD-like receptor signaling. Motif analysis further identified that transcription factors significantly enriched in the SR group included CTCF and heterodimers composed of multiple members of the ETS and FOX transcription factor families. Through integrative analysis, seven transcription factors (CTCF, Spi1, ETV2::FOXI1, FOXJ2::ELF1, FOXO1::ELK1, SPIC, and FOXO1::ELF1) were found to be significantly enriched in core promoter regions. To further screen for differentially expressed genes directly regulated by chromatin accessibility changes, an overlapping analysis was performed between 629 predicted target genes and 2656 differentially expressed genes (DEGs), resulting in the identification of 71 candidate genes. Among these, three immune-related genes (, , and ) belonging to the ETS and FOX families were identified. This study reveals the dynamic chromatin accessibility landscape of largemouth bass in response to LMBV infection and demonstrates that increased chromatin accessibility in core promoter regions is closely associated with the resistant phenotype. Heterodimers of ETS and FOX family transcription factors may participate in antiviral immune responses by regulating the expression of key immune genes such as , , and , providing potential epigenetic molecular markers for disease resistance breeding in fish. - Source: PubMed
Publication date: 2026/05/05
Sun HuiHua JixiangTao YifanLu SiqiWang WenDong YalunZhang LinbingHe JixiangHe JieQiang Jun - Salmonella enterica serovar Enteritidis is a principal cause of foodborne and invasive infections worldwide. Ciprofloxacin continues to be a primary treatment for invasive cases, but resistance has emerged in several regions. In Morocco, although S. Enteritidis is frequently isolated, no ciprofloxacin-resistant isolates have been reported to date. - Source: PubMed
Publication date: 2026/04/30
Elmourabit HajarKarraouane BouchraBouchrif BrahimBelahrach BouchraKopprio GermánFazza OumaimaNchioua ZakariyaSoraa NabilaElmehrach Khadija - Polycystic ovary syndrome (PCOS) is associated with an increased risk of type 2 diabetes mellitus (T2DM), and the risk of PCOS increases in patients with T2DM of reproductive age. The bidirectional link between PCOS and T2DM has been confirmed through experimental and epidemiological evidence; however, the genetic factors that contribute to deeper insights into the shared pathogenesis of these two diseases remain unclear. We aimed to identify shared immune- and inflammation-related genes and pathways in PCOS and T2DM, further explore the molecular mechanisms in developing this comorbidity, and predict drugs with potential effects to develop novel therapeutic strategies. - Source: PubMed
Publication date: 2026/04/16
Liu XuemengWang YanleiBi QiuhanZhang YingWang ShuminYang PanPei JieZhu WeixiChen YijingZhang ZhiguoChen BeiliZhang QiuZhang YiJiang Tian - Microglial polarization plays a key role in the process of chronic neuropathic pain (CNP). This study aims to investigate the molecular mechanism by which the transcription factor SPI1 mediates microglial polarization and participates in CNP by regulating NOD-like receptor C4 (NLRC4) expression. The GSE124272 dataset (blood samples of 8 intervertebral disc degeneration patients and 8 controls) was obtained from the GEO database, and the differentially expressed genes (DEGs) were screened. The intersection of DEGs with neuropathic pain related genes in GeneCards was taken. Support vector machine-recursive feature elimination algorithm was used to identify hub genes. Human microglia (HMC3) were stimulated with lipopolysaccharides (LPS) to construct an inflammation model. qRT-PCR, western blot, ELISA, flow cytometry, and reactive oxygen species (ROS) detection were used to evaluate gene expression, inflammatory factor levels, cell polarization, and ROS levels. ChIP and dual-luciferase reporter assay were used to verify the binding of SPI1 to NLRC4 promoter and its transcriptional regulation. A rat model of chronic constriction injury (CCI) was established to evaluate the effect of shNLRC4 on CNP in vivo. After screening and machine learning, NLRC4 was one of the five hub genes, and its expression was significantly upregulated in LPS-induced HMC3 cells. NLRC4 knockdown inhibited LPS-induced M1 polarization, the release of pro-inflammatory factors, ROS production, and the expression of microglia activation marker Iba1, while promoted the expression of M2 polarization markers. SPI1 could directly bind to the NLRC4 promoter to increase its transcription. Overexpression of NLRC4 reversed the inhibitory effect of SPI1 knockdown on LPS-induced microglial activation and inflammation. In CCI rat model, knocking down NLRC4 significantly alleviated mechanical and thermal hyperalgesia, and reduced the levels of NLRC4 and inflammatory factors (TNF-α, IL-1β, and IL-6) in the spinal cord tissues. SPI1 acts as a transcription factor to directly increase NLRC4 transcription, thereby promoting microglial activation and neuroinflammatoion, and ultimately accelerating the development of CNP. - Source: PubMed
Publication date: 2026/05/07
Qin LiyuanFu QiangWang XiaolingLi Quanbo