Ask about this productRelated genes to: EPSTI1 Blocking Peptide
- Gene:
- EPSTI1 NIH gene
- Name:
- epithelial stromal interaction 1
- Previous symbol:
- -
- Synonyms:
- BRESI1, MGC29634
- Chromosome:
- 13q14.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-05
- Date modifiied:
- 2016-10-05
Related products to: EPSTI1 Blocking Peptide
Related articles to: EPSTI1 Blocking Peptide
- Nervous necrosis virus (NNV) is a major viral pathogen that causes viral nervous necrosis in a wide range of fish species and poses a serious threat to global aquaculture. However, the antiviral responses of mandarin fish (Siniperca chuatsi) to NNV infection remain poorly understood. In this study, we investigated host antiviral responses using Chinese perch brain (CPB) cell line and in vivo infection models. Transcriptome sequencing of red-spotted grouper nervous necrosis virus (RGNNV)-infected CPB cells revealed extensive transcriptional reprogramming, with numerous interferon-stimulated genes (ISGs) significantly upregulated. Comparative transcriptomic analysis across multiple teleost species identified a conserved set of ISGs induced during RGNNV infection, including CMPK2, RSAD2, DHX58, IRF3, and EPSTI1. Among these genes, CMPK2 showed strong induction in both infected CPB cells and mandarin fish brain tissues. Functional assays further demonstrated that CMPK2 overexpression significantly inhibited RGNNV replication in CPB cells and was accompanied by increased expression of several interferon-related genes. These findings provide the first functional evidence that CMPK2 restricts RGNNV infection in S. chuatsi. Our study highlights a conserved interferon-responsive antiviral module in teleost fish and identifies CMPK2 as a potential antiviral effector involved in host defense against RGNNV infection. - Source: PubMed
Publication date: 2026/07/17
Qin ChanxiaHuang JinlongLi LinmiaoLiang YingFeng HaiqingJiang HaiyingChen JiarongChen JinpingOu WeihaoYu Yepin - This study aimed to develop a robust transcriptomic diagnostic signature for Sjögren's disease (SjD; formerly Sjögren's syndrome) and elucidate key biomarker functions by integrating machine learning and single-cell analysis. - Source: PubMed
Publication date: 2026/07/10
Li JianbinLi RenheWang WenwenGesang YuzhenLiu Wei - Human immunodeficiency virus (HIV) is a lentivirus belonging to the retrovirus subclass. HIV specifically targets and infects human CD4 + T lymphocytes, and T cell exhaustion (TEX) plays an important role in disease progression. However, the specific molecular mechanisms have not been fully elucidated. In this study, we explored the potential mechanisms by analyzing transcriptomic data and TEX-related genes, and screened novel markers closely associated with HIV neutralization and T cell function to assess TEX severity and guide precise immunotherapy. - Source: PubMed
Publication date: 2026/07/09
Zhang YanYong YutaoLiu WenqingHu DieJi ChengjieMa Chunyu - The dengue virus (DENV) can cause various clinical syndromes and organ damage, known as dengue fever, with the probability of developing severe dengue. However, the underlying mechanisms of host response against DENV infection remain unclear, and there is still no specific medicine for dengue fever. In the present study, we revealed the transcriptomic features of the host factor in patients with DENV infection and explored potential therapeutic medication. - Source: PubMed
Publication date: 2026/04/30
Liu ChengxinYu XinboChen JiafanZhong MingYe BeiWang KaiJiang YongLi GengZhan Shaofeng - Spontaneous ovarian hyperstimulation syndrome (OHSS) is closely associated with follicle stimulating hormone receptor (FSHR) functional mutations. We observed that estrildid finches naturally carry the gain-of-function FSHR p.Thr449Ala mutation found in humans, yet do not develop OHSS, thereby providing a novel and system to study aspects of OHSS prevention. Cross-species single-cell analysis revealed that macrophages, the most abundant immune cells in ovaries, play a pivotal role in OHSS progression. Macrophage depletion exacerbates the manifestations of OHSS in both birds and rats. Pharmacological activation of the G protein-coupled receptor 183 (GPR183) in ovarian macrophages, significantly alleviates OHSS symptoms. Mechanistically, GPR183 activation in macrophages maintains ovarian immune homeostasis by downregulating inflammatory factors (Interleukin 1 alpha: IL1A, Interleukin 6: IL6, Interleukin 1 beta: IL1B) and upregulating immune regulators responsive to external stimuli (sphingomyelin phosphodiesterase acid like 3A: Smpdl3a, Macrophage-expressed gene 1: Mpeg1, Epithelial stromal interaction 1: Epsti1, Unc-93 homolog B1: Unc93b1, Apolipoprotein B mRNA editing enzyme catalytic subunit 1: Apobec1). It markedly altered CD44 molecule (CD44)/Syndecan-4 (SDC4) -mediated intercellular communication between macrophages and endothelial/stromal cells, thereby modulating the ovarian microenvironment. This study identifies ovarian macrophages as a key therapeutic target for OHSS and proposes GPR183 as a novel receptor target for precision macrophage-based interventions. - Source: PubMed
Publication date: 2026/05/05
Yan XiaofeiHuang YongjieYang JiabaoMa SuLiu SongsongHuang XuanBrosius JuergenZheng HuapingYao BingChen LiLai ShanshanDeng Cheng