ELISA Mouse , IP-10
- Known as:
- Enzyme-linked immunosorbent assay test Mouse , IP-10
- Catalog number:
- RBMS6018R
- Product Quantity:
- 96 wells (1 kit)
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- ELISA Mouse IP-10
Related genes to: ELISA Mouse , IP-10
- Gene:
- BBIP1 NIH gene
- Name:
- BBSome interacting protein 1
- Previous symbol:
- NCRNA00081
- Synonyms:
- bA348N5.3, BBIP10, BBS18
- Chromosome:
- 10q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-09-02
- Date modifiied:
- 2016-10-05
- Gene:
- CXCR3 NIH gene
- Name:
- C-X-C motif chemokine receptor 3
- Previous symbol:
- GPR9
- Synonyms:
- CKR-L2, CMKAR3, IP10-R, MigR, CD183
- Chromosome:
- Xq13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-01
- Date modifiied:
- 2016-10-05
- Gene:
- MED24 NIH gene
- Name:
- mediator complex subunit 24
- Previous symbol:
- THRAP4, CRSP4
- Synonyms:
- TRAP100, KIAA0130, DRIP100, CRSP100, MED5
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-30
- Date modifiied:
- 2016-10-05
- Gene:
- PPIAP10 NIH gene
- Name:
- peptidylprolyl isomerase A pseudogene 10
- Previous symbol:
- PPIAL2, PPIP10
- Synonyms:
- CRP
- Chromosome:
- 20q13.2
- Locus Type:
- pseudogene
- Date approved:
- 1998-10-12
- Date modifiied:
- 2017-08-21
- Gene:
- PRPF40A NIH gene
- Name:
- pre-mRNA processing factor 40 homolog A
- Previous symbol:
- FNBP3
- Synonyms:
- FLJ20585, FBP11, HYPA, NY-REN-6, HIP10, FBP-11, FLAF1, Prp40
- Chromosome:
- 2q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-28
- Date modifiied:
- 2018-11-19
Related products to: ELISA Mouse , IP-10
Related articles to: ELISA Mouse , IP-10
- Heart failure is a syndrome where immune cells play a crucial role in its development and progression. Although the recruitment of T cells driven by C-X-C motif chemokine receptor 3 activation has been reported, the specific contribution of C-X-C motif chemokine ligand 10 (CXCL10), one of its ligands, remains unclear. Here, we investigate the role of CXCL10 in pressure overload-induced cardiac remodeling, both in the early phase of remodeling and during heart failure progression. We used the transverse aortic constriction model to induce pressure overload in mice and assessed the role of CXCL10 in cardiac remodeling. Our study shows that the genetic deletion of CXCL10 attenuates early cardiac remodeling and with more pronounced effects 6 weeks after transverse aortic constriction, as CXCL10-/- mice exhibit reduced hypertrophy and fibrosis and are protected from the development of cardiac dysfunction, which was observed in wild-type animals. Notably, CXCL10-/- mice do not show T-cell expansion and activation in the draining lymph nodes, particularly in the CD4+ T-cell subset. Using bone marrow chimeras, we show that CXCL10 from recruited macrophages accelerates pathologic cardiac remodeling. Our findings establish CXCL10 as a key mediator of heart failure, acting through immune cell recruitment and activation. These results suggest that targeting CXCL10 could provide a novel therapeutic strategy to mitigate inflammation-driven heart failure progression. - Source: PubMed
Souza-Neto FernandoLe PrestonAbdrabbo MobeenAlamgir AshabWang HaiguangFerreira de Araujo NataliaMikkila Jennifer LSanches BrunoParthiban PreethyMoon RyanHerman AdamAdams Andrew BPrins Kurt WGuatimosim SilviaSchuldt NathanRevelo Xavier Svan Berlo Jop H - Perivascular inflammation induced by abnormal hemodynamic stress is increasingly recognized as a key driver of secondary microvasculopathy in chronic thromboembolic pulmonary hypertension. Although circulating CXCL10 (C-X-C motif chemokine ligand 10) is elevated in chronic thromboembolic pulmonary hypertension and correlates with pulmonary hemodynamics, its mechanistic contribution to vascular remodeling remains unclear. - Source: PubMed
Publication date: 2026/04/22
Lu JianminLiao HuizhaoHuang ZijieBao ChangleiSun TingtingChen HaimingGuo WenliangWu XiaofengLu GuoliangTang HaiyangWang JianHong Cheng - BackgroundCerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by mutations in the NOTCH3 gene. Previous research has predominantly focused on vascular smooth muscle cell pathology, whereas the role of brain microvascular endothelial cells (BMECs) in the disease remains unclear.ObjectiveTo investigate the impact of the NOTCH3-R544C mutation on BMECs function and to elucidate the underlying mechanisms of endothelial dysfunction in CADASIL.MethodsUsing CADASIL transgenic mice and endothelial cell (EC) models stably expressing NOTCH3-R544C, the impact of the mutation on endothelial function was assessed through immunofluorescence staining, RNA-seq analysis, protein-protein interaction (PPI) network mapping, and lipid and cellular function assays.ResultsSignificant NOTCH3 extracellular domain (NOTCH3ECD) deposition and reduced microvascular density are observed in CADASIL mice. R544C mutant cells exhibit abnormal NOTCH3ECD accumulation alongside pronounced gene expression dysregulation, predominantly enriched in pathways related to inflammation, cell migration. The PPI network centers on CXCL10 as a pivotal hub, forming a core "inflammation-migration" pathological axis. R544C cells exhibit heightened inflammatory responses, cholesterol accumulation, reduced cell viability, and increased sensitivity to inflammatory stimuli.ConclusionsThe NOTCH3-R544C mutation disrupts inflammatory regulation, migratory capacity, and lipid metabolic homeostasis in BMECs, leading to endothelial dysfunction and revealing a key mechanism of endothelial injury in CADASIL. - Source: PubMed
Publication date: 2026/04/21
Sun RuihuaLi WanyueLiu NingJi XiaoyiZhao ZhenxiangChe NingningLi AnqiHu WenjianZhang Jiewen - Gastric cancer poses a formidable therapeutic challenge due to high heterogeneity and aggressive invasiveness. To address this challenge, we first prepared chiral BiMoO nanoparticles (NPs) that exhibited a strong circular dichroism signal of approximately 160 mdeg at 920 nm wavelength. Notably, intraperitoneal injection of -BiMoO NPs achieved complete tumor clearance, as evidenced by extended survival, maintained body weight, and reduced tumor burden. Mechanistically, -BiMoO NPs initially activated PI3K-Akt and NF-κB signaling pathways via the Toll-like receptor 2 (TLR2) in splenic macrophages, thereby increasing interleukin-6 (IL-6) production. Notably, reactive oxygen species (ROS) generated from molybdenum valence change further amplified the NF-κB pathway. Subsequently, IL-6 was transported to the tumor site via the circulation to activate the JAK-STAT signaling pathway in mouse forestomach carcinoma (MFC) cells, leading to the upregulation of C-X-C motif chemokine ligand 16 (CXCL16). This CXCL16 then recruited intestinal-derived group 3 innate lymphoid cells (ILC 3s), which elevated CXCL10 expression. Ultimately, CXCL10 activated T cells and natural killer (NK) cells, thereby mediating tumor elimination. These findings highlight -BiMoO NPs as a promising candidate for tumor immunotherapy. - Source: PubMed
Publication date: 2026/04/20
Huang LuShi BaimeiGe YuxiXu LiguangHu ShudongQu AihuaXu ChuanlaiSun MaozhongKuang Hua - This study aims to investigate the pathogenic hallmarks in various subtypes of idiopathic inflammatory myopathies (IIM) using single-cell transcriptomic approaches. - Source: PubMed
Publication date: 2026/04/20
Wang ZhiqinLi YanmeiLi XiaowenZhang JianlinXu JingHan FengDu JunYang TongChen MingGuo YingWang GaoyaXu YongHou HouSun WenwenZhang NaLi DongZhang HuafengCai ZhigangWei Wei