RANTES protein (Mouse)
- Known as:
- RANTES protein (Mouse)
- Catalog number:
- 30r-ar003
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- RANTES protein (Mouse)
Related genes to: RANTES protein (Mouse)
- Gene:
- CCL5 NIH gene
- Name:
- C-C motif chemokine ligand 5
- Previous symbol:
- D17S136E, SCYA5
- Synonyms:
- RANTES, SISd, TCP228, MGC17164
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-05
- Date modifiied:
- 2016-03-01
Related products to: RANTES protein (Mouse)
Related articles to: RANTES protein (Mouse)
- Peritoneal fibrosis, driven by M2 macrophage polarization, limits the long-term application of peritoneal dialysis (PD). Although ADAM19 is known to mediate fibrosis in other organs, its specific role in PD-associated peritoneal fibrosis remains unclear. PD patients were enrolled in a single center and divided into three groups depending on the PD time. Demographic and clinical data were collected. We detected the expressions of ADAM19, Notch1, Fibrosis-associated protein, chemokines and inflammatory factors in the peritoneum dialysis effluent by real-time PCR and western-blot assays. Macrophages were identified through flow cytometry. Then we analysis the relationship between ADAM19 and clinical data in PD patients. Furthermore, we established mouse models for peritoneal fibrosis to verify the biological function of ADAM19 in regulating macrophage polarization. In the long-term group, the fibrotic proteins (Fibronectin, α-SMA) and inflammatory factors (IL-6, IL-10) and chemokines (CCL5, CCL2, CXCL16) were higher than short-term group and more macrophages polarized towards M2. ADAM19 expression was linearly correlated with dialysis time and Kt/v. The AUROC of ADAM19 was 0.738 to identify the predictive value for peritoneal dialysis adequacy. The cut-off of ADAM19 RNA level was 7.84. In logistic regression models, higher ADAM19 (≥ 7.84) was also independently associated with lower Kt/v (< 1.67). Additionally, the results revealed a moderate increment of M1 macrophage (CD86+) and enormous rise of M2 macrophage (CD206+) with high-glucose dialysis fluid in mice model. Furthermore, the 8-week G4.25% group showed significant growth of M2 macrophage compared to the 4-week G4.25% group, indicating that prolonged dialysis duration has a more pronounced effect on promoting M2 polarization of macrophages via ADAM19/Notch1 signaling pathway. Through stimulating chemokines and inflammatory factors, ADAM19 regulated macrophage polarization and was correlated to the progression of peritoneal fibrosis. ADAM19 is expected to be a novel indicator for detecting peritoneal ultrafiltration function in PD patients. - Source: PubMed
Publication date: 2026/05/02
Xu KunyueYu JinHe MinhuiJiang XueYuan Yuan - Conventional type-1 dendritic cells (cDC1) are the main mediators of crosspresentation of tumor antigens to CD8+ T cells and provide a context of costimulatory molecules and cytokines that lead to cytotoxic T lymphocyte (CTL) responses. We analyzed bulk RNA sequences from 7 key clinical trials testing checkpoint inhibitors across multiple cancer types. cDC1- and CD8-associated gene signatures were analyzed. Multiplex tissue immunofluorescence was used to quantify cDC1 in melanoma, urothelial cancer, and non-small-cell lung cancer (NSCLC) samples and assess cDC1 tissue neighborhoods. Melanoma samples were studied with Xenium spatial transcriptomics (ST) and one series of NSCLC was analyzed using GeoMX-DSP. Strong associations across tumor types were found between cDC1 and CD8+ T cell transcripts with clinical outcomes. As mechanistically expected, transcripts for the CCL4 and CCL5 chemokines and the growth factor FLT3-L showed associations with cDC1 abundance. Tissue immunofluorescence showed a strong correlation of cDC1 and CD8+ T cell infiltration with clinical benefit upon treatment with checkpoint inhibitors (CPIs). Moreover, short distance between cDC1 and CD8+ T cells was found to define tissue niches associated with favorable outcomes. ST revealed recent T cell activation within immune cDC1-rich niches. cDC1 abundance, which determines CD8+ T lymphocyte density and activation in tumor tissues across cancer types, is strongly associated with clinical response to CPI-based immunotherapies. - Source: PubMed
Publication date: 2026/05/01
Lopez-Janeiro AlvaroGonzález-Gomariz JoséIssa FadiHester JoannaPorciuncula AngeloTeijeira AlvaroLuri-Rey CarlosRuiz-Guillamon DavidPerez-Gracia Jose LuisPerez-Ruiz ElisabethBarragan IsabelMartín-Algarra SalvadorSanmamed Miguel FOrtego IgnacioRodriguez-Ruiz Maria EAlexandru RalucaRodriguez InmaculadaArrieta-Aranzueque SaioaRimm DavidAung ThazinSchalper Kurt Ade Andrea Carlos EMelero Ignacio - Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide, characterized by a highly immunosuppressive tumor microenvironment (TME) that facilitates immune evasion and tumor progression. - Source: PubMed
Publication date: 2026/04/15
Bian YiboHuangfu ChaonanLu Yuanyuan - Piroplasmosis, including Theileriosis and Babesiosis, poses a threat to livestock health and productivity worldwide. However, the molecular mechanisms underlying breed-specific differences in resistance to piroplasmosis remain poorly understood. Compared to Bos taurus, Bos indicus generally exhibits greater resistance to diseases such as piroplasmosis and trypanosomiasis, as well as enhanced adaptability to hot and humid environments. Yunnan humped cattle, an indigenous B. indicus breed, are well adapted to coarse feed and harsh environments, yet the molecular basis of their disease resistance has not been systematically investigated. - Source: PubMed
Publication date: 2026/04/30
Chen YumingChen XiaonaLiu RongLi ChunqingXiao HengChen Shanyuan - Acquired resistance to Epidermal Growth Factor Receptor (EGFR) tyrosine kinase inhibitors (TKIs), such as gefitinib, remains a major therapeutic challenge in EGFR-mutant non-small cell lung cancer (NSCLC). Here, we report that cepharanthine (CEP), a natural bisbenzylisoquinoline alkaloid, effectively reverses gefitinib resistance through concurrent suppression of the AKT/P70S6K survival axis and activation of the Stimulator of Interferon Genes (STING)-mediated innate immune pathway. In gefitinib-resistant H1975 cells (EGFR L858R/T790M), CEP monotherapy significantly inhibited proliferation and induced mitochondrial apoptosis. Notably, CEP synergized with gefitinib to enhance therapeutic efficacy. RNA sequencing and functional validation revealed that CEP activates the STING/TANK-Binding Kinase 1 (TBK1)/Interferon Regulatory Factor 3 (IRF3) signaling cascade, resulting in robust production of T-cell chemoattractants C-X-C Motif Chemokine Ligand 9 (CXCL9), C-X-C Motif Chemokine Ligand 10 (CXCL10), and C-C Motif Chemokine Ligand 5 (CCL5). Critically, the STING inhibitor H-151 abolished CEP's antitumor effects in vitro. Our findings reveal a novel dual mechanism action of CEP and nominate it as a potential candidate for overcoming TKI resistance in NSCLC. - Source: PubMed
Kang Li-PingChen Hui-HuiLv Tong-TongHuang Hua-JingHuang Dong-HuiChen Ying-QingJiang Ze-Bo