RANTES CCL5, Human
- Known as:
- RANTES CCL5, Human
- Catalog number:
- Z02832-20
- Product Quantity:
- 20,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- RANTES CCL5 Human
Related genes to: RANTES CCL5, Human
- 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 CCL5, Human
Related articles to: RANTES CCL5, Human
- Epidemiological studies link long-term air pollution to an increased risk of hepatocellular carcinoma (HCC), but the underlying toxicological targets remain poorly understood. We used an integrative computational framework to identify and prioritize candidate molecular mediators potentially linking pollutant-associated gene signatures with hepatocarcinogenesis. - Source: PubMed
Publication date: 2026/07/19
Yang LinQing XinWang Jiaxing - The treatment with immune checkpoint inhibitors is not universally effective, and the efficacy is challenging to predict using a single biomarker. Breast cancer (BC) cells develop within a complex microenvironment, which includes tumor cells, immune cells, and extracellular matrix, and they may interact through paracrine signaling. Elucidating the mechanisms of immune microenvironment regulation and intercellular interactions in BC is fundamental for screening efficacy markers and developing new immunotherapeutic targets. Based on the immune phenotype cellular infiltration characteristics and transcriptomic changes, we constructed a two-way orthogonal partial least square (O2PLS) model to identify immune cell infiltration (ICI) genes, quantitatively characterizing the immune microenvironment within BC to predict patient prognosis, select sensitive populations for immunotherapy, and provide a theoretical basis for the combination of immunotherapy with radiotherapy and chemotherapy. We described the T cell differentiation trajectories and intercellular communication landscapes and revealed the synergistic effects of receptors and ligands (CXCL9-CXCR3, CCL5-ACKR1, and GZMA-F2R) on the immune microenvironment and prognosis. These findings may contribute to elucidating the factors that shape the immune microenvironment and identifying new therapeutic targets. - Source: PubMed
Yang ZeyuDu Tianjing - Obesity significantly alters the adipose-tumor microenvironment and enhances colorectal cancer (CRC) progression. Visceral adipose tissue (VAT) becomes metabolically and immunologically activated, driving adipocyte dedifferentiation into cancer-associated adipocytes (CAAs). CAAs secrete adipokines, cytokines, chemokines, and lipid substrates that activate the JAK/STAT3, NF-κB, PI3K/AKT, and HIF-1α pathways in CRC cells, thereby enhancing proliferation, the epithelial-mesenchymal transition (EMT), angiogenesis, and immune escape. Increased fatty acid release and CD36/FABP-mediated uptake further support metabolic rewiring and metastatic potential. Key chemokine axes, CCL2/CCR2, CCL5/CCR5, and CXCL12/CXCR4, coordinate stromal recruitment and organ-specific dissemination, linking VAT inflammation to metastasis. New therapeutic concepts - including inhibition of lipid exchange between adipocytes and tumor, modulation of adipokine and chemokine signaling, and reprogramming of the CAA phenotype - highlight the clinical potential of targeting adipose-mediated tumor progression. In this review, we summarize and systematize the current mechanistic evidence on the interactions between adipose tissue and CRC, highlighting their importance in metastasis and therapy resistance. Despite significant progress, key aspects of adipose tissue modulation of CRC biology remain unexplored, underscoring the need for further mechanistic and translational research. - Source: PubMed
Publication date: 2026/07/17
Litwiniuk AnnaKalisz MałgorzataStępień DominikaSławkowska NataliaRoszkowski RafałRemyzovska OlgaGrala BartłomiejBik WojciechKwiatkowski Andrzej - Death-associated protein kinase 1 (DAPK1), a Ca²+/calmodulin-regulated serine/threonine kinase, plays a pivotal role in epidermal homeostasis, tissue repair, and cutaneous wound healing. However, its role in oral mucosal repair remains unclear. In this study, we established a global knockout mouse model to create 1.5-mm circular palatal wounds in mice aged 8 to 12 wk. Our results demonstrated that DAPK1 deficiency significantly accelerated oral wound closure. In vitro experiments further confirmed that DAPK1 modulates the proliferation and migration of human oral keratinocytes. Mechanistic investigations through transcriptome sequencing revealed activation of the Wnt signaling pathway in knockout mice following injury, characterized by pronounced upregulation of , , and , alongside downregulation of innate immune mediators, including , , , , and . These findings suggest that loss of DAPK1 enhances epithelial proliferation and migration while attenuating local inflammation. Furthermore, we developed a novel microneedle patch for drug delivery, consisting of GelMA tips encapsulating the DAPK1 inhibitor (HS-38) and a hyaluronic acid substrate. This system facilitated efficient mucosal penetration and localized delivery. Application of the microneedle patch significantly improved wound healing in both normal and diabetic mouse models. Collectively, these findings uncover a previously unrecognized role of DAPK1 in oral mucosal repair and highlight its potential as a molecular target to accelerate wound healing. - Source: PubMed
Publication date: 2026/07/17
Li YHu MYin HCao YWu JYang MZhang XZhou JFang XLuo JHu MLi DLiu D - Hirschsprung-associated enterocolitis (HAEC), a lethal complication of Hirschsprung disease (HSCR)-a prevalent congenital disorder with high morbidity-has a poorly understood pathogenesis. We investigated how aberrant immune-stromal crosstalk drives mucosal injury in HSCR. - Source: PubMed
Publication date: 2026/07/16
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