RANTES Synthetic Protein
- Known as:
- RANTES Synthetic Protein
- Catalog number:
- x1248c
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Exalpha
- Gene target:
- RANTES Synthetic Protein
Related genes to: RANTES Synthetic Protein
- 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 Synthetic Protein
Related articles to: RANTES Synthetic Protein
- Postnatal choline supplementation improves memory, non-verbal IQ, executive function, and white-matter microstructure in children with fetal alcohol spectrum disorder (FASD) across randomized controlled trials; however, peripheral and brain biomarkers of these effects are uncharacterized. - Source: PubMed
Publication date: 2026/09/16
Tran Phu VMaxim Zia LEckerle Judith KZeisel Steven HGeorgieff Michael KWozniak Jeffrey R - Excessive inflammation is a critical contributor to impaired oral mucosal wound healing, yet effective therapeutic strategies are still lacking. Although dehydrocorydaline (DHC) has been reported to exhibit anti-inflammatory and analgesic properties, its role in wound healing and the underlying mechanisms have not been fully elucidated. This study aimed to investigate whether DHC accelerates palatal wound healing and to elucidate the role of the p38 mitogen-activated protein kinase (MAPK)/CCL2 signaling axis in DHC-mediated regulation of macrophage chemotaxis. , macrophages were stimulated with 1 μg/mL lipopolysaccharide (LPS) and treated with DHC at 0.1, 1, and 10 μM. The chemotactic response and inflammatory function of macrophages were assessed using real-time PCR, ELISA, Western blotting, and Transwell assays. Molecular docking simulations and Western blotting analyses were performed to examine the regulatory effect of DHC on MAPK signaling pathway. , a full-thickness palatal mucoperiosteal wound extending from the left maxillary first to third molars was established in mice by scalpel scraping. The effects of topical 10 μM DHC gel on wound healing were evaluated using stereomicroscopy, histological staining, and real-time PCR at 0, 3, and 5 days post-modeling. , DHC effectively downregulated the expression of chemokines, including C-C motif chemokine ligand 2 (), , , C-X-C motif chemokine ligand 10 (), and , with the most significant inhibitory effect on (70.8% inhibition). In Transwell assays, DHC reduced macrophage migration by 68.2%. Mechanistically, DHC prominently inhibited the activation of the MAPK signaling pathway. , DHC treatment accelerated wound healing and markedly reduced macrophage infiltration in mouse palatal wound tissues. These findings demonstrated that DHC accelerated palatal wound healing 1.6-fold in mice. DHC suppressed macrophage chemotaxis by 68.2% through modulation of the MAPK signaling pathway. - Source: PubMed
Publication date: 2026/08/27
Chen YingyiLiu ZhaonaWang YijiaXia GuiyangLiu YitongXia HuanWang MinfengLin ShengLiu Yi - Necrotic enteritis (NE), caused by Clostridium perfringens(C. perfringen) type G carrying the NetB gene, represents a major infectious disease threatening the global poultry industry. Following the ban on in-feed antibiotic growth promoters, the incidence of NE has increased markedly, highlighting the urgent need for safe and effective prevention and control strategies. To address this challenge, we developed a novel probiotic-based oral immunization strategy.We constructed a recombinant Lactobacillus plantarum (L. plantarum) NC8 strain surface-displaying the FimB antigen [NC8(pYL515)] and orally co-immunized broiler chickens with the previously developed NC8(pYL590) strain co-expressing FimA, FBA, and NetB, together with Enterococcus faecalis EF32, to evaluate their protective efficacy against NE in broilers. In vitro, EF32 demonstrated a strong ability to promote the maturation of chicken bone marrow-derived DCs, as evidenced by the upregulation of CD83, CD86, CCL5, and CCR7 expression. Prior to challenge, the combination of live EF32 and multi-antigen recombinant strains established an enhanced systemic immunity (significantly elevated IgG), mucosal immunity (early activation of IgM and marked increase in sIgA) and cellular immunity (enhanced splenic lymphocyte proliferation and increased expression and secretion of IFN-γ and IL-4). In addition, the co-administration also significantly upregulated the mRNA levels of intestinal CCR7, CCR9, and CD86. Finally, in a broiler challenge model, this combined immunization strategy significantly alleviated intestinal lesions and mitigated growth suppression. Notably, live EF32 bacteria, as a key component exerting synergistic effects in this combined immunization strategy. Our findings demonstrate that combined immunization with recombinant L. plantarum co-expressing multiple antigens and live EF32 synergistically enhances the immunogenicity and protective efficacy of an oral vaccine, offering a promising antibiotic-free strategy for NE control. - Source: PubMed
Publication date: 2026/09/08
Xu YaoZhang YuxiLiu HuanyuLu XinWen XinWang TongDu LinhaiWang YijieHuang HaibinWang ZhannanWang ChunfengJiang Yanlong - Cardiac fibrosis is driven by dynamic crosstalk between cardiac fibroblasts and macrophages, yet how tissue mechanics regulate these interactions remains poorly defined. Here, we introduce a viscoelastic coculture platform that enables precise interrogation of mechanical and paracrine signaling in a physiologically relevant context. Counterintuitively, we found that soft, viscous environments promote human-induced pluripotent stem cell-derived cardiac fibroblast activation and macrophage healing phenotypes, while stiff environments bias macrophages toward inflammation. Coculture in soft, viscous matrices amplifies reciprocal pro-fibrotic signaling, while sequential exposure to inflammatory and then healing macrophages, which mimic in vivo dynamics, further exacerbates fibroblast activation. Mechanistically, we identified a STAT1 and AP-1 mediated, viscoelasticity-driven positive feedback loop involving inflammatory cytokines IL6, CCL5, and CCL2 as well as healing cytokines VEGFA and CTGF. This work establishes tissue viscoelasticity as a central regulator of immune-stromal interactions and provides a broadly applicable platform for dissecting mechanobiological drivers of fibrosis. - Source: PubMed
Publication date: 2026/09/24
Atcha HamzaBishop Carrie TMolley Thomas GBanerjee AbhinabaBalayan AlisEngler Adam J - Isaridin E (ISE), a marine-derived fungal cyclodepsipeptide, possesses antiplatelet activity in vitro and antithrombotic efficacy in a FeCl-induced carotid artery thrombosis mouse model without prolonging bleeding time. In this study, we investigated the antiplatelet and neuroprotective effects of prophylactic and therapeutic administration of ISE in a transient middle cerebral artery occlusion (tMCAO) mouse model. We found that both prophylactic administration (50 and 100 mg/kg) and therapeutic administration (50 mg/kg) of ISE significantly reduced cerebral infarct volume, alleviated neurological deficits, and attenuated neuronal injury. Furthermore, therapeutic administration of ISE suppressed platelet hyperactivity, as evidenced by reduced P-selectin expression, downregulated platelet secretion-related proteins (SNAP23, VAMP8), and decreased plasma levels of platelet-derived pro-inflammatory cytokines (IL-1β, PF4, and CCL5). Moreover, ISE attenuated microglial inflammatory activation in the peri-infarct region in vivo. Mechanistically, in vitro studies revealed that this effect may be mediated through the LRP1/IκB/NF-κB signaling pathway. In conclusion, these results suggest that ISE protects mice against ischemic stroke by concurrently suppressing platelet hyperactivity and LRP1-associated microglial neuroinflammation. - Source: PubMed
Publication date: 2026/09/20
Mi Yu-ChenLi Zi-ChengJiang Qi-QiLiu LanChen Sen-HuaPan NiWang Guan-Lei