Rat RANTES (CCL5)
- Known as:
- Rat RANTES (CCL5)
- Catalog number:
- GEM-300-513P1
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- SeraLab
- Gene target:
- Rat RANTES (CCL5)
Related genes to: Rat RANTES (CCL5)
- 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: Rat RANTES (CCL5)
α - Calcitonin Gene Related Peptide, α - CGRP, rat'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala13)-Apelin-13 (human, bovine, mouse, rat) 98% C63H107N23O16S CAS: 568565-11-7(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala96)-Myelin Basic Protein (87-99) (human, bovine, rat) 98% C70H110N20O17 CAS:(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2 Related articles to: Rat RANTES (CCL5)
- Herpes zoster (HZ) results from reactivation of latent varicella-zoster virus (VZV), and postherpetic neuralgia (PHN) is a major chronic pain complication. We performed parallel analyses of two independent public blood transcriptomic cohorts: GSE242252 (n=80; HZ onset, 1-year recovery, and controls) and PRJNA1142765 (n=23; 15 HZ and 8 PHN). Because the cohorts differed in platform, library preparation, design, and sampling structure, expression matrices were not merged; cross-cohort interpretation was restricted to within-cohort results and pathway-level directional concordance. HZ onset showed strong type I interferon (IFN)-dominated activation (HALLMARK_INTERFERON_ALPHA_RESPONSE, NES = 2.21, adjusted p=4.4x10-10), with recovery-associated attenuation of the sample-level IFN score (onset vs. recovery, p=0.005). In the smaller PHN cohort, only two genes met the strict differential-expression threshold, but Hallmark GSEA showed positive IFN-alpha and IFN-gamma enrichment. Ranking-sensitivity analysis confirmed IFN-alpha and IFN-gamma as the top two positively enriched Hallmark pathways using either log2 fold change or the DESeq2 Wald statistic, with leading-edge Jaccard similarities of 0.848 and 0.897, respectively. Exact patient-label permutation of the sample-level IFN score was not significant (two-sided p=0.297), although the PHN-minus-HZ direction remained positive in all 23 leave-one-out iterations. The new biological information is therefore an asymmetry of evidence: acute HZ IFN activation and recovery-associated attenuation are strongly supported, whereas the PHN-associated IFN pattern is stable at the pathway-ranking level but statistically uncertain at the patient level. Accordingly, the prior interpretation of persistent IFN activation in PHN is narrowed rather than reinforced. A structured external-replication search did not identify a suitable independent public human blood/PBMC transcriptomic cohort containing PHN samples; external evidence was therefore treated as literature-based concordance and supportive context rather than validation. Restricted computational prioritization highlighted IFN-related and CCL5/CCR5-associated axes for future study. - Source: PubMed
Publication date: 2026/09/23
Zhang HuiyingZhu YidongShao WeijieXu Kai - Keratinocytes play a crucial role in the pathogenesis of canine atopic dermatitis (cAD). Tumor necrosis factor (TNF)-α, a proinflammatory cytokine, is highly expressed in the lesional skin of dogs with atopic dermatitis. Additionally, interferon (IFN)-γ, a T-helper (Th)1-type cytokine, and interleukin (IL)-13, a Th2-type cytokine, are also detected in the lesional skin during the acute and/or chronic phases of cAD. However, their effects on chemokine expression in canine keratinocytes remain unclear. This study investigated the effects of TNF-α on chemokine mRNA expression in canine keratinocytes and how IFN-γ or IL-13 modulates these responses. Canine progenitor epidermal keratinocyte (CPEK) cells were stimulated with TNF-α alone or in combination with IFN-γ or IL-13. Chemokine mRNA expression was analyzed by real-time PCR. TNF-α induced the mRNA expression of chemokines, including , and . Co-stimulation with IFN-γ enhanced TNF-α-induced and mRNA expression, but reduced TNF-α-induced , and mRNA expression. IL-13 augmented TNF-α-induced mRNA expression, while suppressing TNF-α-induced and mRNA expression. IL-4, another Th2-type cytokine, was also confirmed to have effects similar to those of IL-13. These results indicate that TNF-α induces multiple chemokine genes in canine keratinocytes and that IFN-γ, IL-13, and IL-4 modulate this induction in a chemokine-specific manner, producing both enhancement and suppression. As these findings were obtained exclusively at the mRNA level in a canine keratinocyte cell line, their relevance to the pathogenesis and phases of cAD remains to be determined . - Source: PubMed
Publication date: 2026/09/22
Hasegawa TakehiroKaida YuzukiTakahashi KahoYoshimatsu RinaAndo MioriOhmori Keitaro - Small cell lung cancer (SCLC) and tuberculosis (TB) are both deadly diseases that present with spatially complex lung lesions. These lesions share similarities, including spatial interactions between T cells and macrophages. Both SCLC and TB exhibit heterogeneous disease progression and responses to treatment; current experimental methods have few tools to investigate the spatiotemporal evolution of these lesions within human lungs. We have applied our computational agent-based model (ABM), GranSim, to extensively study heterogeneity of TB granuloma formation and treatment efficacy. We introduce TumorSim, an analogous ABM designed to understand heterogeneity of SCLC lung tumors. TumorSim mechanistically captures immune-tumor interactions, many of which are well-studied in isolation, including cytokine-based recruitment of immune cells and PD-1/PD-L1-based inhibition of cytotoxic T cells. Drawing from lung immunology literature, we define and explore wide parameter ranges to characterize TumorSim behavior using global sensitivity analysis. We compare factors that drive both tumor and granuloma outcomes. As model validation, sensitivity analysis captures several well-known correlates of improved SCLC outcomes including macrophage-mediated cytotoxic T-cell recruitment. Surprisingly, both models predict a two-phase formation process occurring with an abrupt change in tumor/granuloma dynamics upon arrival of adaptive immune cells into the lung. Simulations suggest that while C-C motif chemokine ligand 5 (CCL5) is associated with improved tumor control later during tumor growth, CCL5 plays a pro-tumor role early during tumor growth by recruiting regulatory T cells. We find that, like virtual granulomas, TumorSim tumors become enlarged when immunosuppressive mechanisms outweigh pro-inflammatory responses. This novel tumor model enables future studies of both immunotherapeutics and anti-cancer drugs. - Source: PubMed
Publication date: 2026/10/06
Michael Christian TBudak MaralKirschner Denise - Anxiety is clinically associated with impaired fracture healing, but the underlying immunological mechanism remains unclear, and no targeted therapy is available. In a mouse model of chronic restraint stress (CRS)-induced anxiety with femoral fracture, we observed expansion of TGFβ1CCR5 double-positive neutrophils in the bone marrow. These neutrophils inhibited osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) via TGFβ1 secretion, while BMSC-derived CCL5 reciprocally promoted neutrophil activation, forming a detrimental feedback that disrupted fracture repair. Mechanistically, CRS activated the NF-κB-CCR5 axis to upregulate CCR5 and sustain this neutrophil subset. We found that acetyl-11-keto-β-boswellic acid (AKBA) directly bound YAP1, relieved YAP1-mediated suppression of ubiquitin-specific peptidase 31 (USP31), and consequently inhibited NF-κB phosphorylation and CCR5 expression, reducing the pathogenic neutrophil population and restoring BMSCs' osteogenic function. In order to overcome the problems of poor solubility, low bioavailability and tissue non-selectivity of AKBA, we developed a NIMP-R14 aptamer-modified epigallocatechin gallate (EGCG)-coated nanocarrier (AKBA@E-N), which can achieve enhanced uptake and local retention of neutrophils in the acidic microenvironment of the fracture site. In vivo, AKBA@E-N significantly accelerated fracture healing compared with free AKBA. This study reveals a neutrophil-mediated mechanism linking stress to impaired bone repair and provides a targeted nanotherapeutic strategy. - Source: PubMed
Publication date: 2026/09/24
Ouyang LizhiZhang YunhuaLiao JiewenZhang ZhenheHe XiLin ZeTao RanyangXie XudongAl-Smadi FawwazZhou WuXue HangHu YiqiangYang DongLiu Guohui - Zika virus (ZIKV) infection can cause severe neurological complications, particularly when antiviral immune responses are impaired. Here, we investigated how type I interferon (IFN-I) signaling influences the cellular inflammatory response and immunopathology in the central nervous system (CNS) during ZIKV infection. ZIKV infection induced early IFN-α and IFN-β expression in the CNS of wild-type (WT) mice. In contrast, mice lacking the IFN-I receptor (IFNAR) exhibited higher CNS viral loads, severe clinical symptoms, weight loss, increased mortality, and histopathological alterations characterized by extensive leukocyte accumulation and ZIKV antigen detection. Flow cytometry and UMAP analysis revealed that IFN-I signaling restrains leukocyte accumulation in the CNS. IFNARmice showed increased accumulation of myeloid and lymphoid cells, including inflammatory monocytes, monocyte-derived dendritic cells, and activated CD4 and CD8 T cells, whereas WT mice displayed limited leukocyte accumulation. Loss of IFN-I signaling was associated with elevated levels of pro-inflammatory cytokines (IL-6, IL-1β, TNF, and IFN-γ), chemokines (CCL2, CCL4, and CCL5), and inducible nitric oxide synthase (iNOS). Notably, CNS-resident microglia from IFNAR mice were highly susceptible to cell death, including among ZIKV antigen-negative cells, suggesting that inflammatory signals generated during infection may contribute to injury in uninfected microglia. In contrast, myeloid cells were predominantly ZIKV antigen-positive but remained largely viable. CD45 non-leukocyte cells constituted the major ZIKV antigen-positive population in the CNS and displayed resistance to cell death, indicating that this compartment may represent an important cellular population associated with ZIKV antigen detection during acute infection. Together, these findings demonstrate that IFN-I signaling is essential for controlling ZIKV replication, restraining neuroinflammation, and limiting CNS immunopathology. Its absence leads to increased viral burden, dysregulated immune cell accumulation, and severe neurological disease. - Source: PubMed
Publication date: 2026/10/04
Benevides Lucianada Silva HerculanoPioto FrancieleRigoni Thais da SilvaPiccin Mariela Pires CabralSouza Juliano de PaulaArruda EuricoCarregaro VanessaSilva João S