MIP-5 CCL15, Human
- Known as:
- MIP-5 CCL15, Human
- Catalog number:
- Z02838-25
- Product Quantity:
- 25,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- MIP-5 CCL15 Human
Related genes to: MIP-5 CCL15, Human
- Gene:
- CCL15 NIH gene
- Name:
- C-C motif chemokine ligand 15
- Previous symbol:
- SCYA15
- Synonyms:
- HCC-2, NCC-3, SCYL3, MIP-5, Lkn-1, MIP-1d, HMRP-2B
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-11
- Date modifiied:
- 2016-03-01
Related products to: MIP-5 CCL15, Human
Related articles to: MIP-5 CCL15, Human
- Intestinal fibrosis presents a major clinical challenge in Crohn's disease (CD) due to the lack of effective pharmacological interventions. The underlying mechanisms of intestinal fibrosis remain largely elusive. Reanalysis of the single-cell RNA-seq data from full-thickness CD tissue identifies a distinct profibrotic macrophage subset characterized by high S100A8 and S100A9 expression. CellChat analysis indicates strong communication between this S100A8/A9-high (S100A8/A9) macrophage subset and fibroblasts. Adoptive transfer of S100A8/A9 macrophages exacerbate intestinal fibrosis in mice with chronic dextran sulfate sodium (DSS)-induced colitis. Consequently, pharmacological inhibition of S100A8/A9 significantly ameliorates intestinal fibrosis in murine chronic colitis. Proteomic analysis further identifies murine CCL6 (mCCL6) as the key pro-fibrotic mediator secreted by S100A8/A9 macrophages, which acts via CC chemokine receptor 1 (CCR1) to regulate fibroblasts. Antibody blockade of mCCL6 alleviates established intestinal fibrosis in a DSS-induced colitis model. Mechanistically, S100A8/A9 macrophages drive mCCL6 production via STAT3 activation. Similarly, the human ortholog of CCL6, CCL15 (hCCL15), exerts pro-fibrotic effects on fibroblasts via the CCR1 receptor. Our findings reveal that targeting S100A8/A9 macrophage may be a therapeutic strategy against intestinal fibrosis in CD. - Source: PubMed
Publication date: 2026/06/29
Wang ShuWang JiayunLin JunjieYe ZipingZhou GeyujiaMa JingjingSun JunjianYu JiangZhang YingdiTang NanaJiao ChunhuaZhao XiaojingZhang Hongjie - Dual declines in cognitive status and physical performance increase dementia risk but shared biological mechanisms between processes remain unclear. We investigated plasma proteomic signatures underlying dual decline in older adults from the Invecchiare in Chianti cohort (n = 774; age ≥ 60). Group-based trajectory models with up to 15 years of data on cognitive status (global Mini-Mental State Examination scores) and 4-m gait speed identified three trajectories that included no decline, physical decline, or dual decline groups. At baseline, 1301 plasma proteins were measured with aptamer-based proteomics (SomaScan). Adjusted multinomial regressions identified proteins associated with group membership. Additional analyses included Reactome functional enrichment and partial least squares discriminant analysis (PLS-DA). Collectively, eight proteins were associated with differences across trajectory groups. Higher PI3, GDF15, TFF3, CCL15, TNNT2, and AGRP were associated with greater odds of dual decline, whereas higher CKM and GHR were linked to lower odds. PLS-DA confirmed and extended these findings. The top discriminators by variable-importance were PTN, TFF3, GDF15, IGFBP-2, and CHRDL1. Hierarchical clustering found PTN, IGFBP-2, PI3, GDF15, and TFF3 formed a coherent module. Functional enrichment highlighted overrepresentation of regulation of IGF transport and uptake by IGF binding proteins across decline trajectories and exploratory enrichment of post-translational protein phosphorylation and diseases of homeostasis. Older adults with dual declines showed a proteomic profile marked by cellular stress, inflammation, barrier injury, reduced IGF-1 bioavailability, and cardiovascular-metabolic strain. These findings support system-level hypotheses of dual decline and warrant replication, longitudinal proteomics, and evaluation of module-level markers. - Source: PubMed
Publication date: 2026/06/16
Rathbun Alan MChen ChixiangTian QuTanaka ToshikoFerrucci LuigiShardell Michelle D - In the tumor microenvironment, immune, stromal and cancer cells interact. They communicate in paracrine and autocrine manners via secreted cytokines, altering anti-tumor immunity. The pattern consisting of the relative secretions of these proteins is referred-to as the "immune secretome". To date, the immune secretome of human cancers remains largely unexplored. Herein, we describe the dominant cytokines released by human tumors. - Source: PubMed
Publication date: 2026/06/05
Kuksin MariaMouraud SeverineBredel DelphineRadulescu CameliaMohamed-Djalim ChifaouAdam JulienTerrier Philippede Montpréville Vincent ThomasZitvogel LaurenceScoazec Jean-YvesBigorgne Amelie ERouanne MathieuMarabelle Aurélien - Pancreatic ductal adenocarcinoma (PDAC) represents a highly fatal malignancy with a huge public health burden. There is a critical need to better understand its etiology for developing innovative strategies for effective prevention and treatment. Leveraging genetic variants as instrumental variables, Mendelian randomization and proteome-wide association study have identified dozens of protein biomarkers associated with PDAC risk, yet potential nonlinear associations have largely been underexplored. In this study, we applied a nonlinear modeling approach, combining two-stage sliced inverse regression (2SIR) with nonlinear transformations via adjusted inverse regression (AIR), to investigate associations between genetically predicted protein concentrations in plasma and PC risk, by integrating blood proteome and genome data from the INTERVAL study (n = 3301), and a large genome-wide association study of PC risk (8275 cases and 6723 controls). We identified 25 genetically predicted proteins associated with PDAC risk after multiple comparison correction, including 22 that had been previously reported using linear modeling methods, and an additional three novel proteins (APOF, CCL15, and CHIT1). Importantly, there has been some level of evidence in the literature supporting potentially important roles of some of these novel proteins in PDAC development. Our study underscores the importance of accounting for nonlinear relationships in uncovering novel proteins associated with PDAC risk. If validated in further studies, our findings could improve the understanding of PDAC pathogenesis and inform future therapeutic and risk assessment strategies to reduce the burden from this deadly cancer. - Source: PubMed
Publication date: 2026/06/01
Zhu JingjingWu ChongMoaven OmeedYamazaki HajimeWei YumengDai BenWu Lang - To analyze the effect of metabolic disorders and immunological parameters on the functional outcome (FO) of acute ischemic stroke (IS) in patients with metabolic syndrome (MS). - Source: PubMed
Tynterova A MBarantsevich E RShusharina N NKhoimov M SRogovskaya M S