Ask about this productRelated genes to: MCP3 antibody
- Gene:
- CCL7 NIH gene
- Name:
- C-C motif chemokine ligand 7
- Previous symbol:
- SCYA6, SCYA7
- Synonyms:
- MCP-3, NC28, FIC, MARC, MCP3
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-04
- Date modifiied:
- 2016-10-05
Related products to: MCP3 antibody
Related articles to: MCP3 antibody
- Ovarian cancer (OC) remains a malignancy characterized by obscure risk factors and unfavorable prognosis. While 3-tert-butyl-4-hydroxyanisole (3-BHA) is suspected of exerting toxic effects on ovarian health, the precise molecular mechanisms underlying its impact remain elucidated. This study aims to systematically investigate the potential pathogenic mechanisms of 3-BHA in the progression of OC.Integrated transcriptomic data from the GEO database (GSE18520 and GSE40595) were analyzed. A synergistic computational framework was employed, incorporating Differentially Expressed Genes (DEGs) identification, Weighted Gene Co-expression Network Analysis (WGCNA), multiple machine learning algorithms, and SHapley Additive exPlanations (SHAP) analysis to achieve high-interpretability feature selection.Five hub genes-CXCR4, CCL7, CXCL8, CXCR2, and CX3CL1-were identified, all demonstrating robust diagnostic efficacy with AUC values of 0.911, 0.882, 0.823, 0.772, and 0.837, respectively. Prognostic profiling via GEPIA3 highlighted CXCR2 overexpression as a potential critical biomarker driving poor clinical outcomes in OC. Furthermore, molecular docking validated the strong binding affinity of 3-BHA with CX3CL1 and CXCR2. Subsequent 100 ns molecular dynamics simulations and thermodynamic stability assessments confirmed the structural stability of the 3-BHA-CXCR2 complex.By integrating bioinformatics and computational toxicology, this study deciphers the potential mechanistic landscape through which 3-BHA influences OC. These findings not only refine the toxicological understanding of 3-BHA but also provide novel candidates for early diagnosis and prognostic risk stratification in OC. - Source: PubMed
Publication date: 2026/05/03
Shi YifeiNiu DongJin Chunhui - Urinary tract infections (UTIs) caused by uropathogenic (UPEC) are prevalent among women. UPEC infection can lead to kidney injury, and currently, there are no effective methods to mitigate this damage. Previous studies have shown that macrophage infiltration is closely associated with kidney injury induced by UTIs. However, the mechanisms underlying macrophage recruitment to the kidneys remain unclear. In this study, IL-17B may play a critical role in protecting against UPEC-induced kidney injury by modulating macrophage infiltration and bacterial colonization. Compared with wild-type (WT) mice, IL-17B mice exhibited significantly higher mortality and more M1-type macrophage infiltration, which was associated with renal injury. rIL-17B treatment significantly reduced macrophage infiltration in the kidneys of CFT073-infected mice. Additionally, analysis of chemokines indicated that IL-17B is a key regulator of macrophage recruitment by influencing the expression of CCL2, CCL3, and CCL7. Overall, IL-17B can serve as a crucial cytokine for treating urinary tract infections and mitigating kidney damage. - Source: PubMed
Publication date: 2026/05/01
Wang ChangyingLiu MinWang LuyueZhang YixinNiu ZihanLiu XueXiong Huabao - Skin diseases frequently coexist with other disorders, such as metabolic syndrome, diabetes mellitus, depression, psoriatic arthritis, and cardiovascular disease. Altered levels of distinct chemokines, like CCL5/RANTES, CXCL12/SDF-1a, CCL7/MCP-3, CCL2/MCP-1, CXCL1/GROa, and the eotaxin family, contribute to the development and/or exacerbation of inflammation, which is a common feature of numerous skin diseases as well as metabolic syndrome. The pathological and molecular connections between chronic inflammatory skin diseases and metabolic syndrome are increasingly recognized as being driven by shared inflammatory pathways, oxidative stress, and adipokine dysregulation. While systemic inflammation acts as a common thread, the precise mechanisms for some conditions remain partially understood. Nevertheless, the exact pathological and molecular connections between skin diseases (i.e., psoriasis, atopic dermatitis, pemphigus vulgaris, acute and chronic spontaneous urticaria, bullous pemphigoid, squamous cell carcinoma, alopecia areata, systemic sclerosis, discoid lupus erythematosus, diffuse large B-cell lymphoma) and metabolic syndrome are not yet fully understood. This narrative review summarizes the robust association between various chronic inflammatory skin diseases and metabolic syndrome in the context of pro-inflammatory chemokines. - Source: PubMed
Publication date: 2026/04/10
Matwiejuk MateuszMyśliwiec HannaMikłosz AgnieszkaChabowski AdrianFlisiak Iwona - Photosensitivity is central to cutaneous lupus erythematosus and dermatomyositis (DM), but the mechanisms linking UVB exposure to tissue-specific autoimmunity are poorly defined. Using single-cell RNA sequencing, spatial transcriptomics, proteomics, UVB provocation and in vitro modeling, we identify MMP9⁺CD14⁺ myeloid cells as critical mediators of photosensitivity. These cells expand significantly in lesional skin, produce interferon-β (IFNβ) and colocalize with cytotoxic CD4⁺ T cells at the dermal-epidermal junction. Keratinocytes activate fibroblasts in the superficial dermis, prompting them to release chemokines (CCL2, CCL19, CCL7, CCL8) that recruit MMP9⁺CD14⁺ cells. In vitro, type I interferon-primed keratinocytes exposed to UVB release cytokines activating dendritic cells, mirroring in vivo responses. UVB irradiation of non-lesional skin of patients with DM rapidly recruits these myeloid cells. In a clinical proof-of-concept study, anti-type I interferon treatment with anifrolumab prevented UVB-induced myeloid infiltration and reduced photosensitivity. Therefore, targeting MMP9⁺CD14⁺ cells may offer therapeutic potential for managing photosensitive autoimmune skin conditions. - Source: PubMed
Publication date: 2026/04/24
Wang YuqingAfshari KhashayarHaddadi Nazgol-SadatLopes Carolina SalomãoEng Chee-Huat LinusWhiteman Leah MMartinez NuriaKyawe Pyae PAnufrieva Ksenia SWei KevinFrieda KirstenRosenbach MishaVleugels Ruth AnnGallucci StefaniaHarris John ERashighi MehdiGarber Manuel - To investigate the effects of a matrikine, fibronectin fragment (FN7-10), on human osteoarthritic (OA) synovial fibroblasts and implications for inflammation and cartilage degradation. - Source: PubMed
Publication date: 2026/04/20
Fernandez Davila Jorge GAlberto Ralph AByun SeyounD'Costa SusanShine JacquelineAlvarez CarolinaYanke Adam BOlcott Christopher WDiekman Brian OPhanstiel Douglas HLoeser Richard F