CCL20
- Known as:
- CCL20
- Catalog number:
- Y214388
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CCL20
Related genes to: CCL20
- Gene:
- CCL20 NIH gene
- Name:
- C-C motif chemokine ligand 20
- Previous symbol:
- SCYA20
- Synonyms:
- LARC, MIP-3a, exodus-1, ST38, CKb4
- Chromosome:
- 2q36.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-10
- Date modifiied:
- 2016-03-01
Related products to: CCL20
anti-CCL20anti-CCL20anti-CCL20 (Internal)anti-CCL20 type: Primary antibodies host: MouseAnti-CCL20, Goat Polyclonal to CCL20, Isotype , Host GoatAnti-human MIP-3 alpha CCL20 (MAB), Source: Monoclonal Murine, MABAnti-human MIP-3 alpha (CCL20), bt, Source: Polyclonal bt. Rabbit, PABAnti-human MIP-3 alpha (CCL20), bt, Source: Polyclonal bt. Rabbit, PABAnti-human MIP-3 alpha (CCL20), bt, Source: Polyclonal bt. Rabbit, PABAnti-human MIP-3 alpha (CCL20), Source: Polyclonal Rabbit, PABAnti-human MIP-3 alpha (CCL20), Source: Polyclonal Rabbit, PABAnti-human MIP-3 alpha (CCL20), Source: Polyclonal Rabbit, PABAnti-human MIP-3 alpha / CCL20 (MAB), Source: Monoclonal Murine, MABAntibodies: CCL20 HOST: Goat Clonality: pAbAntigens CCL20, 27-96aa, Human, His tag, E.coli, Recombinant Related articles to: CCL20
- The identification of novel therapeutic targets and agents to overcome chemoresistance remains a central challenge in triple-negative breast cancer (TNBC). Here, we report three key innovations: the discovery of a novel oncogenic circRNA, circPARPBP, as a driver of chemoresistance; the elucidation of its mechanism through the recruitment of the SRCAP complex to activate CCL20 transcription and cancer stemness; and the demonstration that the natural compound isoliquiritigenin (ISL) effectively suppresses this axis to overcome chemoresistance. TNBC is the most aggressive subtype of breast cancer with poor prognosis and limited treatment options. In this study, we identified circPARPBP, a circRNA (hsa_circ_0000432) derived from PARPBP gene, which was aberrantly upregulated in TNBC tissues and cells. Clinically, the upregulation of circPARPBP was notably associated with TNBC chemoresistance. In vitro and in vivo experiments demonstrated that circPARPBP promoted TNBC progression and chemoresistance. Mechanistically, circPARPBP recruited the SNF2-related CBP activator protein (SRCAP) complex to activate C-C motif chemokine ligand 20 (CCL20) transcription and thus contributed to cancer stemness and chemoresistance. ISL, a key bioactive substance extracted from licorice root, effectively suppressed the circPARPBP-SRCAP-CCL20 signaling pathway. Notably, patient-derived xenograft models demonstrated that ISL treatment effectively overcame TNBC chemoresistance, with a superior benefit when in combination with conventional chemotherapy. Collectively, our study identifies circPARPBP as a novel regulator of TNBC progression and chemoresistance via SRCAP-mediated CCL20 activation, and provides a preclinical rationale for the clinical development of ISL as a potential therapy targeting this axis. - Source: PubMed
Publication date: 2026/05/21
Chen BoMa KangZhong WenhuanWang YunjieLong ChengMao XueyanTang HailinZhu XudongYang AnliLiu Peng - species are emerging pathogens associated with adverse gynaecologic, obstetric and neonatal sequelae, including bacterial vaginosis, preterm birth, chorioamnionitis, non-gonococcal urethritis and HPV-mediated cervical carcinogenesis. Yet, their pathogenicity is poorly understood due to their fastidious nature. Here, we conducted infection assays using multiple strains of and to evaluate host responses in an 3D organotypic model of the human cervix. We profiled a broad array of proteins, including antimicrobial peptides, cytokines, growth factors, mucins, matrix metalloproteinases and proteins related to apoptosis and cellular stress. Both species induced similar pro-inflammatory signatures. Notably, all strains robustly induced IL-6 and IL-8/CXCL8 ( from 0.02 to <0.0001), which are clinical markers associated with preterm birth, vaginal dysbiosis and cervical carcinogenesis. Most strains also induced the two chemokines IP-10/CXCL10 and MIP-3/CCL20. Conversely, no significant induction of matrix metalloproteinases or apoptosis-related proteins was observed. Furthermore, co-infection with both species elicited similar cytokine patterns with no synergistic effects observed. Collectively, investigation of multiple strains confirms that both species trigger a conserved immune-mediated response. This reveals a shared pathogenic mechanism that represents a potential pathway toward adverse gynaecologic and obstetric outcomes. - Source: PubMed
Åaniewski PaweÅGarwolinska AnitaAnwyl GwenllianHerbst-Kralovetz Melissa M - The airway epithelial barrier is the primary defense line of the lungs against allergens, such as house dust mite (HDM). A disrupted airway epithelial barrier plays a major role in asthma development. Short-chain fatty acids (SCFAs) are bacterial fermentation products that are associated with prevention against allergic inflammation. In this study, we aim to elucidate the direct preventative effects of SCFAs, particularly butyrate, on the HDM-induced bronchial epithelial cell (BEC) activation and barrier disruption in-vitro. - Source: PubMed
Publication date: 2026/05/19
Verstegen Roos E MHotie JenniferBikineeva Margaritavan Brummelen SuzeGarssen JohanFolkerts GertWillemsen Linette E M - Lynch syndrome (LS) is the most common hereditary cause of colorectal cancer (CRC) and results from pathogenic germline variants affecting mismatch repair. The tissue microenvironment that contributes to this elevated risk of CRC is poorly characterised particularly during the early precancerous stages. - Source: PubMed
Publication date: 2026/05/19
Yang HairuDungan MichaelaMadhu BhoomiBeyries KeelyWang XinKilpatrick RobertChen BaronOh SangmiBerkowitz MarissaSmith DavidZhou ChaotingKoralov Sergei BAxelrad JordanLengner Christopher JBelle NicoleBewtra MeenakshiKatona Bryson WCadwell Ken - Knee osteoarthritis (KOA) is clinically characterized by recurrent and progressively worsening episodes; however, its underlying pathological mechanisms remain incompletely understood. Phenotypic changes and the specific migration of circulating monocytes may be key factors contributing to the recurrence and progressive exacerbation of synovial inflammation in KOA. In this study, we report a specific subtype of circulating monocytes in KOA that highly express interleukin 1A (IL1A), IL1R1, tumor necrosis factor, CXCL12, CXCL3, CXCL2, CCL20, and G0S2. These monocytes exhibit a trained immune phenotype, and their CXCR4-dependent migration to the synovium exacerbates synovial inflammation. HMGB1 (high mobility group protein B1) primes the trained immunity of this subtype, resulting in increased chromatin accessibility, and the transcriptional storage of multiple proinflammatory factors enables them to exhibit a more positive inflammatory response when restimulated by HMGB1. In addition, we find that MyD88, downstream of HMGB1, recruits cytoplasmic interferon regulatory factor 1 to the nucleus and then stabilizes interferon regulatory factor 1 in chromatin through SUMOylation of tripartite motif containing 28 to exert transcriptional activity and epigenetic enhancement of proinflammatory factor expression. Finally, we found that KOA inflammation was effectively attenuated by blocking HMGB1. Taken together, this study reveals the mechanism by which trained immunity of circulating monocytes promotes the progression of synovial inflammation, supporting a future therapeutic approach in the management of KOA. - Source: PubMed
Publication date: 2026/05/14
Jie LishiMao JunZhang LiFu HouyuLi XiaochenLiao TaiyangWei YibaoLiu DerenDu JiaojiaoWu PengYin SongjiangZhang NongshanCao MengWang Peimin