Anti_Mouse, mab CCR6 Source Rat
- Known as:
- Anti_Mouse, mab CCR6 Source Rat
- Catalog number:
- 103-M340
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab CCR6 Source Rat
Related genes to: Anti_Mouse, mab CCR6 Source Rat
- Gene:
- CCR6 NIH gene
- Name:
- C-C motif chemokine receptor 6
- Previous symbol:
- STRL22
- Synonyms:
- CKR-L3, GPR-CY4, CMKBR6, GPR29, DRY-6, DCR2, BN-1, CD196
- Chromosome:
- 6q27
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-21
- Date modifiied:
- 2016-03-14
Related products to: Anti_Mouse, mab CCR6 Source Rat
Related articles to: Anti_Mouse, mab CCR6 Source Rat
- Inflammatory bowel disease (IBD) is a chronic condition characterized by recurrent intestinal ulceration. The rising global incidence of IBD in recent years has increased disease burden and highlighted the urgent need for more effective and safer treatments. Small-molecule therapeutics targeting critical pathogenic pathways represent a rapidly advancing area of IBD drug development, offering the advantages of stronger target binding affinity, better specificity, and more favorable pharmacokinetic performance compared to conventional therapies. This review summarizes the progress made in IBD small-molecule drugs in the past 5 years, covering the association between related targets and IBD pathogenesis, a series of new compounds acting on distinct molecular targets, including those that have advanced recently to clinical trials as well as those demonstrating promising anti-IBD activity in preclinical studies. The targets include key proteins (BRD4, PDE4, NLRP3), kinases (JAK, RIPK, SIK, IRAK), and G protein-coupled receptors (CCR6, CXCR4). For preclinical compounds, we highlighted the key structural modification process and structure-activity relationship (SAR) studies, summarizing their anti-inflammatory and intestinal protective activities demonstrated in both in vitro and in vivo experiments. Overall, this review aims to facilitate the rational development of next-generation, more effective, and safer small-molecule therapeutics for IBD. - Source: PubMed
Publication date: 2026/06/18
Lin HuihengWen ShunHuang YujieWang Siyuan - C-C motif chemokine ligand 20 (CCL20) is widely expressed in various human tissues and immune cells, playing a critical role in immune cell migration and inflammation. As the sole ligand of CCL20, C-C motif chemokine receptor 6 (CCR6) is a G protein-coupled receptor mainly expressed in immune cells and mediates chemotactic function of CCL20. The CCL20-CCR6 axis actively participates in immune homeostasis and activation. Dysregulation of CCL20-CCR6 axis is regarded as an imperative part of the pathogenic mechanism of autoimmune diseases and cancers, and a multitude of therapeutic strategies have been developed to target CCL20-CCR6 axis. In this review, we comprehensively summarized researches of CCL20-CCR6 axis and introduced the biology and functions of CCL20-CCR6 under normal conditions. We further discussed the pivotal pathogenic roles of CCL20-CCR6 axis in progression of autoimmune diseases as well as cancers from multiple directions. The article also explored recent advancements in the field of CCL20-CCR6 axis inhibition in autoimmune diseases and cancers, shedding light on its potential as a promising therapeutic target. A systematic understanding of CCL20-CCR6 axis in progression of autoimmune diseases and cancers is crucial for realizing the full potential of CCL20-CCR6 axis-based interventions, heralding the promise of improved outcomes for patients. - Source: PubMed
Publication date: 2026/06/18
Yu GuanhuaZhang AnLiu YixiaoFan TaoWen XinghaoLi ChunxiangJiang Zheng - Chemokine CCL20, secreted by gut epithelial cells, demonstrates markedly increased expression during episodes of chronic inflammation and infection. Mucosal barriers recruit more CCR6+ B cells and have higher immunogloblin A (IgA) Ab levels during normal, infectious, and inflammatory states. Ig isotypes at the mucosal surface are pivotal in modulating inflammatory responses and controlling infections. However, the intrinsic signaling pathway mediated by CCR6-CCL20 in B cells-in particular, its impact on Ig isotype expression-remains insufficiently investigated. In this study, the dextran sodium sulfate (DSS)-induced gut inflammation model in C57BL/6 mice was used. Our findings indicate that DSS administration elevates CCL20 production in the gut epithelium, which, in turn, enhances the differentiation of IgA+ B cells in gut-associated lymphoid tissues, while concurrently reducing both IgG1+ B-cell populations and serum IgG1 levels, in a CCR6-dependent manner. Furthermore, stimulation with CCL20 through CCR6 induces phosphorylation of the AKT/mTOR/STAT3 signaling pathways in B cells. Pharmacological inhibition of mTOR signaling with rapamycin effectively abrogated CCL20-driven differentiation of IgA+ B cells. Collectively, these results suggest a significant role for CCR6-CCL20 signaling, alongside other costimulatory mechanisms, in regulating Ig isotype switching at the mucosal barrier during intestinal inflammation, thereby offering important insights into CCR6-mediated inflammatory pathologies. - Source: PubMed
Padghan Priyanka DPathak ManishaLal Girdhari - To characterise long-term immune dysregulation and persistent inflammatory signalling in paediatric burn survivors with hypertrophic scarring. - Source: PubMed
Publication date: 2026/05/22
Langley DonnaHolland Andrew J AStefanutti GiorgioKimble Roy MKenna TonyCuttle Leila - Immunosuppression greatly drives oral squamous cell carcinoma (OSCC) progression and impairs patient prognosis, so exploring microbial regulators of the tumor immune microenvironment carries essential research value. While oral bacteria are tightly associated with worsening OSCC, it remains poorly understood how critical periodontal bacteria reshape immune cell composition to support tumor expansion. Here, we demonstrate that the common periodontal pathogen Porphyromonas gingivalis (P. gingivalis, P. g) stimulates cancer cells to secrete C-C motif chemokine ligand 20 (CCL20). This key signaling protein specifically recruits immunosuppressive regulatory T cells (Tregs). This bacterium elevates immune regulatory molecules, strengthens local immune suppression, and accelerates tumor growth in experimental OSCC models. Clinically, abundant P. gingivalis relates to advanced disease and poorly prognosis, and blocking C-C chemokine receptor type 6 (CCR6)-the immune cell receptor for CCL20-reverses the tumor-promoting effect. This study establishes a novel immune-mediated connection between periodontal infection and OSCC progression, and provides promising molecular targets to improve future prevention and targeted treatment for OSCC. - Source: PubMed
Publication date: 2026/06/12
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