CXCR6
- Known as:
- CXCR6
- Catalog number:
- Y214498
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CXCR6
Related genes to: CXCR6
- Gene:
- CXCR6 NIH gene
- Name:
- C-X-C motif chemokine receptor 6
- Previous symbol:
- -
- Synonyms:
- TYMSTR, STRL33, BONZO, CD186
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-23
- Date modifiied:
- 2016-10-05
Related products to: CXCR6
Anti Human CXCR6 Polyclonal AntibodyAnti Human CXCR6 Polyclonal AntibodyAnti Human CXCR6 Polyclonal AntibodyAnti Human CXCR6 Polyclonal Antibodyanti-CXCR6anti-CXCR6anti-CXCR6anti-CXCR6anti-CXCR6 (C-Terminus)anti-CXCR6 (N-Terminus)anti-CXCR6 (N-Terminus)Anti-CXCR6, Goat Polyclonal to CXCR6, Isotype , Host GoatAnti-CXCR6, Rabbit Polyclonal to CXCR6, Isotype , Host Rabbitanti-CXCR6, Rabbit polyclonal to CXCR6, Isotype IgG, Host RabbitAnti-human CXCR6, Source: Monoclonal Murine, MAB Related articles to: CXCR6
- Loss-of-function mutations in AT-rich interactive domain-containing protein 1 A (ARID1A), accompanied by reduced protein expression, are common in endometrial carcinoma (EC) and correlate with shorter progression-free survival. Alterations in the EC cells secretome play a critical role in shaping the tumor microenvironment (TME), thereby promoting disease progression, metastasis, and therapeutic resistance. Here, we demonstrate that ARID1A-deficient EC cells display a reprogrammed soluble secretome that alters tumor-stromal communication. Among the secreted factors, CXCL16 emerges as the predominant chemokine, promoting epithelial-to-mesenchymal transition and enhancing tumor cell invasiveness. Mechanistically, CXCL16 activates MAPK and Paxillin/FAK pathways, driving YAP/TAZ signaling and reinforcing pro-tumorigenic features. Elevated CXCL16 levels within the tumor niche also promote the conversion of stromal cells into cancer-associated fibroblasts (CAFs) in both preclinical models and patient samples of ARID1A-deficient EC. Importantly, genetic or pharmacological inhibition of CXCL16 or its receptor CXCR6 disrupts these pathogenic interactions, impairing EC cell migration and reducing metastatic burden. These findings identify the secretome of ARID1A-deficient EC cells as a key driver of tumor progression and underscore the CXCL16-CXCR6 axis as a promising therapeutic target in EC. - Source: PubMed
Publication date: 2026/04/10
Megino-Luque CristinaAlbertí-Valls ManelOlave SaraSisó PolBonifaci NúriaMacià AnnaMatias-Guiu XavierGatius SòniaLlobet-Navas DavidEritja Núria - CD4 tissue-resident memory T cells (TRM) are crucial adaptive immune components involved in preventing influenza A virus (IAV) infection. Despite their importance, their physiological role in the upper respiratory tract, the first site of contact with IAV, remains unclear. Here, we find that, after IAV infection, antigen-specific CD4 TRM persist in the nasal tissue (NT) compartment after infection and provide protection upon heterosubtypic challenge. Single-cell RNA-sequencing analysis reveals that NT CD4 TRM are heterogeneous and transcriptionally distinct as compared with their lung counterparts. Mechanistically, we demonstrate that the CXCR6-CXCL16 axis promotes CD4 TRM residency in the NT. Furthermore, we show that the NT of mice and humans contains a high frequency of Th17 CD4 TRM that aid in local viral clearance and in reducing tissue damage. Collectively, our results support a robust physiological role for NT CD4 TRM in local protection during heterosubtypic IAV infection. - Source: PubMed
Publication date: 2026/04/06
Mathew Nimitha RGailleton RomainScharf LydiaSchön KarinEnriquez JosueAxelsson HannesStrömberg AnneliLycke NilsBemark MatsTang Ka-WeiAngeletti Davide - Acute kidney injury (AKI) can progress to chronic kidney disease (CKD) in the setting of maladaptive repair characterized by tubular atrophy, inflammation, and fibrosis. Programmed cell death is a key driver of proximal tubule (PT) loss, yet how immune infiltration promotes tubular injury and death remains incompletely understood. Using a mouse model of maladaptive repair, we integrated bulk and single-cell RNA sequencing with immunohistochemistry and protein analyses to define immune-epithelial interactions during AKI-to-CKD transition. Injured kidneys exhibited loss of healthy PTs, expansion of injured PT subsets, and late-stage T cell accumulation. Apoptotic and necroptotic signaling pathways were markedly upregulated, particularly in VCAM1+ PT cells. Cell-cell interaction analysis identified macrophage-derived Cxcl16 as the dominant chemokine mediating recruitment of Cxcr6+ T cells. Genetic deletion of Cxcr6 reduced renal T cell accumulation, cytotoxic effector expression, and activation of apoptotic (cleaved caspase-3, Bax) and necroptotic signaling (MLKL, phospho-MLKL) in PT cells. Accordingly, Cxcr6 mice displayed preserved PT differentiation, reduced fibrosis, and improved renal function. Together, these findings identify Cxcr6+ T cells as key mediators of immune-driven tubular cell death during maladaptive repair and suggest that targeting the CXCL16-CXCR6 axis may mitigate tubular injury and slow AKI-to-CKD progression. - Source: PubMed
Publication date: 2026/03/24
Li XiaoxuMelchinger IsabelChen YuchuGuo JiankanCantley Lloyd GXu Leyuan - The objective of this study was to investigate the regulatory effect of CXCL16 on macrophage polarization within the microenvironment of chronic atrophic gastritis (CAG), thereby providing a theoretical foundation for understanding the pathogenesis of CAG and developing effective therapeutic strategies. - Source: PubMed
Publication date: 2026/01/19
Ma XiuzhenLiu NingningCui WentingMai Ping - - Source: PubMed
Publication date: 2026/03/17
Zhao YangYan HaoChen XindaZhang XiaolinLu MujunZhang Ming