Anti_Mouse, mab CXCL14 Source Rat
- Known as:
- Anti_Mouse, mab CXCL14 Source Rat
- Catalog number:
- 103-M357
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab CXCL14 Source Rat
Related genes to: Anti_Mouse, mab CXCL14 Source Rat
- Gene:
- CXCL14 NIH gene
- Name:
- C-X-C motif chemokine ligand 14
- Previous symbol:
- SCYB14
- Synonyms:
- BRAK, NJAC, bolekine, Kec, MIP-2g, BMAC, KS1
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-30
- Date modifiied:
- 2016-10-05
Related products to: Anti_Mouse, mab CXCL14 Source Rat
Related articles to: Anti_Mouse, mab CXCL14 Source Rat
- Advanced renal cell carcinoma frequently acquires resistance to immune checkpoint blockade (ICB), underscoring the pivotal influence of the tumor immune microenvironment (TME) on therapeutic efficacy. While recent studies have implicated multicellular crosstalk within the TME as a central driver of ICB resistance, the precise multicellular programs (MCPs) that orchestrate this process remain poorly defined. Here, through integrative single-cell and spatial transcriptomic profiling of clear cell RCC (ccRCC) cohorts, we delineated a previously unrecognized MCP associated with ICB resistance, distinguished by heightened lysosomal activity, adipogenic signaling, and rewired fatty acid metabolism. Within this program, we uncover a coordinated interplay among TAM_APOE, ccRCC_CXCL14, and endothelial cells, whereby ccRCC_CXCL14 recruits TAM_APOE, which subsequently promotes tumor lipid metabolic reprogramming and angiogenesis, forming a pro-tumorigenic feedforward loop. Spatial mapping revealed a malignant gene topic colocalizing with this MCP in tumor cores, which robustly predicted both unfavorable survival and resistance in ICB-treated patients. Functional assays confirmed that the CXCL14-TAM axis promotes metabolic reprogramming, while dual CXCR4 and PD-1 blockade synergistically reverses the resistant phenotype by restoring CD8⁺ T-cell cytotoxicity. Multiplex immunofluorescence further validated the enrichment of this MCP specifically in non-responders. Collectively, our study defines a spatially organized, functionally coordinated multicellular niche that drives ICB resistance in ccRCC, establishing both a predictive biomarker for patient stratification and a mechanistic framework for therapeutic intervention. - Source: PubMed
Publication date: 2026/07/21
Yao WenbinQi JiabaoZheng XinyiWu KeZheng ZhongYao ZhixianHu Sang - Carotid body tumors (CBTs) exhibit pronounced clinical heterogeneity, particularly in fibrotic progression, yet the underlying cellular mechanisms remain poorly defined. Here, we performed single-cell RNA sequencing on 64,944 cells from three fibrotic CBT (FCBT) and three non-fibrotic CBT (nFCBT) specimens to construct a high-resolution cellular atlas of CBT fibrosis. Integrated analyses revealed that FCBTs are distinguished by a FOXP2+ chief cell subpopulation exhibiting a metabolic shift toward mitochondrial respiration and enhanced MIF signaling, which may facilitate macrophage recruitment. Endothelial cells expanded in FCBTs and acquired pro-angiogenic signatures driven by macrophage-derived CXCL signaling. Notably, CXCL14+ fibroblasts emerged as the principal effectors of extracellular matrix deposition, with lineage inference suggesting their origin from smooth muscle cells. Immune cells, including T/NK and mast cells, further modulated the fibrotic niche through cytokine interactions. This study provides the first comprehensive single-cell dissection of CBT fibrosis, identifies FOXP2+ chief cells as initiators of stromal remodeling, and highlights CXCL14+ fibroblasts as key matrix-producing effectors. These findings nominate FOXP2 and CXCL14 as potential therapeutic targets for mitigating fibrosis in CBT patients. - Source: PubMed
Publication date: 2026/06/25
Cao KangxiYu JiazhiAo GuangnanHan ZongliWang ZhongzhengHan YunfengWang Tao - The poor prognosis of head and neck squamous cell carcinoma (HNSCC) is primarily attributed to lymphatic or systemic metastasis. The cellular identity plasticity provides carcinocytes with the motility phenotype fluctuations, which indicates the intensified metastasis. Aiming at elucidating this lineage evolution, this study integrated single-cell RNA sequencing data from 12 primary lesions, 12 lymphatic metastases, and 12 distant metastases to portray the pan-metastatic cellular landscape. With the escalation of metastasis, there was a dramatic increase in the proportion of cancer-associated fibroblasts (CAFs). The spatiotemporal RNA alternative splicing and trajectory tracing methods with/without histopathological constraint observed that the SCGB3A1 malignant epithelial cells, which become conspicuous in metastasis, undergo partial epithelial-mesenchymal transition (pEMT) to exhibit a CXCL14 CAF phenotype, and B2M CAFs serve as a transdifferentiation terminal. Moreover, multimodal genetic detection identified WD repeat domain 54 (WDR54) as a potential initiator of cellular identity reshaping. Functional experiments demonstrated that WDR54-launched dedifferentiation preserves lineage plasticity via epithelial signature erosion and markedly enhances cellular invasion, migration, and MDSC-mediated immune evasion. Homologous protein structural congruence alignment and CUT&Tag profiling revealed that WDR54 initiates the TGF-β-driven pEMT program by selective H3K4me3 and H4K16ac modifications. Clinically, the practical utility of WDR54 as a diagnostic, prognostic and therapeutic target has received validation from a real-world perspective. In summary, the research establishes WDR54 as an epigenetic regulator that initializes cell identity and triggers metastasis in HNSCC. - Source: PubMed
Publication date: 2026/06/30
Feng QiushiShan XiaofengXia YangyangLiao LingziKang YifanLi ZimengDai ZiweiChai YingyueZhang XinyuanWang LumingXie ShangCai Zhigang - Osteoarthritis (OA) is a globally prevalent degenerative joint disorder that imposes significant socioeconomic burdens. While traditionally viewed as a localized "wear-and-tear" disease, emerging evidence supports a systemic pathogenesis involving the gut-joint axis. The oral-gut-joint pathway remains underexplored in OA pathophysiology. - Source: PubMed
Publication date: 2026/06/22
Liu YuchiGong JinhuaZhang YuyingWang HongyuFeng Haotian - Sinonasal inverted papilloma (IP) carries a 10% risk of malignant transformation to IP-associated sinonasal squamous cell carcinoma (IP-SNSCC), yet the molecular and immune drivers of this progression remain poorly defined. This study integrates single-cell RNA sequencing, multiplexed spatial proteomics, whole-exome sequencing, and functional assays across IP and IP-SNSCC cohorts to define mechanisms of malignant transformation. Respiratory epithelial basal cells are identified as the putative cell of origin, with progression marked by recurrent loss and mutations. Spatial profiling reveals immune reorganization at the lesional interface in IP-SNSCC, characterized by enrichment of alternatively activated M2 macrophages. CXCL14 is shown to directly induce an immunosuppressive myeloid phenotype that suppresses T-cell IFNγ production through an IDO-pathway-dependent mechanism. Integration of these multimodal datasets defines a previously unrecognized CXCL14-IDO mechanism that constrains anti-tumor immunity at the tumor-stroma interface. These findings establish IDO-targeted immunomodulation as a rational adjuvant strategy and provide a comprehensive molecular framework for understanding IP-SNSCC pathogenesis. - Source: PubMed
Publication date: 2026/06/04
Olonisakin Tolani FZamuner Fernando TVu KennyGunti SreenivasuluDing YimingHou YueYang XinpingViswanathan RamyaHuynh AngelComoglio FedericoNotaro MarcoCherry ChristopherPatatanian MichaelWong NathanDeKlotz Timothy RKim JeanKoch WayneLane Andrew PRamanathan MurugappanRowan Nicholas RLechner MattUdager AaronIzumchenko EvgenyAllen Clint TLondon Nyall R