Recombinant Human BRAK (CXCL14) BRAK
- Known as:
- Recombinant Human BRAK (CXCL14) BRAK
- Catalog number:
- chm-001
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human BRAK (CXCL14)
Related genes to: Recombinant Human BRAK (CXCL14) BRAK
- 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: Recombinant Human BRAK (CXCL14) BRAK
Related articles to: Recombinant Human BRAK (CXCL14) BRAK
- Elderly sepsis (ES), characterized by dual insults of aging and sepsis, is associated with substantial morbidity and mortality and exhibits distinct pathophysiological features. Elucidating these unique mechanisms is critical for developing precise therapeutic strategies and improving patient prognoses. - Source: PubMed
Publication date: 2026/05/26
Gou YiXia ZiyuHaireti NazilaAikepaer AilikutiYang JianzhongLi Dandan - Lung cancer (LC), particularly lung adenocarcinoma, is a leading cause of cancer-related mortality, while systemic sclerosis-associated interstitial lung disease (SSc-ILD) is a chronic fibrotic autoimmune disorder. Growing evidence suggests shared molecular mechanisms between these conditions, although their genetic overlap remains insufficiently characterized. In this study, integrative bioinformatics approaches were applied to identify common differentially expressed genes (DEGs) and regulatory networks linking LC and SSc-ILD. Comparative transcriptomic analysis revealed 72 shared DEGs, including 10 hub genes: , , and (upregulated), and , , , , , , and (downregulated). Regulatory network analysis identified key miRNAs (hsa-miR-34a-5p, hsa-miR-126-3p, hsa-miR-335-5p) and central transcription factors (FOS, JUN, NFKB1). Pathway enrichment highlighted interleukin-10 signaling as a critical shared pathway, implicating immune regulation and extracellular matrix remodeling. Molecular docking suggested a potential interaction between doxycycline and MMP7 (binding affinity -6.4 kcal/mol), while X-ray diffraction and Rietveld refinement confirmed its crystalline purity. Additionally, doxycycline demonstrated antibacterial activity against via minimum inhibitory concentration assays. Overall, these findings provide preliminary insights into shared molecular features between LC and SSc-ILD and suggest doxycycline as a potential repurposed candidate warranting further experimental and clinical validation. - Source: PubMed
Publication date: 2026/05/27
Dasgupta SanjuktaGhosh MoupiyaSadhukhan SukhenduSet Srijit - CXCL14 is a highly conserved chemokine with potential roles in tumor progression and immune modulation. This study investigates the functional impact of CXCL14 on colon cancer by exploring its effects on tumor cell behavior and the immune microenvironment. We generated stable cell lines overexpressing CXCL14 in mouse MC38 and CT26 cells and human HCT15 colon cancer cells, and used these models to assess tumor growth, invasion, and immune cell infiltration. Our results demonstrate that CXCL14 suppresses colon cancer cell proliferation, migration, and metastasis. In vitro, CXCL14 inhibited the expression of matrix metalloproteinases (MMPs), key regulators of epithelial-mesenchymal transition (EMT), suggesting a role in promoting mesenchymal-epithelial transition (MET). Additionally, in vivo studies using a subcutaneous tumor model showed that CXCL14 not only suppressed tumor growth but also enhanced the infiltration of immune cells, including NK cells, dendritic cells (DCs), and T cells, converting the tumor microenvironment from a "cold" to a "hot" phenotype. RNA sequencing and pathway analyses revealed that CXCL14 regulates the expression of genes associated with angiogenesis, immune response, and cell signaling, particularly through the MAPK pathway. Furthermore, CXCL14's influence on tumor progression was confirmed in a spleen-to-liver metastasis model, where its overexpression reduced metastatic spread. In conclusion, CXCL14 inhibits colon cancer progression by modulating both tumor cell behavior and the immune landscape, making it a promising candidate for targeted immunotherapy. Our findings highlight CXCL14's potential to enhance anti-tumor immunity and provide new insights into its therapeutic applications in colon cancer. - Source: PubMed
Publication date: 2026/05/08
Zhang YinjieWang SiyiNiu YuchenWang YanjingMa BuyongLi Jingjing - Metastasis is the primary cause of mortality in patients with breast cancer. This study aimed to develop a prognostic signature based on metastasis- and cancer-associated differentially expressed genes (M-CA-DEGs) and to identify potential novel therapeutic genes. - Source: PubMed
Publication date: 2026/05/11
Yao YuanZheng YunshengXie JiancongLiu HonghaoChen ChenCao JieYin Ting-Ting - Hepatocellular carcinoma (HCC) develops within a complex microenvironment in which cancer-associated fibroblasts (CAFs) are abundant, yet their heterogeneity and functional roles remain incompletely understood. Here, we integrated multi-site single-cell RNA sequencing of Normal liver, primary Tumor, portal vein tumor thrombus (PVTT), and metastatic Lymph node samples with bulk transcriptomic analysis, cell-cell communication inference, and functional assays to define stromal programs associated with HCC progression. We identified four transcriptionally distinct CAF subsets: SGCA mCAFs, POSTN mCAFs, TDO2 CAFs, and CXCL14 iCAFs, each showing site-specific distribution and distinct prognostic relevance. Among them, POSTN mCAFs were enriched for extracellular matrix organization and integrin signaling, and their signatures were consistently associated with poor overall survival across independent cohorts. Ligand-receptor analysis identified POSTN mCAFs as highly connected stromal hubs communicating with malignant and myeloid cells through ECM-integrin, collagen-SDC4, and chemokine pathways. Consistently, tumor-derived POSTN-high fibroblasts promoted hepatoma cell proliferation, migration, and invasion in vitro. Together, these findings identify POSTN mCAFs as a transcriptionally distinct and functionally pro-tumorigenic stromal subset in HCC, supporting POSTN-centered stromal programs as candidate markers of aggressive tumor microenvironments and a basis for future mechanistic investigation. - Source: PubMed
Publication date: 2026/05/22
Chen YalinLiu TingtingZhang ShichaoWu Dong