Ask about this productRelated genes to: COL16A1 antibody
- Gene:
- COL16A1 NIH gene
- Name:
- collagen type XVI alpha 1 chain
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p35.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-14
- Date modifiied:
- 2016-10-05
Related products to: COL16A1 antibody
Related articles to: COL16A1 antibody
- Osteoarthritis is a degenerative joint disease that can currently only be treated by alleviating pain or, ultimately, by a total joint replacement. The bone morphogenetic protein 7-derived peptide p[63-82] offers a potentially novel molecular treatment option for osteoarthritis. Mapping peptide-induced transcriptomic changes in human articular chondrocytes is expected to help reveal how p[63-82] confers its chondrocyte phenotype modulating bioactivity. - Source: PubMed
Publication date: 2026/04/07
Steijns Jessica S Jvan den Akker Guus G HWelting Tim J MCaron Marjolein M J - Diabetic foot ulceration (DFU) imposes major global health burdens due to high morbidity and recurrence rates. Current therapies (debridement and offloading) show limited efficacy, highlighting the need to uncover molecular mechanisms of diabetic wound repair. Multi-omics analyses of DFU and healthy skin identify fibroblast-derived COL16A1 as a wound healing mediator. In vitro, COL16A1 overexpression or knockdown in fibroblasts is employed to assess its regulatory effects on cellular function and collagen secretory capacity. In vivo, localized adenoviral delivery of COL16A1 is administered to evaluate its therapeutic impact on wound closure in diabetic mice. DNA pull-down plus LC-MS/MS, ChIP-qPCR, and luciferase reporter assays are systematically implemented to delineate the upstream regulatory mechanism of COL16A1 expression. Transcriptomic profiling of skin specimens identifies fibroblast-derived COL16A1 as a key regulatory gene in DFU repair. Subsequent in vitro and in vivo experiments demonstrate COL16A1 enhances fibroblast activation and restores normal repair processes in diabetic wounds. Notably, Brahma-related gene 1 (BRG1) is identified as the key transcription factor governing COL16A1 expression. BRG1 directly binds to the COL16A1 promoter, upregulating its transcription and thereby accelerating diabetic wound healing. BRG1-COL16A1 axis is a critical regulatory pathway and proposes novel therapeutic targets for chronic diabetic wounds. - Source: PubMed
Publication date: 2026/03/02
Wang PenghuiSun JiamingWang YingRen BichenLiu YuxinLiu YunhanChen LiangYu LuDai TaoYu LiDong Zhihui - Breast cancer is the most commonly diagnosed cancer in women globally. Our previous MIRACLE trial (NCT02313051) demonstrated that everolimus plus letrozole (E + L) significantly improves progression-free survival compared with letrozole (L) monotherapy in premenopausal patients with endocrine therapy-resistant, hormone receptor-positive, HER2-non-amplified advanced breast cancer. This study aims to investigate spatially resolved biomarkers linked to survival benefits from E + L to guide precision therapies. Patients from MIRACLE were stratified by overall survival (OS ≤ 3 vs. >3 years). Spatial Whole Transcriptome Atlas analysis was used to evaluate tumor-, immune-, and stroma-specific gene expression, co-expression network patterns, and survival correlations. Among patients with shorter survival (OS ≤ 3 years), we identified a distinctive gene interaction network characterized by tumor-derived S100A9 and CALML5, which is associated with mTORC1 activation. This finding suggests that tasquinimod, an S100A9 inhibitor, could be a viable therapeutic option. Additionally, an interaction between CALML5 and SLPI across tumor and immune areas indicated a potential role in maintaining tumor integrity and mitigating immune-mediated damage. Conversely, patients with longer survival (OS > 3 years) exhibited SERPINA1 as a hub gene linked to estrogen receptor activation, and an interaction between FKBP5 and SESN3 associated with AKT/mTORC1 inhibition within tumor-rich regions. Furthermore, the interaction between MMP11 and COL16A1 in stroma-rich regions suggests that cancer-associated fibroblasts may contribute to improved outcomes. Our study underscores the critical role of spatial gene expression analysis in elucidating the tumor microenvironment and its impact on prognosis in patients undergoing E + L treatment, thereby opening new avenues for targeted interventions. - Source: PubMed
Publication date: 2026/02/18
Xue XueminJi DanyangXue LiyanTan YujingWang BingzhiWang JiayuMa FeiLuo YangLan BoChen ShanshanYing JianmingXu BingheFan Ying - Hepatic stellate cell (HSC) activation plays a crucial role in the progression from chronic liver disease to hepatocellular carcinoma (HCC) by establishing disorganized extracellular matrix (ECM) and facilitating immune evasion. However, the effects of HSC on the tumor microenvironment (TME) in lenvatinib (LEN)-treated HCC have not been well explored. In the present study, CCL11 secretory levels elevated in both the serum of HCC patients and the supernatant of HSCs following LEN treatment. In HSCs, CCL11 protein increased, while a CCR3 inhibitor decreased, expression of CCL11- and ECM-related genes: Col3a1 and Col16a1. Based on the expression of Ccl11 and its top 10 related genes, TCGA HCC samples (n = 371) were stratified into high- (n = 175) and low-expression (n = 196) groups. The pathways related to ECM and cell chemotaxis were upregulated in the high-expression group through GO and KEGG analyses. Tumor-associated- macrophages (TAMs) and neutrophils (TANs) and their marker genes (Cd206 and S100a9) were also enriched in this group. Mechanically, the over-production of CCL11 activates HSCs through the CCL11/CCR3 signaling pathway, resulting in the augmented CCL26 secretion to promote the infiltration of TAMs and TANs. In mice, LEN showed weaker tumor control and increased COL3A1, CD206, and S100A9 expression in tumors co-transplanted with HSCs versus tumor cells alone. Combining a CCR3 inhibitor with LEN reversed these effects. In conclusion, CCL11 over-production drives HSC activation, creating an ECM-disorganized and immunosuppressive TME via the CCL11/CCR3 axis in LEN-treated HCC. Combination therapy with CCR3 inhibitor and LEN might represent a novel therapeutic strategy. - Source: PubMed
Publication date: 2025/11/26
Qiang NaLan ChengLin AnKanzaki HiroakiInoue MasanoriKanogawa NaoyaKondo TakayukiOgasawara SadahisaNakamura MasatoNakamoto ShingoCui DaweiLv HangXu QiuranChen GuipingAo Junjie - Caloric restriction is so far the most effective strategy for weight management. Based on their weight loss response, individuals can be classified as hypo-responders or hyper-responders. Therefore, efforts have been made to understand the molecular mechanisms underlying these differential responses to develop more effective and personalized weight loss interventions. This study aimed to identify changes in gene expression patterns between hyper- and hypo-responders selected from a dietary intervention based on caloric restriction. - Source: PubMed
Publication date: 2025/10/14
Vela-Vásquez Diana ADelgado-Enciso IvánSifuentes-Rincón Ana M