DDR2 siRNA_Lentivectors
- Known as:
- DDR2 siRNA_Lentivectors
- Catalog number:
- i005816a
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- DDR2 siRNA_Lentivectors
Related genes to: DDR2 siRNA_Lentivectors
- Gene:
- DDR2 NIH gene
- Name:
- discoidin domain receptor tyrosine kinase 2
- Previous symbol:
- TYRO10, NTRKR3
- Synonyms:
- TKT
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-17
- Date modifiied:
- 2016-10-05
Related products to: DDR2 siRNA_Lentivectors
Related articles to: DDR2 siRNA_Lentivectors
- Chronic antibody-mediated rejection (AMR) is a leading cause of late kidney allograft loss, yet sensitive non-invasive biomarkers are lacking. Discoidin domain receptor 2 (DDR2), a collagen-binding tyrosine kinase implicated in fibrosis, may play a role in its pathogenesis. This study aimed to investigate the expression and clinical relevance of DDR2 in patients with chronic AMR. - Source: PubMed
Publication date: 2026/03/26
Li GuanghuiLiu LuhaoHu YuyangGuo YuheWan JiaoFang JialiSu JinChen Zheng - Type X collagen (COL10A1) is an extracellular matrix protein primarily expressed by hypertrophic chondrocytes and is essential for endochondral ossification and skeletal mineralization. Although traditionally regarded as cartilage-specific, recent studies have reported its re-expression in a range of solid tumors. This shift in expression pattern suggests that COL10A1 may have functions beyond development, particularly within the tumor microenvironment (TME). Elevated COL10A1 levels have been reported in cancers such as breast, gastric, colorectal, and lung cancers, where both tissue expression and circulating levels are frequently associated with advanced disease stage and poor clinical outcomes. These observations support COL10A1 as a potential diagnostic and prognostic biomarker. Beyond its clinical associations, accumulating evidence indicates that COL10A1 actively contributes to tumor progression. It is involved in extracellular matrix remodeling, angiogenesis, epithelial-mesenchymal transition (EMT), and alterations in immune cell infiltration, and possibly immunotherapy response. In addition, its enrichment in specific subsets of cancer-associated fibroblasts (CAFs) highlights its essential role in tumor-stroma interactions. At the mechanistic level, COL10A1 has been linked to multiple oncogenic signaling pathways, including TGF-β1/SOX9, as well as downstream DDR2/FAK and ITGB1/PI3K/AKT pathways, which may collectively promote tumor invasion, metastasis, and therapy resistance. However, its biological functions are not yet fully defined, and tumor heterogeneity continues to complicate its clinical application. Further studies are needed to clarify how COL10A1-functions within the tumor microenvironment and to determine its clinical value as a biomarker and a potential therapeutic target in solid cancers. - Source: PubMed
Publication date: 2026/04/15
Zhu TianxiangLiang YutingDong WanyuDeng RushuangHu WenshiWei RongWang QianLu YaojuanQiao LongweiHe Tong-ChuanZheng Qiping - Olaparib is registered for use in ovarian, breast, pancreatic and prostate cancers with a BRCA1/2 mutation and/or mutations in other homologous recombination deficiency (HRD) genes. HRD gene mutations are also found in other cancer types, and these cancers may also benefit from olaparib therapy. We aimed to evaluate the efficacy of olaparib in advanced cancers harboring a (likely) pathogenic germline or somatic mutation in a gene involved in homologous recombination (HR). - Source: PubMed
Publication date: 2026/05/08
Joris SDenys HCollignon JRasschaert Mde Roodenbeke D TDuhoux F PCanon J LTejpar SMebis JDecoster LAftimos PDe Grève J - Angiotensin II (Ang II), a potent profibrotic stimulus, exhibits pleiotropic effects on cardiac cells. The fate of c-Kit cells in an Ang II-elevated injured myocardium remains poorly defined. This study investigated, in vitro, the effect of Ang II on the phenotype of non-hematopoietic non-endothelial c-Kit cardiac interstitial cells (CICs), expressing OCT4. Our findings demonstrate that Ang II directly drives the phenotypic transition of c-Kit CICs into α-SMA-expressing myofibroblasts, accompanied by significant upregulation of prominent myofibroblast markers, SM22-α, collagen type IA, and its crosslinking enzyme, lysyl oxidase. Through targeted silencing experiments, we confirmed that Ang II-mediated phenotypic transition occurs via activation of the ERK1/2 MAPK pathway, triggered by collagen receptor Discoidin domain receptor 2 (DDR2), and involves the transcription factor, serum response factor (SRF). These results indicate that c-Kit CICs are susceptible to myofibroblast transition in the infarcted myocardium, and may serve as an additional source of myofibroblasts contributing to repair and remodeling alongside resident fibroblasts. Additionally, we observed that overexpression of c-Kit attenuated Ang II-induced α-SMA upregulation by downregulating DDR2-ERK1/2-SRF signaling in c-Kit CICs, highlighting the pivotal role of c-Kit expression levels in regulating cell fate. Furthermore, overexpression of c-Kit in Ang II-treated cardiac fibroblasts significantly reduced the expression of myofibroblast proteins, α-SMA, SM22-α, periostin, collagen type IA, collagen receptor DDR2, and lysyl oxidase, and resembled c-Kit CICs in morphology. Collectively, these results suggest that c-Kit expression in myofibroblasts may potentially mitigate the adverse effects of cardiac fibrosis and promote favorable remodeling in the long term. - Source: PubMed
Devidasan IndrajaRadhakrishnan SruthiGopal SarayuNair Geethu SMundackal Sivaraman DivyaPillai Vivek VMohan Neethu - Liver fibrosis is the principal histological determinant of mortality in metabolic dysfunction-associated steatohepatitis (MASH), yet the mechanisms driving progression from steatosis to fibrosis remain incompletely defined and effective anti-fibrotic therapies are limited. Although hepatocyte-derived exosomes under lipotoxic stress promote hepatic stellate cell (HSC) activation, the pathogenic protein cargos remain undefined. This study sought to identify lipotoxicity-induced hepatocyte-derived exosomal proteins that drive MASH fibrogenesis and to define their mechanistic and therapeutic relevance. - Source: PubMed
Publication date: 2026/05/08
Wang YadiWu LiangliangLi ZhaozhiHuang PanfengLuo YinLiao ZhezhenLi JiaoyangJiang XiaoZhu JinLi ShuyanRan LiYang FeiLiu JianghuaLu YanXiao Xinhua