DDR2, Active
- Known as:
- DDR2, Active
- Catalog number:
- 7760-5
- Product Quantity:
- 5 μg
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- DDR2 Active
Related genes to: DDR2, Active
- 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, Active
Related articles to: DDR2, Active
- 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 - Atypical fibroxanthoma (AFX) and pleomorphic dermal sarcoma (PDS) are rare cutaneous mesenchymal tumours sharing clinical and histopathological features. Compared to AFX, PDS has an increased risk of local recurrence and metastasis. A precise diagnosis is critical to ensure proper clinical management and follow-up. AFX and PDS show a similar genetic background, but also a heterogeneous pattern of different molecular abnormalities still poorly investigated due to the rarity of these tumours. Multiple data from different institutions and geographical areas, facilitate the identification of molecular alteration/s of valuable diagnostic and/or sub-classification power. We investigated the DNA profile of 32 AFX and PDS samples using a custom targeted Next-Generation Sequencing panel including 228 cancer genes. We confirm a common pattern of gene mutations affecting TP53, CDKN2A and NOTCH1. Differences appeared in less frequently detected genes (e.g. TSC2) and in NF2 harbouring novel genetic alterations. Integrating our results with published datasets of AFX and PDS mutation profiles we observed a divergent distribution of alterations in genes signalling through angiogenic pathway (KDR, PDGFRB), DNA damage response (ATR), cellular migration/metastasis (DDR2, CDH1). These differences do not reach statistical significance, and histopathological evaluation remains the diagnostic gold standard, however, they offer valuable insights into the pathogenesis of these tumours. - Source: PubMed
Publication date: 2026/05/03
Caprini ElisabettaScaglione Giovanni LucaScarponi ClaudiaMorelli MartinaMadonna StefaniaMarani CarlaSebastiani ValeriaScala EnricoAlbanesi CristinaRahimi Siavash - Bladder cancer (BC) is a prevalent malignant tumor worldwide, posing a significant public health burden and challenge to human society. Current therapeutic modalities for BC include surgical treatment, radiotherapy, chemotherapy, targeted therapy, and immunosuppressive therapy. However, almost all patients experience disease progression and ultimately succumb to BC. Our study demonstrated that elevated expression of Heat Shock Protein Beta-6 (HSPB6) correlated with higher clinical grades and stages, establishing it as an independent prognostic risk factor for BC. Enrichment analysis indicated that HSPB6 is associated with the extracellular matrix in BC. Experimental validation revealed that HSPB6 overexpression inhibits the proliferation of BC cell line T24. This effect may be achieved by inhibiting the PI3K/Akt signaling pathway, which in turn leads to inhibition of epithelial-mesenchymal transition (EMT). Furthermore, we developed a prognostic risk model that incorporated DDR2, DPYSL3, MFAP5, PDGFRB, and SPOCD1, allowing accurate prediction of patient outcomes based on immunological status. In conclusion, this study highlights that HSPB6 overexpression can restrain the proliferation of BC cells and inhibit EMT, underscoring its potential as a diagnostic marker and therapeutic target in BC. - Source: PubMed
Publication date: 2026/04/20
Wang Jian-SheQiu Yi-FanZhang LuJi BoLiang SenWang Ya-XuanZhu Hai-Xia - Glioblastoma (GBM) is a highly aggressive brain tumor with a poor prognosis, and its etiology involves both genetic and environmental factors. Triphenyl phosphate (TPHP), an organophosphorus flame retardant widely used in various consumer products, has raised public health concerns due to its environmental prevalence and detection in human samples. However, its potential role in GBM pathogenesis remains unclear. This study combined machine learning and molecular simulation docking technology to investigate the effects of TPHP on the pathogenesis and related molecular mechanisms of glioma. - Source: PubMed
Publication date: 2026/03/24
Wang ZiyuCui KaiWang JialinMa RongWang Yanyang