DDR2 antibody Monoclonal Antibodies Primary antibodies
- Known as:
- DDR2 (anti-) Monoclonal Antibodies Primary antibodies
- Catalog number:
- orb117275
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- DDR2 antibody Monoclonal Antibodies Primary antibodies
Related genes to: DDR2 antibody Monoclonal Antibodies Primary antibodies
- 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 antibody Monoclonal Antibodies Primary antibodies
Related articles to: DDR2 antibody Monoclonal Antibodies Primary antibodies
- Doxorubicin (DOX) is a highly effective anthracycline chemotherapeutic drug. However, the clinical application is limited due to its dose-dependent cardiotoxicity. Discoidin domain receptor 2 (DDR2), the main collagen-binding receptor tyrosine kinase is a major player of various degrees of fibrosis or tissue restructuring in pathological conditions and unknown its role for DOX-induced heart injuries. We investigated the impacts of DDR2 deficiency from acute DOX cardiotoxicity in vivo, by utilizing DDR2-knockout (DDR2) and wild-type (Wt) mice. Genetic deletion of DDR2 significantly reduced DOX-induced cardiac dysfunction. Furthermore, we observed a substantial reduction in reactive oxygen species generation within the vasculature of DDR2 + DOX mice, along with decreased mRNA expression of Hmox1 and Nfe2l2 in cardiac tissue. Additionally, DDR2 deficiency suppressed the DOX-induced Inflammatory cytokines. Finally, DDR2 attenuated DOX-induced cardiac fibrosis. The work demonstrates that DDR2 plays a pivotal role in the pathogenesis of DOX-mediated cardiotoxicity. - Source: PubMed
Publication date: 2026/09/17
Zhang YihanXu BoweiFeng JunqiangSun ChuangJia Qingge - -associated skeletal dysplasias affect cartilage extracellular matrix and endochondral growth, but patient growth-plate tissue is largely inaccessible. We generated chondrogenically induced urine-derived cells (chUDCs) from three individuals with heterozygous pathogenic variants and three healthy controls. Classical differentiation was assessed by Alcian blue and Alizarin red staining, bulk RNA sequencing compared patient-derived and control chUDCs, and single-cell RNA sequencing was performed in two patient-derived lines. -mutant chUDCs retained overt chondrogenic and osteogenic staining capacity without a clear patient-control separation. In contrast, bulk RNA sequencing identified a small set of consistently differential extracellular-matrix remodeling genes enriched for matrix and ossification-related programs; and remained significant in leave-one-donor-out, age-adjusted and cell-composition-adjusted models. Single-cell profiling resolved multiple chUDC states, including chondrogenic, fibroblastic extracellular-matrix, IGF1R-high, and osteogenic-associated states. IGF1 co-treatment was associated with reduced osteogenic-associated module scores and increased fibroblastic/anabolic extracellular-matrix programs. Because no IGF1-treated control-donor line was profiled, IGF1-associated changes are reported as exploratory and are not claimed to be -specific. These findings support chUDCs as a non-invasive system for exploring selected transcriptional programs relevant to cartilage biology and growth-factor responsiveness in -associated growth disorders. - Source: PubMed
Publication date: 2026/09/01
Schulz AlexanderSchubert MichaelBrockmann Emily MEkici Arif BUebe SteffenThiel Christian T - Collagen specifically binds discoidin domain receptor 2 (DDR2) to regulate cellular behaviors such as adhesion and spreading. Although its molecular structure is highly susceptible to physicochemical modifications, the quantitative impact of these alterations on DDR2 engagement and downstream cellular responses remains poorly understood. Herein, we systematically investigated the effects of physical treatments including cryogenic milling, heating, and irradiation on the structural integrity of bovine Achilles tendon collagen and its subsequent DDR2 binding capacity. Structural parameters were quantified using circular dichroism and SDS-PAGE, and CAL27 squamous carcinoma cells were used as the cellular model. The affinity of collagen for DDR2 showed an exponential positive correlation with triple-helix integrity (R = 0.92) and an exponential negative correlation with molecular fragmentation (R = 0.96). Binding capacity also exhibited a strong linear correlation with CAL27 cell adhesion efficiency (R = 0.91). Progressive structural degradation significantly compromised cell adhesion, restricted cellular spreading, and downregulated surface DDR2 expression. This study provides a quantitative framework linking collagen structural parameters to DDR2 engagement and establishes exponential correlation models. These insights may inform the rational design of advanced collagen biomaterials and targeted receptor therapeutics. - Source: PubMed
Publication date: 2026/09/10
Hou YuanjingWang FeiHan QingqiuFan DeshengZhang JuntaoWei BenmeiKou HuizhiWang Haibo - The tunica adventitia of blood vessels is a highly heterogeneous microenvironment comprising diverse cell types. Beyond providing structural scaffolding, adventitial fibroblasts act as dynamic, responsive cells that contribute to vascular homeostasis mainly through regulation of collagen, fibronectin and elastin expression and paracrine effects that promote vascular inflammation. Their dysregulation leads to the onset and progression of several diseases. Signaling pathways in adventitial fibroblasts, particularly DDR2, hypoxia-ERK1/2 MAPK and PI3K/Akt signaling, impact cell proliferation, pro-fibrotic gene expression and cellular response to stress. Furthermore, non-coding RNAs and novel epigenetic mechanisms significantly impact adventitial fibroblast function. Adventitial fibroblasts promote sex-related variations in the prevalence and severity of vascular diseases. Rapid advances in single-cell transcriptomics, biomarker development and other molecular and imaging techniques promise deeper insights into adventitial fibroblast biology, unravelling their heterogeneity and functional variability, and their role in extracellular matrix remodeling and paracrine signaling. These in turn would pave the way for innovative strategies to target pro-fibrotic fibroblast subpopulations and prevent adverse vascular remodeling. This review provides an overview of adventitial fibroblast function and the role of these cells in atherosclerosis, hypertension, diabetes, aneurysm and age-related vascular dysfunction, underscoring the need for a paradigm shift in vascular biology, positioning the adventitia as a critical regulator of vascular health and disease. - Source: PubMed
Publication date: 2026/08/24
Sebastian ManiVijayakumar AnupamaJayachandran ParvathyWang MingyiKailasam Shivakumar - Dedifferentiated liposarcoma (DDL) is defined by amplification of chromosome 12q13-15 but exhibits substantial morphologic heterogeneity, including variable stromal composition. This study aimed to determine whether prominent stromal patterns in DDL are associated with distinct immunophenotypic and genomic profiles. - Source: PubMed
Choi Nam-KyuKim So-WoonKim Dong-HoonDO Sung-ImYamamoto HidetakaNa Kiyong