DDR2 (3B11E4 )
- Known as:
- DDR2 (3B11E4 )
- Catalog number:
- NBP1-28883
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- DDR2 (3B11E4 )
Related genes to: DDR2 (3B11E4 )
- 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 (3B11E4 )
Active DDR2Active DDR2anti-DDR2anti-DDR2anti-DDR2anti-DDR2 (3B11E4)Anti-DDR2 Antibodyanti-DDR2 type: Primary antibodies host: MouseAnti-DDR2, Mouse Monoclonal to DDR2, Isotype IgG2a, Host MouseCD167 antigen-like family member B,DDR2,Discoidin domain receptor 2,Discoidin domain-containing receptor 2,Discoidin domain-containing receptor tyrosine kinase 2,Homo sapiens,Human,Neurotrophic tyrosiCD167 antigen-like family member B,Ddr2,Discoidin domain receptor 2,Discoidin domain-containing receptor 2,Mouse,Mus musculus,Neurotrophic tyrosine kinase, receptor-related 3,Ntrkr3,Receptor protein-tCD167b DDR2 Ig antibody Ab host: RabbitCD167b DDR2 Ig antibody Ab host: RabbitCD167b DDR2 IgG antibody Ab host: RabbitCD167b DDR2 IgG2a antibody Ab host: Mouse Related articles to: DDR2 (3B11E4 )
- Orofacial clefting (OFC) is among the most common birth defects and can occur either as part of a syndrome or in isolation (nonsyndromic, ns). Cleft palate only (CPO) is an OFC subtype. Here, we searched for novel nsCPO risk genes carrying homozygous and compound-heterozygous variants, by analyzing exome data from six sibling pairs with nsCPO born to unaffected parents. After stringent quality control and filtering, we identified 6 homozygous variants and 32 compound-heterozygous variants in 5 and 16 candidate genes, respectively. We prioritized DDR2, a collagen-activated receptor-tyrosine-kinase influencing extracellular matrix composition, as our top candidate for functional follow-up, since variants in this gene can cause Warburg-Cinotti syndrome, the phenotypic spectrum of which includes palatal abnormalities. Knock-down and knock-out of DDR2-orthologs in zebrafish caused craniofacial abnormalities resembling CPO in humans. Zebrafish immunostaining indicated that DDR2-orthologs were expressed in mature head muscle cells, while murine single-cell RNA-Sequencing data detected Ddr2 expression only in head muscle progenitor cells; the latter finding was confirmed in human embryo sections stained for DDR2. DDR2-expressing head muscle progenitor cells may influence extracellular matrix composition through DDR2-mediated signaling, thereby affecting outgrowth, elevation, and fusion of the palatal shelves, a previously postulated mechanism involved in palatogenesis. Most established OFC genes (e.g. CDH1, CTNND1, IRF6, and GRHL3) act via mechanisms related to epithelial integrity and periderm differentiation, whereas our data provide evidence supporting DDR2 as a risk gene for nsOFC that functions by influencing extracellular matrix composition. - Source: PubMed
Capecki Julia AShkuro HelenaYilmaz ÖznurSchmitt LisaChannab KhadijaLindenberg Tobias TKruse TeresaAchterrath SarahCrespo BertaSiewert AnnaBakhshi MostafaPantel LeandraLudwig Kerstin UGeyer MatthiasMangold ElisabethOdermatt BenjaminIshorst Nina - Cardiac calcification is an age-associated pathological process that contributes to cardiac dysfunction, arrhythmia, and sudden cardiac death, yet its underlying mechanisms remain unclear. Cardiac fibroblasts (CFs) have emerged as key mediators of ectopic calcification through osteogenic differentiation. Proprotein convertase subtilisin/kexin type 9 (PCSK9), a key regulator of cholesterol metabolism, has been implicated in cardiovascular pathology beyond its canonical role, but its involvement in cardiac calcification is unknown. In this study, aged mice exhibited cardiac dysfunction, interstitial fibrosis, and myocardial calcium deposition, accompanied by upregulation of osteogenic markers, including Runx2, OCN, and Osx. PCSK9 expression was increased in aged hearts and enriched in DDR2-positive cells. In vitro, senescent CFs displayed enhanced osteogenic differentiation, characterized by increased calcium deposition, alkaline phosphatase activity, and elevated expression of osteogenic markers. Recombinant PCSK9 promoted osteogenic differentiation in young CFs, whereas genetic deletion of PCSK9 attenuated these effects in senescent CFs. Pharmacological experiments suggest that PCSK9-mediated osteogenic differentiation is associated with activation of the ATF4 pathway and upregulation of Runx2 expression. These findings support a role for the PCSK9-ATF4-Runx2 signaling axis in osteogenic differentiation of CFs, providing new insights into age‑related cardiac calcification and identifying this pathway as a hypothesis‑generating candidate for future investigation. - Source: PubMed
Publication date: 2026/06/19
Liu GangCai QiuyaYe LinPan BinbinYe ChenjiZhang ShuhongSun YongkunCui ChaochuLu ChengbiaoWang Xianwei - Human induced pluripotent stem cell (hiPSC) technologies offer human-relevant cardiac models for biomedical applications. However, workflows for differentiation of cardiac stromal cells and fabrication of engineered heart tissue (EHT) commonly rely on animal serum, contrary to growing policy demands to reduce use of these products. Applying marker analysis via COL-I, DDR2 and GATA4 for cardiac fibroblasts or CD31, CD34 and CD144 for endothelial cells, we tailored Panexin, a defined serum substitute, to support high efficiency differentiation of cardiac stromal lineages to 85% purity without additional purification steps. We evaluated fabrication of EHTs using hiPSC-cardiomyocytes only (monoculture) or further combined with cardiac fibroblasts and endothelial cells (triculture; 70%:15%:15%, respectively). Panexin poorly supported fabrication and contractility of EHTs, a finding unaltered by modulating spontaneous cardiac myofibroblast activation via TGFβ inhibition. In contrast, human serum enabled fabrication of mono- and tri-culture EHTs, wherein constructs made without TGFβ signalling inhibition delivered the strongest contractile forces and exceeded comparator tissues engineered using animal serum. Our data show that iterative evaluation of serum substitutes, human serum, cell combinations and signalling pathway modulators can mitigate use of animal serum for functional EHT generation, aligning with the UK government's roadmap for alternative methods. - Source: PubMed
Publication date: 2026/06/16
Vo Nguyen T NChung KelvinNasir AishahPavlovic DavorDenning Chris - Extracellular matrix (ECM) stiffening is a biophysical hallmark of solid tumors. Cutaneous melanoma is an aggressive malignancy characterized by high heterogeneity and phenotypic plasticity in which melanoma cells switch from a proliferative and differentiated phenotype to an invasive, dedifferentiated and therapy-resistant state. However, the impact of ECM stiffness on the diverse cellular phenotypes of melanoma remains poorly defined. Here, we show that melanoma cell subpopulations differ in their responses to mechanical signals. Compared to melanocytic/transitory cells, dedifferentiated cells exhibited heightened sensitivity to stiff collagen matrices, characterized by increased cell spreading, focal adhesion maturation, YAP nuclear translocation and contractility. ECM stiffening enhanced proliferation, migration and invasion in dedifferentiated cells, whereas highly proliferative and poorly migratory melanocytic/transitory cells were less affected by collagen stiffness. Importantly, a soft ECM sensitized dedifferentiated cells, but not melanocytic/transitory cells, to BRAF/MEK inhibition. Mechanistically, the mechanosensitivity of dedifferentiated cells relies on collagen receptors DDR1 and DDR2, which control cytoskeleton reorganization and YAP mechanosignaling. Genetic or pharmacological inhibition of DDR, actomyosin contractility, or YAP suppressed stiffness-induced proliferation and migration, reduced traction forces, and restored sensitivity to targeted therapy in dedifferentiated cells. Conversely, ectopic DDR1/DDR2 expression confers mechanosensitive properties to melanocytic cells. Our results thus reveal that phenotypic plasticity endows dedifferentiated melanoma cells with increased addiction to mechanical cues and implicate DDR1/2-YAP-dependent signaling in this aggressive behavior. - Source: PubMed
Publication date: 2026/06/13
Lecacheur MargauxBerestjuk IlonaCarminati AlexandrineRabbaa MiraBouvet OcéaneDiazzi SerenaBiber PierricRovera ChristopherIrondelle MarieLarbret FrédéricProd'homme VirginieGirard Christophe ADeckert MarcelTartare-Deckert Sophie - Collagen receptors orchestrate vital extracellular matrix signaling, yet the inability to distinguish functional receptor activation from mere expression in real-time has obscured our understanding of fibrotic progression. Here, we develop a fluorescent triple-helical collagen-mimetic peptide (CMP) probe, [GVMGFO], designed to selectively target the ligand-engaging conformation of Discoidin Domain Receptor 2 (DDR2)─the sole receptor tyrosine kinase family that signals collagen. In pulmonary fibrosis, this probe identifies active fibrotic niches and directly tethers to disease-driving activated fibroblasts to enable precise mapping, all without perturbing baseline signaling. Utilizing this tool, we decipher the long-standing mystery of DDR2's characteristically slow, hours-long activation kinetics. We reveal that while monomeric collagen engagement fails to override constitutive DDR2 internalization, supramolecular fibrillar collagen provides a multivalent physical anchor that arrests DDR2 trafficking at the cell-matrix interface to sustain receptor clustering and phosphorylation. To recapitulate this biophysical requirement, we engineered Zn-coordinated supramolecular assemblies of a histidine-modified CMP, [H-GVMGFO-H], triggering rapid DDR2 activation within minutes. Our work transforms CMPs from structural models of collagen into programmable chemical tools for dissecting the spatiotemporal dynamics of collagen-receptor interplay, offering a platform for imaging and modulating fibrotic disease. - Source: PubMed
Publication date: 2026/06/05
Liu YinghuaWang XufeiMa XiaotongHuang LuYang PenghuiLi TaoWu WenjunZhou DaoningSu JinLi Yang