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Human Monoclonal DDR2 Primary Antibody für ICC, IHC - ABIN969083
Leitinger, Kwan: The discoidin domain receptor DDR2 is a receptor for type X collagen. in Matrix biology : journal of the International Society for Matrix Biology 2006
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Human Polyclonal DDR2 Primary Antibody für IF (p), IHC (p) - ABIN755218
Wang, Wang, Zhao, Li, Deng: Angiotensin II upregulates K(Ca)3.1 channels and stimulates cell proliferation in rat cardiac fibroblasts. in Biochemical pharmacology 2013
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Human Monoclonal DDR2 Primary Antibody für CyTOF, FACS - ABIN4899816
Ali, Ranjbarvaziri, Talkhabi, Zhao, Subat, Hojjat, Kamran, Müller, Volz, Tang, Red-Horse, Ardehali: Developmental heterogeneity of cardiac fibroblasts does not predict pathological proliferation and activation. in Circulation research 2014
DDR2 mutations were observed in 4% of cases of lung squamous cell carcinoma of European descent; no clinical characteristics were significantly associated with DDR2 mutation
The Epithelial-to-Mesenchymal Transition inducing factor TWIST1 drives expression of discoidin domain receptor 2 (DDR2). The collagen receptor DDR2 is critical for multiple steps of ovarian cancer progression to metastasis.
DDR2 expression is upregulated by matrix stiffening. DDR2 controls the epithelial-mesenchymal-transition markers via c-Myb acetylation upon matrix stiffening.
Higher DDR2 expression was associated with lower miR-182 levels.
High DDR2 expression is associated with Gallbladder Squamous Cell/Adenosquamous Carcinomas
Mutations of KRAS and DDR2 were found in large cell carcinoma (LCC) and squamous cell carcinoma (SCC) subtypes, respectively, whereas mutations of TP53 were seen in SCC and lung adenocarcinoma subtypes with higher frequencies and LCC subtype with lower frequency in Iranian patients.
Our data indicate that DDR2 is a potent biomarker that can be used as an effective therapeutic target for treating oral squamous cell carcinoma patients with lymph node metastasis.
DDR2 localisation is independent of integrin activation and the key DDR2 signalling effector SHC1. Structure-function analysis reveals that DDR2 mutants defective for collagen binding or kinase activity are unable to localise to the cell surface, demonstrating for the first time that both collagen binding and kinase functions are required for spatial localisation of DDR2.
report the identification and characterization of a selective, extracellularly acting small molecule inhibitor (WRG-28) of DDR2 that uniquely inhibits receptor-ligand interactions via allosteric modulation of the receptor. By targeting DDR2, WRG-28 inhibits tumor invasion and migration
Our results suggest that a mutation in DDR2 occurs naturally with a frequency of about 2% in Korean lung SCC patients. In addition, we showed that each of the novel DDR2 mutations were located in a kinase domain and induced an increase in cell proliferation rate.
Overexpression of DDR2 might contribute to tumor progression in lung SQCC. The overexpression of DDR2 could be potential molecular target of lung SQCC.
DDR2 overexpression is independently associated with tumor progression and poor survival rates in urothelial carcinoma patients.
The DDR2 E655K mutation can play a role in cancer progression.
collagen II-activated phosphorylated-DDR2 induces CYR61 through activation of transcription factor activator protein 1 (AP-1). The elevated CYR61, in turn, accelerates MMP1 production via ETS1 (ETS proto-oncogene 1).
these data suggest that biological collagen aging could increase tumor cell proliferation by reducing the activation of the key matrix sensor DDR2
Female ddr2-deficient mice homozygous for the slie mutation show inefficient spontaneous BC metastasis.
This study suggested that DDR1 and DDR2 knockdown alters brain immunity and significantly reduces the level of triggering receptor expressed on myeloid cells (TREM)-2 and microglia.
This work identifies DDR2 as a potential therapeutic target that controls breast cancer metastases through its action in both tumor cells and tumor-stromal cells at the primary tumor site.
The group of patients with colorectal cancer with high DDR2 expression had significantly higher frequencies of T4, lymph node metastasis, and peritoneal dissemination compared to the group with low DDR2 expression.
DDR2 showed high expression in gastric cancer tissues and cells. In xenograft models, DDR2 overexpression promoted tumor formation. Furthermore, DDR2 expression impacted on the invasion and motility of GC cells, accompanied by changes in EMT marker expression. Finally, our results revealed that DDR2 facilitates GC cell invasion and EMT through mTORC2 activation and AKT phosphorylation.
DDR2 is important for maintenance of osteoblast activity and suppression of marrow adipogenesis in vivo and these actions are related to changes in MAPK-dependent RUNX2 and PPARgamma phosphorylation.
circulating fibroblast precursors expressing DDR2, in an exposure-induced model of pulmonary fibrosis, is reported.
The progressive process of articular cartilage degeneration was significantly delayed in the knee joints of Ddr2-deficient mice in comparison to their control littermates. Articular cartilage damage in the knee joints of the mice was associated with increased expression profiles of both Ddr2 and matrix metalloproteinase 13.
DDR2 mutation can drive lung cancer initiation in vivo and provide a novel mouse model for lung cancer therapeutics studies.
Study showed that Nrp1 expression paralleled with that of DDR2 during osteoblast differentiation. Nrp1 assisted the promoting role of DDR2 in osteoblast differentiation, via activation of DDR2-mediated downstream signaling.
Data show that discoidin domain receptor (DDR) 2 siRNA-mediated suppression of extracellular regulated kinase (ERK) 1 and 2 and nuclear factor of kappa B (NF-kappaB) could down-regulate the expressions of matrix metalloproteinase (MMP) 2 and 9.
RESULTS Data show that DDR2 (discoidin domain receptor 2) suppresses osteoclast differentiation and activity.
DDR2 signaling regulates cell proliferation and extracellular matrix synthesis, which are key aspects of fibroblast contribution to tissue healing [review]
Germline deletion of the DDR2 results in smaller hearts, shorter cardiomyocytes, lower interstitial cardiac collagen density and abnormalities in cardiac function.
Taken together, our data demonstrated that DDR2 might play a systemic role in the regulation of body size thorough skeletal formation and fat metabolism.
Loss of DDR2 suppresses tumor angiogenesis and tumor metastasis to the lung.
DDR2 is involved in the collagen I-induced IL-12 production via NF-kappaB and JNK pathway
these data demonstrated that DDR2 might play a local and essential role in the proliferation of chondrocytes.
DDR2 deficiency predisposes hepatic tissue to colon carcinoma metastasis. DDR2 deficiency fosters myofibroblast transdifferentiation of tumour-activated hepatic stellate cells (HSCs), generating a prometastatic microenvironment in the liver.
DDR2 regulated the transactivity of Runx2, a master transcription factor involved in skeletal development, by modulating its phosphorylation.
Reduction of DDR-2 expression attenuates the articular cartilage degeneration of knee joints induced either by type XI collagen deficiency or by surgical destabilization of the medial meniscus.
Study results show that Ddr2 significantly reduced the persistence length and Young's Modulus of collagen type I fibers.
since soluble forms of DDR1 and DDR2 containing its ECD are known to naturally exist in the extracellular matrix, in this work we investigated if these soluble DDR ECDs may have a functional role in modulating collagen fibrillogenesis
Results indicate that discoidin domain receptor 2 signaling plays a critical role in the maintenance of male spermatogenesis.
DDR2 activation may be effected by single triple-helices rather than fibrillar collagen
Receptor tyrosine kinases (RTKs) play a key role in the communication of cells with their microenvironment. These molecules are involved in the regulation of cell growth, differentiation, and metabolism. In several cases the biochemical mechanism by which RTKs transduce signals across the membrane has been shown to be ligand induced receptor oligomerization and subsequent intracellular phosphorylation. This autophosphorylation leads to phosphorylation of cytosolic targets as well as association with other molecules, which are involved in pleiotropic effects of signal transduction. RTKs have a tripartite structure with extracellular, transmembrane, and cytoplasmic regions. This gene encodes a member of a novel subclass of RTKs and contains a distinct extracellular region encompassing a factor VIII-like domain. Alternative splicing in the 5' UTR results in multiple transcript variants encoding the same protein.
CD167 antigen-like family member B
, cell migration-inducing protein 20
, discoidin domain receptor 2
, discoidin domain receptor family, member 2
, discoidin domain-containing receptor 2
, discoidin domain-containing receptor tyrosine kinase 2
, hydroxyaryl-protein kinase
, migration-inducing gene 16 protein
, neurotrophic tyrosine kinase receptor related 3
, neurotrophic tyrosine kinase, receptor-related 3
, receptor protein-tyrosine kinase TKT
, tyrosine-protein kinase TYRO10
, tyrosylprotein kinase
, discoidin domain receptor tyrosine kinase 2
, CD167b antigen
, tyrosine-protein kinase TYRO 10