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circulating fibroblast precursors expressing DDR2, in an exposure-induced model of pulmonary fibrosis, is reported.
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 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 (show MMP13 Proteins).
DDR2 mutation can drive lung cancer initiation in vivo and provide a novel mouse model for lung cancer therapeutics studies.
Study showed that Nrp1 (show NRP1 Proteins) expression paralleled with that of DDR2 during osteoblast differentiation. Nrp1 (show NRP1 Proteins) assisted the promoting role of DDR2 in osteoblast differentiation, via activation of DDR2-mediated downstream signaling.
Data show that discoidin domain receptor (DDR (show DDR1 Proteins)) 2 siRNA-mediated suppression of extracellular regulated kinase (ERK) 1 (show MAPK3 Proteins) and 2 and nuclear factor of kappa B (NF-kappaB (show NFKB1 Proteins)) could down-regulate the expressions of matrix metalloproteinase (MMP) 2 (show MMP2 Proteins) 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.
Female ddr2-deficient mice homozygous for the slie mutation show inefficient spontaneous BC metastasis.
This study suggested that DDR1 (show DDR1 Proteins) and DDR2 knockdown alters brain immunity and significantly reduces the level of triggering receptor expressed on myeloid cells (TREM)-2 (show TREM2 Proteins) and microglia.
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 (show ITK Proteins) marker expression. Finally, our results revealed that DDR2 facilitates GC cell invasion and EMT (show ITK Proteins) through mTORC2 (show CRTC2 Proteins) activation and AKT (show AKT1 Proteins) phosphorylation.
DDR2 mediates collagen-induced activation of MT1-MMP (show MMP14 Proteins) in human fibroblasts
Study strongly suggests that during pulmonary fibrosis, DDR2 not only participates in both the initiation and maintenance of fibrotic reaction, but also affects both ECM (show MMRN1 Proteins) production and angiogenesis.
signaling pathway, effectively suppressed peritoneal dissemination. DDR2 was identified as a driver gene for Gastric Cancer dissemination from the combined expression signature and can potentially serve as a novel therapeutic target for inhibiting Gastric Cancer peritoneal dissemination.
Ang II (show AGT Proteins) induces cardiac fibrosis by enhancing DDR2 expression in cardiac fibroblasts via p38 MAPK (show MAPK14 Proteins)-mediated activation of NF-kappaB (show NFKB1 Proteins).
DDR2 Missense mutation is associated with spondylo-meta-epiphyseal dysplasia, short limb-abnormal calcification type.
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