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The data suggest that the absence of DDR1 provides a growth and adhesion advantage that favors the expansion of basal cells, potentiates fibrosis, and enhances necrosis/hypoxia and basal differentiation of transformed cells to increase their aggression and metastatic potential.
DDR1 kinase activity is required for regulating collagen IV (show COL4 Antibodies) synthesis.
DDR-1 interacts with the TGF-beta (show TGFB1 Antibodies) pathway to restrict calcifying extracellular vesicle-mediated mineralization and fibrosis by smooth muscle cells.
alpha5(IV), but not alpha1(IV), promotes lung cancer cell proliferation and tumor angiogenesis through non-integrin collagen receptor (show ITGA2 Antibodies) DDR1-mediated ERK (show EPHB2 Antibodies) activation.
DDR1 malfunction causes outer hair cells deformation and the separation of the lateral wall, the location of the cellular motor responsible for the electromotile property, explicitly in those regions showing DDR1 and NM-IIA co-localization.
the collagen receptors DDR1 and integrin a2b1 contribute to regulate GBM-maturation and to control matrix accumulation.
Extensive co-localization and relationship of Jag1 (show JAG1 Antibodies) and Ddr1 in bile ducts and blood vessels in postnatal liver.
Genetic inhibition of discoidin domain receptor 1 protects mice against crescentic glomerulonephritis.
Data identifyies Syk (show SYK Antibodies) as a potent inhibitor of epithelial migration and describes a first functional consequence of the interaction with the collagen receptor (show ITGA2 Antibodies) DDR1.
Results show that DDR1 promotes cell-cell adhesion and differentiation through stabilization of E-cadherin (show CDH1 Antibodies), which is mediated by Cdc42 (show CDC42 Antibodies) inactivation.
E2F1 (show E2F1 Antibodies) knockdown decreased the expression of discoidin domain receptor 1 (DDR1) which plays a crucial role in many fundamental processes such as cell differentiation, adhesion, migration and invasion.
Furthermore, the inhibition of DDR1 with 7rh showed striking efficacy in combination with chemotherapy in orthotopic xenografts and autochthonous pancreatic tumors where it significantly reduced DDR1 activation and downstream signaling, reduced primary tumor burden, and improved chemoresponse.
These findings demonstrate a critical role of miR (show MLXIP Antibodies)-199a-3p/DDR1 pathway in ovarian cancer development.
findings demonstrate that, in human breast cancer cells, DDR1 regulates IR expression and ligand dependent biological actions. This novel functional crosstalk is likely clinically relevant
These results support an activation mechanism of DDR1 whereby collagen induces lateral association of DDR1 dimers and phosphorylation between dimers.
Data suggest that IGF-I (show IGF1 Antibodies)/IGF-IR system triggers stimulatory actions through both GPER (show GPER Antibodies) and DDR1 in aggressive tumors as mesothelioma and lung tumors.
we further analyzed the CpG methylation levels at the DDR1 promoter in EOC cells and found that the CpG methylation levels of DDR1 promoter correlated negatively with the expression of DDR1 along the EMT (show ITK Antibodies) spectrum. Therefore, EMT (show ITK Antibodies) stratification could be a potential biomarker to predict patient response to DDR1-targeting drugs.
This study suggested that DDR1 and DDR2 (show DDR2 Antibodies) knockdown alters brain immunity and significantly reduces the level of triggering receptor expressed on myeloid cells (TREM)-2 (show TREM2 Antibodies) and microglia.
Isoform b of DDR1 is responsible for collagen I-induced up-regulation of N-cadherin (show CDH2 Antibodies) and tyrosine 513 of DDR1b is necessary.
Reduced DDR1 expression may be implicated in impaired melanocyte adhesion process involved in vitiligo (show MITF Antibodies) pathogenesis
Receptor tyrosine kinases play a key role in the communication of cells with their microenvironment. These kinases are involved in the regulation of cell growth, differentiation and metabolism. The protein encoded by this gene belongs to a subfamily of tyrosine kinase receptors with homology to Dictyostelium discoideum protein discoidin I in their extracellular domain, and that are activated by various types of collagen. Expression of this protein is restricted to epithelial cells, particularly in the kidney, lung, gastrointestinal tract, and brain. In addition, it has been shown to be significantly overexpressed in several human tumors. Alternatively spliced transcript variants encoding different isoforms have been described for this gene.
discoidin domain receptor family, member 1
, discoidin domain receptor tyrosine kinase 1
, epithelial discoidin domain-containing receptor 1
, CD167 antigen-like family member A
, cell adhesion kinase
, discoidin receptor tyrosine kinase
, epithelial discoidin domain receptor 1
, protein-tyrosine kinase MPK-6
, tyrosine kinase DDR
, tyrosine-protein kinase CAK
, PTK3A protein tyrosine kinase 3A
, mammary carcinoma kinase 10
, neuroepithelial tyrosine kinase
, neurotrophic tyrosine kinase, receptor, type 4
, protein-tyrosine kinase RTK-6
, neurotrophic tyrosine kinase receptor type 4
, protein-tyrosine kinase 3
, protein-tyrosine kinase PTK-3