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anti-Mouse (Murine) DDR1 Antibodies:
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Human Monoclonal DDR1 Primary Antibody for ELISA, WB - ABIN965982
Foehr, Tatavos, Tanabe, Raffioni, Goetz, Dimarco, De Luca, Bradshaw: Discoidin domain receptor 1 (DDR1) signaling in PC12 cells: activation of juxtamembrane domains in PDGFR/DDR/TrkA chimeric receptors. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2000
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Human Monoclonal DDR1 Primary Antibody for ELISA, WB - ABIN969082
Mohan, Mohan, Wilson: Discoidin domain receptor (DDR) 1 and 2: collagen-activated tyrosine kinase receptors in the cornea. in Experimental eye research 2001
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Human Polyclonal DDR1 Primary Antibody for IHC (p) - ABIN2478753
Coakley, Hawkins, Crinis, McManus, Blake, Nordmann, Sloan, Connelly: An unusual case of variegate porphyria with possible homozygous inheritance. in Australian and New Zealand journal of medicine 1990
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Human Polyclonal DDR1 Primary Antibody for ELISA, WB - ABIN543831
Johnson, Edman, Rutter: A receptor tyrosine kinase found in breast carcinoma cells has an extracellular discoidin I-like domain. in Proceedings of the National Academy of Sciences of the United States of America 1993
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Human Polyclonal DDR1 Primary Antibody for IHC, ELISA - ABIN1847697
Xu, Abe, Liu, Zalivina, Hohenester, Leitinger: Normal activation of discoidin domain receptor 1 mutants with disulfide cross-links, insertions, or deletions in the extracellular juxtamembrane region: mechanistic implications. in The Journal of biological chemistry 2014
Human Polyclonal DDR1 Primary Antibody for ELISA, WB - ABIN560139
Turashvili, Bouchal, Baumforth, Wei, Dziechciarkova, Ehrmann, Klein, Fridman, Skarda, Srovnal, Hajduch, Murray, Kolar: Novel markers for differentiation of lobular and ductal invasive breast carcinomas by laser microdissection and microarray analysis. in BMC cancer 2007
Data (including data from studies using knockout mice) suggest that Ddr1 plays role in promoting mammary tumor growth; tumor-extrinsic Ddr1 appears to be required for promotion of mammary tumors by interleukin-6.
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 synthesis.
DDR-1 interacts with the TGF-beta 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 DDR1-mediated ERK 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 and Ddr1 in bile ducts and blood vessels in postnatal liver.
Discoidin domain receptors are unique receptor tyrosine kinases in collagen-mediated signaling [review]
Genetic inhibition of discoidin domain receptor 1 protects mice against crescentic glomerulonephritis.
Data identifyies Syk as a potent inhibitor of epithelial migration and describes a first functional consequence of the interaction with the collagen receptor DDR1.
Results show that DDR1 promotes cell-cell adhesion and differentiation through stabilization of E-cadherin, which is mediated by Cdc42 inactivation.
Collagen I stimulates the self-renewal of embryonic stem cells mediated by Bmi-1 through alpha2beta1 integrin-dependent ILK, Notch, Gli-1, and DDR1-dependent Ras, PI3K/Akt, and ERK.
Loss of Discoidin domain receptor 1 is associated with inflammation and fibrosis in obstructive nephropathy
Type I collagen induces smooth muscle cell migration through DDR1
DDR1 plays a role in Alport syndrome and may have a universal role in common human inflammatory and fibrotic diseases.
DDR1 expression on resident vessel wall smooth muscle cells limits proliferation, migration and matrix accumulation during atherogenesis.
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
DDR1 mediates an important mechanism for atherosclerotic calcification.
Results suggest that active discoidin domain receptor 1 (DDR1) kinase is a central mediator of SMC migration.
Data (including data from studies using knockout mice) suggest that DDR1 plays role in promoting mammary tumor growth; tumor-extrinsic DDR1 appears to be required for promotion of mammary tumors by interleukin-6.
our study provides a novel regulatory pathway involving TM4SF1, DDR1, MMP2 and MMP9, which promotes the formation and function of invadopodia to support cell migration and invasion in pancreatic cancer.
The three well-conserved seed matched sites for miR-199a/b-5p in the discoidin domain receptor 1 (DDR1) 3'-UTR were targeted, and miRNA binding to at least two sites was required for DDR1 inhibition.
E2F1 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-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/IGF-IR system triggers stimulatory actions through both GPER 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 spectrum. Therefore, EMT stratification could be a potential biomarker to predict patient response to DDR1-targeting drugs.
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.
Isoform b of DDR1 is responsible for collagen I-induced up-regulation of N-cadherin and tyrosine 513 of DDR1b is necessary.
Reduced DDR1 expression may be implicated in impaired melanocyte adhesion process involved in vitiligo pathogenesis
data demonstrate that TGF-beta1 favors linear invadosome formation through the expressions of both the inducers, such as collagen and LOXL2, and the components such as DDR1 and MT1-MMP of linear invadosomes in cancer cells. Meanwhile, our data uncover a new TGF-beta1-dependent regulation of DDR1 expression.
DDR1 overexpression promoted GC cell proliferation (p < 0.05), migration (p < 0.01), and invasion (p < 0.01), and accelerated the growth (p < 0.05) as well as the microvessel formation (p < 0.01) of transplantation tumor in nude mice.
Our results suggest that DDR1 is both a prognostic marker for renal clear cell carcinoma and a potential functional target for therapy
Study concludes that non-canonical DDR1 signaling enables breast cancer cells to exploit the ubiquitous interstitial matrix component collagen I to undergo metastatic reactivation in multiple target organs.
Upregulation of DDR1 collagen receptor is associated with breast cancer.
Knockdown DDR1 reversed the effects of Galpha13 knockdown on cell-cell adhesion and proteolytic invasion in three-dimensional collagen.
Data suggest SCl2 (Streptococcus pyogenes) binds to DDR (DDR1, DDR2) ectodomain w/o stimulating receptor signaling; here, protein engineering was used to construct SCl-like proteins that inhibit collagen-DDR interactions and macrophage migration.
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
, CD167 antigen-like family member A
, cell adhesion kinase
, discoidin receptor tyrosine kinase
, epithelial discoidin domain receptor 1
, epithelial discoidin domain-containing 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
, discoidin domain receptor family, member 1
, neurotrophic tyrosine kinase receptor type 4
, protein-tyrosine kinase 3
, protein-tyrosine kinase PTK-3