Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Human DDR2 Anticorps:
anti-Mouse (Murine) DDR2 Anticorps:
anti-Rat (Rattus) DDR2 Anticorps:
Vous arrivez à notre recherche pré-filtrée.
Human Monoclonal DDR2 Primary Antibody pour ICC, IHC - ABIN969083
Leitinger, Kwan: The discoidin domain receptor DDR2 is a receptor for type X collagen. dans Matrix biology : journal of the International Society for Matrix Biology 2006
Show all 3 Pubmed References
Human Polyclonal DDR2 Primary Antibody pour 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. dans Biochemical pharmacology 2013
Show all 2 Pubmed References
Human Monoclonal DDR2 Primary Antibody pour 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. dans Circulation research 2014
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 (Montrer SHC1 Anticorps). 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 (Montrer CYP11A1 Anticorps) 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 (Montrer CYR61 Anticorps) through activation of transcription factor activator protein 1 (AP-1 (Montrer FOSB Anticorps)). The elevated CYR61 (Montrer CYR61 Anticorps), in turn, accelerates MMP1 (Montrer MMP1 Anticorps) production via ETS1 (ETS (Montrer ETS1 Anticorps) proto-oncogene (Montrer RAB1A Anticorps) 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.
DDR2 is important for maintenance of osteoblast activity and suppression of marrow adipogenesis in vivo and these actions are related to changes in MAPK (Montrer MAPK1 Anticorps)-dependent RUNX2 (Montrer RUNX2 Anticorps) and PPARgamma (Montrer PPARG Anticorps) phosphorylation.
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 (Montrer MMP13 Anticorps).
DDR2 mutation can drive lung cancer initiation in vivo and provide a novel mouse model for lung cancer therapeutics studies.
Study showed that Nrp1 (Montrer NRP1 Anticorps) expression paralleled with that of DDR2 during osteoblast differentiation. Nrp1 (Montrer NRP1 Anticorps) assisted the promoting role of DDR2 in osteoblast differentiation, via activation of DDR2-mediated downstream signaling.
Data show that discoidin domain receptor (DDR (Montrer DDR1 Anticorps)) 2 siRNA-mediated suppression of extracellular regulated kinase (ERK) 1 (Montrer MAPK3 Anticorps) and 2 and nuclear factor of kappa B (NF-kappaB (Montrer NFKB1 Anticorps)) could down-regulate the expressions of matrix metalloproteinase (MMP) 2 (Montrer MMP2 Anticorps) 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.
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