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anti-Human ROR2 Anticorps:
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Human Polyclonal ROR2 Primary Antibody pour FACS, IHC (p) - ABIN392044
Afzal, Rajab, Fenske, Oldridge, Elanko, Ternes-Pereira, Tüysüz, Murday, Patton, Wilkie, Jeffery: Recessive Robinow syndrome, allelic to dominant brachydactyly type B, is caused by mutation of ROR2. dans Nature genetics 2000
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Human Polyclonal ROR2 Primary Antibody pour ELISA - ABIN544343
Oldridge, Fortuna, Maringa, Propping, Mansour, Pollitt, DeChiara, Kimble, Valenzuela, Yancopoulos, Wilkie: Dominant mutations in ROR2, encoding an orphan receptor tyrosine kinase, cause brachydactyly type B. dans Nature genetics 2000
Show all 3 Pubmed References
Human Polyclonal ROR2 Primary Antibody pour IHC (p), WB - ABIN392046
van Bokhoven, Celli, Kayserili, van Beusekom, Balci, Brussel, Skovby, Kerr, Percin, Akarsu, Brunner: Mutation of the gene encoding the ROR2 tyrosine kinase causes autosomal recessive Robinow syndrome. dans Nature genetics 2000
Show all 7 Pubmed References
Here, we show that Wnt/planar cell polarity (PCP) autocrine signaling controls the emergence of cytonemes, and that cytonemes subsequently control paracrine Wnt/beta-catenin signal activation. Upon binding of the Wnt family member Wnt8a, the receptor tyrosine kinase Ror2 becomes activated.
ROR1 and ROR2 play distinct roles in endometrial cancer. ROR1 may promote tumor progression, while ROR2 may act as a tumor suppressor in endometrioid endometrial cancer.
Wnt5a-Ror2 signaling enhanced tongue SCC cell aggressiveness and promoted production of MMP-2 following DeltaNp63beta-mediated EMT
In squamous/adenosquamous carcinoma and adenocarcinoma of the gallbladder positive ROR2 or WNT5a expression is generally associated with a poor prognosis.
Wnt5a suppressed osteoblastic differentiation through Ror2/JNK signaling in periodontal ligament stem cell-like cells.
Data show that receptor tyrosine kinase-like orphan receptor 2 (ROR2) is epigenetically silenced by promoter hypermethylation in colorectal cancer cell lines and in early stages of colorectal neoplasia tissue.
WNT5A and ROR2 are induced by inflammatory mediators through NF-kB and STAT3 transcription factors, and are involved in the migration of human ovarian cancer cell line SKOV-3.
On these bases, we identified that miR-208b targets receptor tyrosine kinase-like orphan receptor 2 gene by which miR-208b can regulate the development of osteosarcoma.
Our findings suggest that receptor tyrosine kinase-like orphan receptor 2 may be an important regulator of epithelial-mesenchymal transition, primarily regulated the non-canonical Wnt signaling pathway in ovarian cancer cells, and may display a promising therapeutic target for ovarian cancer.
Knockdown of Ror2 expression in renal cell carcinoma cells significantly reduced cell proliferation and induced apoptosis.
found no association between ROR2 staining and poor patient survival
Data show that CD13 anntigen and receptor tyrosine kinase-like orphan receptor 2 (ROR2) identify a cardiac lineage precursor pool that is capable of successful engraftment into the porcine heart.
ROR2 gene mutations are associated with autosomal recessive robinow syndrome.
results corroborated previous findings of Ryk-mediated Wnt5a effect, and suggested a role for Ror2 in the Wnt5a machinery in glioblastoma
Data show that silencing receptor tyrosine kinases (RTKs) ROR2 and ROR1 has a strong inhibitory effect on the ability of ovarian cancer cells to proliferate, migrate and invade.
Wnt5a-Ror2 signaling enhances expression and secretion of CXCL16 in mesenchymal stem cells thereby activating CXCR6 expressed on tumor cells to promote proliferation.
the b-catenin-independent WNT score correlated with reduced overall survival only in the metastasized situation . This is in line with the in vitro results of the alternative WNT receptors ROR1 and ROR2, which foster invasion
We present strong evidence that ROR2 could be used as an indicator of poor prognosis and could represent a novel therapeutic target for PDAC.
Findings suggest that high receptor tyrosine kinase-like orphan receptor (ROR) 2 or proto-oncogene protein Wnt-5A (Wnt5a) expression is associated with poor prognosis in non-small cell lung cancer (NSCLC).
This study identifies an interaction between ROR1 and ROR2 that is required for Wnt5a signaling that promotes leukemia chemotaxis and proliferation.
The Ror2-mediated signaling might be activated in response to tissue damage and associated with progression of fibrosis in the submandibular gland (SMG).
Ror2 plays a critical role in regulating the cell cycle progression of reactive astrocytes following brain injury
we uncovered cell state plasticity and adhesion dynamics regulated by Ror2, which influenced Ras Homology Family Member A (RhoA) and Rho-Associated Coiled-Coil Kinase 1 (ROCK1) activity downstream of Dishevelled-2 (Dvl2).
Here, the study of two Ror2 mutants connects aberrant germ cell migration to defects in meiosis and supports the diffusion model of meiotic entry.
Although Ror1-mutant mice show no apparent defects in ureteric bud (UB) formation, Ror1; Ror2-double-mutant mice exhibit either defects in UB outgrowth and branching morphogenesis, associated with the loss of the MM from the UB domain, or ectopic formation of the UB.
The Wnt5a-Ror2 axis promotes the signaling circuit between interleukin-12 and interferon-gamma in colitis
Non-canonical Wnt5a/Ror2 signaling regulates kidney morphogenesis by controlling intermediate mesoderm extension.
Ror2 plays an important role in mammary gland development in mice.
The activation of Wnt5a-Ror2 signaling in epithelial cells undergoing epithelial-to-mesenchymal transition (EMT) may play an important role in disrupting TBM via MMP-2 induction during renal fibrosis.
The results indicate an important role of Wnt5a-Ror2 signaling in morphogenesis of the metanephric mesenchyme to ensure proper epithelial tubular formation of the ureteric bud required for kidney development.
This study provides a method to investigate the effects of the Wnt pathway on the fate of mesenchymal stem cells (MSC) in vivo and for the further improvement of MSC-based therapies.
Show Ror2 expression is higher in highly metastatic cell line than in low metastatic variant cell line. Our data show that Ror2 is a potential factor in the tumorigenesis and metastasis in a Src-dependent manner that is negatively regulated by NRAGE.
Wnt5a-Ror1 and Wnt5a-Ror2 signaling pathways regulated neurogenesis in the developing neocortex.
A soluble form of Ror2 acted as a decoy receptor of Wnt5a and abrogated bone destruction in mouse arthritis models
These findings suggest that Wnt5a-Ror-Dishevelled signaling constitutes a core noncanonical Wnt pathway that is conserved through evolution and is crucial during embryonic development.
these results indicate that Ror2 acts autonomously to permit the polarized response of primordial germ cells to KitL.
Wnt5a-Ror2 signaling might also be required for expression of MMP-13 gene during the development of the cartilaginous tissue.
Wnt5a signaling gradient controls limb elongation by establishing PCP in chondrocytes along the proximal-distal axis through regulating Vangl2 phosphorylation.
Ror2 plays important roles in midgut elongation by means of an epithelial convergent extension mechanism
Indian hedgehog and WNT/beta-catenin signaling, inhibited by receptor tyrosine kinase-like orphan receptor 2 (ROR2) in distal limb mesenchyme, are acting upstream of BMP signaling in the phalanx-forming region
In the Xenopus embryo, Ptk7 functionally interacts with Ror2 to regulate protocadherin papc expression and morphogenesis.
Xenopus adult stem cells originate from the larval absorptive cells expressing Ror2, which require Wnt5a/Ror2 signaling for their dedifferentiation accompanied by changes in cell morphology.
Data show that PAPC signaling via RhoA and Wnt5a/Ror2 activity are required to keep cells aligned in apical-basal orientation during invagination of the ear placode.
Transcriptional regulation of XPAPC by XWnt-5A requires the receptor tyrosine kinase Ror2.
demonstrated that this anti-canonical Wnt activity of Del1 is dependent on the Ror2 pathway, which is activated by the non-canonical Wnt ligands
The protein encoded by this gene is a receptor protein tyrosine kinase and type I transmembrane protein that belongs to the ROR subfamily of cell surface receptors. The protein may be involved in the early formation of the chondrocytes and may be required for cartilage and growth plate development. Mutations in this gene can cause brachydactyly type B, a skeletal disorder characterized by hypoplasia/aplasia of distal phalanges and nails. In addition, mutations in this gene can cause the autosomal recessive form of Robinow syndrome, which is characterized by skeletal dysplasia with generalized limb bone shortening, segmental defects of the spine, brachydactyly, and a dysmorphic facial appearance.
neurotrophic tyrosine kinase receptor-related 2
, tyrosine-protein kinase transmembrane receptor ROR2
, neurotrophic tyrosine kinase, receptor related 2
, neurotrophic tyrosine kinase, receptor-related 2
, receptor tyrosine kinase-like orphan receptor 2
, tyrosine-protein kinase transmembrane receptor ROR2-like
, LOW QUALITY PROTEIN: tyrosine-protein kinase transmembrane receptor ROR2
, receptor tyrosine kinase Xror2
, receptor tyrosine kinase like orphan receptor 2 L homeolog
, receptor tyrosine kinase-like orphan receptor 2 L homeolog