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Receptor tyrosine kinase-like orphan receptor 2

Ror2, BDB
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Wnt5a, CAN, ACID, Frizzled, Staggerer
Papers on Ror2
CD13 and ROR2 Permit Isolation of Highly Enriched Cardiac Mesoderm from Differentiating Human Embryonic Stem Cells.
Ardehali et al., Los Angeles, United States. In Stem Cell Reports, Feb 2016
Here, we identify CD13 and ROR2 as cell-surface markers capable of selecting early cardiac mesoderm emerging during hESC differentiation.
Wnt5a induces ROR1/ROR2 heterooligomerization to enhance leukemia chemotaxis and proliferation.
Kipps et al., In J Clin Invest, Jan 2016
Treatment of CLL cells with Wnt5a induced ROR1 to oligomerize with ROR2 and recruit guanine exchange factors (GEFs), which activated Rac1 and RhoA; siRNA-mediated silencing of either ROR1 or ROR2 or treatment with UC-961 inhibited these effects.
Knockdown of receptor tyrosine kinase-like orphan receptor 2 inhibits cell proliferation and colony formation in osteosarcoma cells by inducing arrest in cell cycle progression.
Wu et al., Jishou, China. In Oncol Lett, Dec 2015
Receptor tyrosine kinase-like orphan receptor 2 (ROR2) has been reported to be dysregulated in human malignancies.
A review of 1α,25(OH)2D3 dependent Pdia3 receptor complex components in Wnt5a non-canonical pathway signaling.
Schwartz et al., Atlanta, United States. In J Steroid Biochem Mol Biol, Aug 2015
Wnt5a initiates its calcium-dependent effects via binding its receptors Frizzled2 (FZD2) and Frizzled5 (FZD5) and receptor tyrosine kinase-like orphan receptor 2 (ROR2), activating intracellular calcium release and stimulating PKC and CaMKII.
Human Cytomegalovirus Modulates Expression of Noncanonical Wnt Receptor ROR2 To Alter Trophoblast Migration.
Rawlinson et al., Sydney, Australia. In J Virol, 2014
Western blot and real-time PCR analyses show increased expression of noncanonical Wnt receptor ROR2 in CMV-infected trophoblasts.
Hair follicle transcriptome profiles during the transition from anagen to catagen in Cashmere goat (Capra hircus).
Li et al., Hohhot, China. In Genet Mol Res, 2014
Many of these up-regulated genes, such as STC2, VEGFR, and ROR2, are known to be transfactors in the process of cell differentiation and in the cell cycle.
ROR1, an embryonic protein with an emerging role in cancer biology.
Zhang et al., Iowa City, United States. In Protein Cell, 2014
Receptor tyrosine kinase-like orphan receptor 1 (ROR1) is a member of the ROR family consisting of ROR1 and ROR2.
The dual role of the novel Wnt receptor tyrosine kinase, ROR2, in human carcinogenesis.
Ward et al., Australia. In Int J Cancer, 2013
The recent discovery that the ROR2 receptor tyrosine kinase (RTK) is a novel Wnt receptor provides the potential to target the non-canonical Wnt pathway for cancer treatments.
Frizzled homolog proteins, microRNAs and Wnt signaling in cancer.
Dahiya et al., San Francisco, United States. In Int J Cancer, 2013
FZDs are one of several families of receptors comprised of FZD/LRP/ROR2/RYK in the Wnt signaling pathway.
Wnt5a signaling is a substantial constituent in bone morphogenetic protein-2-mediated osteoblastogenesis.
Shimauchi et al., Sendai, Japan. In Biochem Biophys Res Commun, 2012
these results suggest that Wnt5a/Ror2 signaling appears to be involved in BMP-2-mediated osteoblast differentiation in a Smad independent pathway.
Isolation of primitive endoderm, mesoderm, vascular endothelial and trophoblast progenitors from human pluripotent stem cells.
Soen et al., Stanford, United States. In Nat Biotechnol, 2012
Functional studies in vitro and in vivo confirmed that ROR2(+) cells produce mesoderm progeny, APA(+) cells generate syncytiotrophoblasts and CD87(+) cells give rise to vasculature.
Loss of Wnt5a and Ror2 protein in hepatocellular carcinoma associated with poor prognosis.
Liu et al., Jinan, China. In World J Gastroenterol, 2012
Data suggest that Wnt5a and Ror2 may serve as tumor suppressor genes in the development of hepatocellular carcinoma, and may serve as clinicopathologic biomarkers for prognosis in HCC patients.
Wnt5a-Ror-Dishevelled signaling constitutes a core developmental pathway that controls tissue morphogenesis.
Greenberg et al., Boston, United States. In Proc Natl Acad Sci U S A, 2012
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.
Wnt5a-Ror2 signaling between osteoblast-lineage cells and osteoclast precursors enhances osteoclastogenesis.
Takahashi et al., Matsumoto, Japan. In Nat Med, 2012
A soluble form of Ror2 acted as a decoy receptor of Wnt5a and abrogated bone destruction in mouse arthritis models
ROR2 gene is associated with risk of non-syndromic cleft palate in an Asian population.
Beaty et al., Beijing, China. In Chin Med J (engl), 2012
Results provided evidence of linkage and association between the ROR2 gene and a gene controlling risk to non-syndromic cleft palate.
FGF and ROR2 receptor tyrosine kinase signaling in human skeletal development.
Mundlos et al., Berlin, Germany. In Curr Top Dev Biol, 2010
Another player of relevance to skeletal development is the unusual receptor tyrosine kinase ROR2, the function of which is as interesting as it is complex.
SNARE-protein-mediated disease resistance at the plant cell wall.
Schulze-Lefert et al., Norwich, United Kingdom. In Nature, 2003
We also isolated barley ROR2 (ref.
Mutation of the gene encoding the ROR2 tyrosine kinase causes autosomal recessive Robinow syndrome.
Brunner et al., Nijmegen, Netherlands. In Nat Genet, 2000
Heterozygous (presumed gain of function) mutations in ROR2 were previously shown to cause dominant brachydactyly type B (BDB; ref. 7).
Recessive Robinow syndrome, allelic to dominant brachydactyly type B, is caused by mutation of ROR2.
Jeffery et al., London, United Kingdom. In Nat Genet, 2000
The recent identification of ROR2, encoding an orphan receptor tyrosine kinase, as the gene mutated in brachydactyly type B (BDB1; ref. 7) and the mesomelic dwarfing in mice homozygous for a lacZ and/or a neo insertion into Ror2 (refs 8,9) made this gene a candidate for RRS.
Dominant mutations in ROR2, encoding an orphan receptor tyrosine kinase, cause brachydactyly type B.
Wilkie et al., Oxford, United Kingdom. In Nat Genet, 2000
We obtained further evidence for this by demonstrating that two patients heterozygous for 9q22 deletions including ROR2 do not exhibit BDB.
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