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RSPO3 encodes a member of the thrombospondin type 1 repeat supergene family. De plus, nous expédions R-Spondin 3 Anticorps (50) et R-Spondin 3 Kits (11) et beaucoup plus de produits pour cette protéine.
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Taken together, we show in this short report that the matricellular protein RSPO3 is a novel permeability factor inducing barrier dysfunction in human primary vascular endothelial monolayers of macro- and micro- vascular origin, and RSPO3 acts synergistically with the prototypic pro-inflammatory mediator IL-1beta.
Knockdown of RSPO3 resulted in significantly increased mRNA expression levels of RUNX2, ALP and OCN and no effects on the proliferation of human adipose-derived stem cells.
For liver transplant-free survival, a genome-wide significant signal was identified and expression of the candidate gene RSPO3 was demonstrated in key liver-resident effector cells and may play a role in primary sclerosing cholangitis disease progression.
The present study identified RSPO fusion transcripts, including three novel transcripts, in one-third of colorectal Traditional serrated adenoma (TSA) and showed that PTPRK-RSPO3 fusions were the predominant cause of RSPO overexpression in colorectal TSA.
RSPOs facilitate HSC activation and promote liver fibrogenesis by enhancing the Wnt pathway
Colorectal cancer cell lines identified VACO6 cells as a carrier of a canonical PTPRK(e1)-RSPO3(e2) fusion; cell line displayed marked in vitro and in vivo sensitivity to WNT blockade by the porcupine inhibitor LGK974. Long-term treatment of VACO6 cells with LGK974 led to the emergence of a resistant population carrying two frameshift deletions of the WNT pathway inhibitor AXIN1, with consequent protein loss.
PTPRK-RSPO3 fusions and RNF43 mutations were found to be characteristic genetic features of traditional serrated adenomas (TSAs).
Using C-mannosylation-defective Rspo3 mutant-overexpressing cell lines, we found that C-mannosylation of Rspo3 promotes its secretion and activates Wnt/beta-catenin signaling.
High RSPO3 expression is associated with breast cancer.
A genome-wide association study of bone mineral density (BMD) found a new BMD locus that harbors the PTCH1 gene, that associates with reduced spine BMD and the RSPO3 associates with increased spine BMD.
results suggest that the expression of RSPO fusion transcripts is related to a subset of colorectal cancers arising in the Japanese population
These findings suggest that aberrant RSPO3-LGR4 signaling potentially acts as a driving mechanism in the aggressiveness of Keap1-deficient lung ADs.
using RNA-seq data, identification of multiple fusion transcripts including recurrent gene fusions involving R-spondin family members RSPO2 and RSPO3 that together occur in 10% of colon tumours
the gene is a novel member of thrombospondin type I repeat supergene family (hPWTSR)
a polymorphism in thrombospondin subtly but significantly sensitizes the calcium-binding repeats to removal of Ca2+ and thermal denaturation
Rspo2 and Rspo3 fusion events are sufficient to initiate hyperplasia and tumour development.
These results shed new light on the role of Rspo3 in heart development and demonstrate that LGR4 is the principal R-spondin 3 receptor in the heart.
Results identify a mechanism through which localized expression of RSPO3 induces proliferation of the coronary arteries at their stems and permits their formation.
Rspo3-LGR4 axis protects hepatocytes from hypoxia/reoxygenation injury via activating beta-catenin.
H. pylori infection increases stromal R-spondin 3 expression and expands the Axin2(+) cell pool to cause hyperproliferation and gland hyperplasia; the ability of stromal niche cells to control and adapt epithelial stem cell dynamics constitutes a sophisticated mechanism that orchestrates epithelial regeneration and maintenance of tissue integrity
We provide in vivo evidence that RSPO3 stimulates the crypt stem cell and niche compartments and drives rapid intestinal tumorigenesis.
Rspo3 function remains essential in adult life to ensure replenishment of lost cells and maintain the properties of the zona glomerulosa
Conditional deletion of Rspo3 in mice disrupts activation of central fate, demonstrating its crucial role in determining and maintaining beta-catenin-dependent zonation.
data identify endothelial RSPO3-driven non-canonical WNT/Ca(2+)/NFAT signaling as a critical maintenance pathway of the remodeling vasculature
Nkx2-5 has a role in regulating cardiac growth through modulation of Wnt signaling by R-spondin3
Rspo3 loss of function mutation in combination with Rspo2 mutation,but not on its own, causes severe limb truncation.
Sexually dimorphic expression patterns were observed for WNT/beta-catenin-responsive genes, and for Wnt2b, Wnt4, Wnt7a, Wnt9b, Wnt10b, Wnt11, Wnt16, and Rspo3 mRNAs.
Data show that Rspo3 binds syndecan 4 and that together they activate Wnt5a/PCP signaling.
suggest a critical role for Rspo3 in the interaction between chorion and allantois in labyrinthine development
identify Rspo3 as a novel, evolutionarily conserved angiogenic factor in embryogenesis
This gene encodes a member of the thrombospondin type 1 repeat supergene family. In addition, the protein contains a furin-like cysteine-rich region. Furin-like repeat domains have been found in a variety of eukaryotic proteins involved in the mechanism of signal transduction by receptor tyrosine kinases.
, R-spondin 3 homolog
, protein with TSP type-1 repeat
, roof plate-specific spondin-3
, thrombospondin type-1 domain-containing protein 2
, thrombospondin, type I, domain containing 2
, R-spondin 3-like protein
, cristin 1
, cysteine-rich and single thrombospondin domain-containing protein 1
, thrombospondin, type I, domain 2