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RSPO3 encodes a member of the thrombospondin type 1 repeat supergene family. De plus, nous expédions R-Spondin 3 Anticorps (51) et R-Spondin 3 Kits (10) et beaucoup plus de produits pour cette protéine.
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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 (Montrer RSPO1 Protéines) fusion transcripts, including three novel transcripts, in one-third of colorectal Traditional serrated adenoma (TSA (Montrer PRDX2 Protéines)) and showed that PTPRK (Montrer PTPRK Protéines)-RSPO3 fusions were the predominant cause of RSPO (Montrer RSPO1 Protéines) overexpression in colorectal TSA (Montrer PRDX2 Protéines).
RSPOs facilitate HSC (Montrer FUT1 Protéines) activation and promote liver fibrogenesis by enhancing the Wnt (Montrer WNT2 Protéines) pathway
Colorectal cancer cell lines identified VACO6 cells as a carrier of a canonical PTPRK (Montrer PTPRK Protéines)(e1)-RSPO3(e2) fusion; cell line displayed marked in vitro and in vivo sensitivity to WNT (Montrer WNT2 Protéines) blockade by the porcupine (Montrer PORCN Protéines) 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 (Montrer WNT2 Protéines) pathway inhibitor AXIN1 (Montrer AXIN1 Protéines), with consequent protein loss.
PTPRK (Montrer PTPRK Protéines)-RSPO3 fusions and RNF43 (Montrer RNF43 Protéines) 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 (Montrer WNT2 Protéines)/beta-catenin (Montrer CTNNB1 Protéines) signaling.
High RSPO3 expression is associated with breast cancer.
A genome-wide association study of bone mineral density (BMD (Montrer BEST1 Protéines)) found a new BMD (Montrer BEST1 Protéines) locus that harbors the PTCH1 (Montrer PTCH1 Protéines) gene, that associates with reduced spine BMD (Montrer BEST1 Protéines) and the RSPO3 associates with increased spine BMD (Montrer BEST1 Protéines).
results suggest that the expression of RSPO (Montrer RSPO1 Protéines) fusion transcripts is related to a subset of colorectal cancers arising in the Japanese population
These findings suggest that aberrant RSPO3-LGR4 (Montrer LGR4 Protéines) signaling potentially acts as a driving mechanism in the aggressiveness of Keap1 (Montrer KEAP1 Protéines)-deficient lung ADs (Montrer AGPS Protéines).
These results shed new light on the role of Rspo3 in heart development and demonstrate that LGR4 (Montrer LGR4 Protéines) 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 (Montrer LGR4 Protéines) axis protects hepatocytes from hypoxia/reoxygenation injury via activating beta-catenin (Montrer CTNNB1 Protéines).
H. pylori infection increases stromal R-spondin 3 expression and expands the Axin2 (Montrer AXIN2 Protéines)(+) 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 (Montrer CTNNB1 Protéines)-dependent zonation.
data identify endothelial RSPO3-driven non-canonical WNT (Montrer WNT2 Protéines)/Ca(2 (Montrer CA2 Protéines)+)/NFAT (Montrer NFATC1 Protéines) signaling as a critical maintenance pathway of the remodeling vasculature
Nkx2-5 (Montrer NKX2-5 Protéines) has a role in regulating cardiac growth through modulation of Wnt (Montrer WNT2 Protéines) signaling by R-spondin3
Rspo3 loss of function mutation in combination with Rspo2 (Montrer RSPO2 Protéines) mutation,but not on its own, causes severe limb truncation.
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