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- Table of Contents
1 Citations 6 Q&As
Facts about R-spondin-3.
Also regulates the canonical Wnt/beta-catenin-dependent pathway and non-canonical Wnt signaling by acting as an inhibitor of ZNRF3, an important regulator of the Wnt signaling pathway. Acts as a ligand for frizzled FZD8 and LRP6.
Mouse | |
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Gene Name: | Rspo3 |
Uniprot: | Q2TJ95 |
Entrez: | 72780 |
Belongs to: |
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R-spondin family |
Cristin 1; CRISTIN1; FLJ14440; hPWTSR; hRspo3; Protein with TSP type-1 repeat; PWTSR; Roof plate-specific spondin-3; RSPO3; R-spondin 3 homolog (Xenopus laevis); RSpondin 3; R-Spondin 3; R-spondin-3; Thrombospondin type-1 domain-containing protein 2; thrombospondin, type I, domain containing 2; THSD2
Mass (kDA):
31.454 kDA
Mouse | |
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Location: | 10|10 A4 |
Sequence: | 10; |
Highly expressed in endothelial cells (PubMed:26766444).
The RSPO3 gene is an important PSC modifer gene. How can you make use of this gene? Continue reading to learn more! We'll be discussing three of the most effective uses of RSPO3.
BoSTER Bio's RNAi libraries revealed that RSPO3 is a crucial PSC moderator, and suggests it could be a candidate for PANK3 transcription factors. This gene is located within the QTL region that is home to PDE10A DHCR7, MFN2, and CCNY. The gene is also located near sscmir103-1, which is believed to regulate PANK3 transcription.
The PSC pathway is controlled by a variety of genes, including RSPO3 (Rose-Sternberg protein 3), and ESXI-1. Both are responsible for controlling Wnt-mediated signaling. The overexpression of RSPO3 in human cancers is a hallmark of translocation-induced cancers, including colon and prostate cancers. These findings highlight the need for more studies on the gene.
A single variant of the RSPO3 gene could increase the likelihood of developing PSC. However, it is not the sole cause. Other genetic determinants like HLA status are thought to have a greater impact on disease risk. It isn't known if a particular exposome will occur. Although PSC risk variants related to HLA are significant, they aren't significant in comparison to the environmental factors that are the cause of PSC risk.
In a recent study, researchers discovered that RSPO3 expression is related to the presence of PSCs. This gene is responsible for the development of an ex Vivo niche in stem cells. It is also responsible for the production of a variety of proteins that are vital to tissue regeneration and could be a target for antimicrobial medications. It has also been demonstrated that RSPO3 is involved in the progression and development of inflammatory bowel disease.
In mice, anti-RSPO3 neutralizing antibodies cause a phenotype which is consistent with the existence of a functional source for RSPO3 in the intestinal lumen. The primary sources of RSPO3 that function are the PdgfRa lineage cells within your intestine.
The study's limitations are a lack of detailed histopathological profiles or vast array of pathobiological markers. Although these limitations limit the practical application of the study the advancements in systems medicine have enabled the identification of these genetic markers. For PSC patients, rs853974 may aid in identifying a potential aggressive disease course. Its hazard ratio is 2.1 (95 percent C.I. 1.7-2.8. In the meantime, polymorphisms in RSPO3 in clinical practice are not relevant.
RSPOs are secreted polypeptides that frequently interact with Wnt genes. At present, there are four paralogous RSPO genes. The first one, RSPO1, is encoded by Xenopus. The two other proteins, RSPO2 and RSPO3, are found in humans. All three proteins have the ability to sensitize cells to the Wnt signaling pathway. RSPO2 and RSPO3 are closely associated with syndecans.
It is a crucial PSC altering gene in the process of intestinal organogenesis. RSPO3 expression promotes the formation of intestinal organoid supports and support in vitro. This makes it an important gene involved in intestinal epithelial stem cell expansion. However, RSPO1 or RSPO2 don't help to counteract the effects of RSPO3.
It has been proposed that RSPO3 regulates homeostasis of the intestinal stem cells and that RSPO3 collaborates with R-spondins as well as Wnts to regulate the growth of the crypts. Both RSPOs and Wnts are essential to maintain the intestinal crypt's homeostasis. Stromal cells are the source of the ligands that are required by intestinal stem cells. Furthermore, Foxl1 and Gremlin1 also regulate the niche of stem cells.
PMID: 16543246 by Nam J.-S., et al. Mouse cristin/R-spondin family proteins are novel ligands for the Frizzled 8 and LRP6 receptors and activate beta-catenin-dependent gene expression.
PMID: 15469841 by Kazanskaya O., et al. R-Spondin2 is a secreted activator of Wnt/beta-catenin signaling and is required for Xenopus myogenesis.
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