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- Table of Contents
Facts about Protein Wnt-7b.
Required for central nervous system (CNS) angiogenesis and blood-brain barrier regulation (PubMed:30026314). .
Human | |
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Gene Name: | WNT7B |
Uniprot: | P56706 |
Entrez: | 7477 |
Belongs to: |
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Wnt family |
protein Wnt-7b; wingless-type MMTV integration site family, member 7B; Wnt7b; Wnt-7b
Mass (kDA):
39.327 kDA
Human | |
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Location: | 22q13.31 |
Sequence: | 22; NC_000022.11 (45920362..45977162, complement) |
Moderately expressed in fetal brain, weakly expressed in fetal lung and kidney, and faintly expressed in adult brain, lung and prostate.
Secreted, extracellular space, extracellular matrix. Secreted.
The WNT7B marker is a canonical Wnt ligand, a protein of 55kDa. It stimulates the proliferation of mesenchymal progenitor cells and induces Sox11 expression. Boster scientists are eligible to receive product credits and special samples. Their results are accepted in all scientific applications around the world. For more information about this protein, please visit the Boster Bio website.
The Glut1 gene encodes a protein of approximately 55kDa. This protein has a single 2.8 kb mRNA transcript, and there are no known splice variants. Glut1 is expressed in the BBB in normal and Def/Deficient mice. The Glut1 protein is detected in various brain tissue samples including rat brain homogenate and primary cultured astrocytes at P0 passage.
Glut1 is an essential neuromuscular protein. Depletion of this protein results in spinal muscular atrophy and motor neuron disease. However, when it is replaced at PND14, the phenotype of Glut1 DS is partially rescued. By PND15, the brain has fully matured, and augmentation of Glut1 expression did not provide any benefit.
Treatment of mutant mice with AAV9-Glut1 improves motor performance. The treatment improved motor performance in the mutant mice injected with AAV9-Glut1, indicating that early Glut1 repletion can lead to improved outcomes. Moreover, in mice injected with AAV9-Glut1, Glut1 RNA did not affect motor performance. These results support the concept that early repletion of Glut1 protein could lead to the same outcomes in human patients.
In a recent study, Glut1 was discovered to be involved in the transport of glucose from the blood to the brain. Researchers found that the mutant mice had increased CSF glucose levels but not blood glucose levels. In addition, the Glut1 protein is found in the brain's microvasculature. Thus, Glut1 is vital in ensuring the transport of glucose from the blood to the brain.
Glut1 transporter proteins are integral membrane glycoproteins that transport glucose into most cells. The protein family contains Glut-1 to Glut-12. Glut-1 is the major transporter in the blood-brain barrier and is expressed at variable levels in many human tissues. Overexpression of Glut-1 has been linked with poor survival in cancer patients. Its molecular weight is 55 kDa, which is comparable to human erythrocyte membrane.
Glut1 has been shown to be phosphorylated in both abluminal and luminal membranes. This phosphorylation alters the conformation of the protein, which is why specific antibodies react with it. The pI of GLUT-1 of the primary isoform of GLUT-1 is 8.0, while the predominant isoform is lower than 8.1.
Wnt7b functions as a canonical Wnt agonist and ligand, and activates canonical Wnt signaling in a cell-dependent manner. Its activity is likely regulated by its ability to bind to specific members of the Fzd family. Wnt7b can bind to four Fzds expressed during lung development. In this study, HA-tagged Wnt7b was incubated with 293 cells and Western blot analysis confirmed Wnt7b expression.
Wnts are highly conserved secreted proteins that activate multiple signaling pathways that regulate critical processes during development and tissue homeostasis in adults. Wnt proteins are hydrophobic, allowing them to travel long distances through extracellular space. Extensive research on Wnt proteins has identified several factors that control Wnt protein secretion and growth patterning.
Wnt7b activates canonical Wnt signaling in VSMCs. During co-transfection with expression plasmids, Wnt7b activated TOPFLASH reporter by sevenfold, while co-expression of Wnt7b and LRP5 increased the activity to over 20-fold.
Wnt7b binds to Fzd1, Fzd10, and Fzd1 in 293 cells. Furthermore, it binds to Fzd7 and Fzd10 in cell culture. These results are promising in terms of the therapeutic potential of WNT7B. With such benefits, Wnt7b can be used to target various types of cancer.
The protein WNT7B in this study binds to Fzd7 and PAC-1. It was obtained by transfection of PAC-1 cells using a commercial RNA reverse transcription kit. After transfection, 5% of the reverse transcribed cDNA was subjected to PCR amplification. For further validation, we used a mouse cell model.
In addition to its potential for treating cancer, WNT7B is also a canonical Wnt agonist. This canonical Wnt ligand has been shown to regulate global asymmetry. A similar study conducted in flies showed that the removal of endogenous Wnts did not affect the PCP pathway.
The co-expression of Wnt7b and Fzd7 in the R2 database using the TCGA-195" dataset showed significant association between the two proteins. The rho=0.548, p=1.07e-16, indicates that Wnt7b is significantly associated with Fzd7 in pancreatic cancer cells. Furthermore, it has an inhibitory effect on b-catenin levels.
This compound stimulates mesenchymal progenitor cell proliferation in a cell culture model by triggering the early attraction of M1 macrophages and endothelial cells to fibrin hydrogels. Moreover, it induces long-term bone healing without engraftment. As a result, it is potentially useful for the treatment of osteoporosis and other degenerative diseases.
Human adult stem cells are one of the most promising cell types for treatment and research, and are currently being evaluated for potential clinical benefits. Studies show that reduced stem cell numbers are associated with a host of dysfunctions. Testosterone, a key androgen, has a major influence on different cell types, including mesenchymal progenitor cells. Studies suggest that testosterone influences stem cell proliferation and stemness.
In a study, human induced pluripotent stem cells enhanced the regeneration of somatosensory cortex, peripheral nerves, and neural tissue. This study provides a basis for further studies on this type of cell. Similarly, the drug inhibits tumorigenesis, thereby promoting cancer cell survival and regeneration. The drug is also FDA-approved for treatment of peripheral nerve injuries.
When a cell is cultured in vitro, the extracellular matrix is supplemented with factors and proteins that mimic the physiologic environment for optimal cell proliferation and differentiation. It has been shown to have anti-inflammatory and pro-resolving/M2 macrophage activity. Further, it promotes the proliferation of mesenchymal progenitor cells. However, there is still more work to be done in order to understand how fibroblasts can stimulate mesenchymal progenitor cell proliferation.
The results of the study demonstrate that WNT7B increases the number of cells in the S phase. In contrast, knockdown of Sox11 completely eliminated the observed changes in cell cycle profile. Furthermore, 5-ethynyl-2''deoxyuridine (EdU) confirmed Wnt7b-dependent proliferation. Thus, Wnt7b induces the proliferation of mesenchymal progenitors.
Sox11 promotes osteogenic differentiation and proliferation of mesenchymal progenitors. It regulates a number of target genes. This article highlights the potential applications of WNT7B in osteoblastogenesis and bone formation. While the WNT7B marker has a plethora of applications in research, it remains a work in progress.
In addition, WNT7B induces Sox11 expression in osteoblasts. This effect is mediated by the Nfatc1-mediated Ca2+ signaling pathway. Moreover, Wnt7b also induces the transcription of Sox11 in osteogenic BMSCs. The results show that the WNT7B marker promotes osteogenic differentiation and stimulates bone-formation.
WNT7B-induced expression in osteoblasts has recently been used to detect the activity of Wnt7b in osteoblasts. By using this marker, researchers can target osteoblasts undergoing bone regeneration. Sox11 expression is a key marker for the treatment of osteoporosis. Boster Bio also provides ccnb1 as a reverse marker in osteoporosis.
PMID: 11562755 by Kirikoshi H., et al. Molecular cloning and characterization of human WNT7B.
PMID: 8168088 by Huguet E.L., et al. Differential expression of human Wnt genes 2, 3, 4, and 7B in human breast cell lines and normal and disease states of human breast tissue.