pCS2-Gpr177 Expression Plasmid
The pCS2-Gpr177 plasmid can be used to express myc-tagged G protein-coupled receptor 177 (Gpr177) full length protein in transfected cells for wnt signaling pathway studies.
Highlights:
- Expresses Gpr177
The Wnt signaling pathways are a group of signal transduction pathways made of proteins that pass signals from outside of a cell through cell surface receptors to the inside of the cell. G protein-coupled receptor 177 (Gpr177) is the mammalian homolog of Drosophila Wntless (Wls; aka Evi, Srt) and is required for Wnt secretion in Wnt-producing cells. Wntless binds to lipid modified Wnts and is mainly localized in the Golgi and trafficking vesicles to modulates intracellular sorting of Wnt proteins. It has been demonstrated that genetic inactivation of Wntless in mice causes similar defects to the loss of canonical Wnt as well as non-canonical Wnt signaling. However, the loss of Wntless does not affect Wnt expression but Wnt secretion in the signal-producing cells. Wntless is also associated with the retromer complex to recycle Wnt from the plasma membrane and the expression pattern of Wntless provides critical information for Wnt-producing cells and source of Wnt in development and disease.
From the laboratory of Wei Hsu, PhD, University of Rochester.
Part of The Investigator's Annexe program.
The pCS2-Gpr177 plasmid can be used to express myc-tagged G protein-coupled receptor 177 (Gpr177) full length protein in transfected cells for wnt signaling pathway studies.
Highlights:
- Expresses Gpr177
The Wnt signaling pathways are a group of signal transduction pathways made of proteins that pass signals from outside of a cell through cell surface receptors to the inside of the cell. G protein-coupled receptor 177 (Gpr177) is the mammalian homolog of Drosophila Wntless (Wls; aka Evi, Srt) and is required for Wnt secretion in Wnt-producing cells. Wntless binds to lipid modified Wnts and is mainly localized in the Golgi and trafficking vesicles to modulates intracellular sorting of Wnt proteins. It has been demonstrated that genetic inactivation of Wntless in mice causes similar defects to the loss of canonical Wnt as well as non-canonical Wnt signaling. However, the loss of Wntless does not affect Wnt expression but Wnt secretion in the signal-producing cells. Wntless is also associated with the retromer complex to recycle Wnt from the plasma membrane and the expression pattern of Wntless provides critical information for Wnt-producing cells and source of Wnt in development and disease.
From the laboratory of Wei Hsu, PhD, University of Rochester.
Part of The Investigator's Annexe program.
| Product Type: | Plasmid |
| Gene/insert name: | Wntless/Gpr177 |
| Accession ID: | Q5T9L3 |
| Antibiotic Resistance: | Amp |
| Fusion Tag(s): | Myc tagged |
| Grow in E. coli at 37 C: | Yes |
| Selectable markers: | Amp |
| Cloning Site 5': | EcoRI |
| Cloning Site 3': | Xhol |
| Insert Size: | 1621 bp |
| Vector Backbone and Size: | pCS2, 4354 |
| High or low copy: | High |
| Storage: | -20C |
| Shipped: | Ambient temperature as liquid |
- Fu J, Jiang M, Mirando AJ, Yu HM, Hsu W. "Reciprocal regulation of Wnt and Gpr177/mouse Wntless is required for embryonic axis formation." Proceedings of the National Academy of Sciences of the United States of America. 2009 Nov 3; 106(44):18598-603.
- Yu HM, Jin Y, Fu J, Hsu W. "Expression of Gpr177, a Wnt trafficking regulator, in mouse embryogenesis." Developmental dynamics : an official publication of the American Association of Anatomists. 2010 Jul; 239(7):2102-9.
- Fu J, Ivy Yu HM, Maruyama T, Mirando AJ, Hsu W. "Gpr177/mouse Wntless is essential for Wnt-mediated craniofacial and brain development." Developmental dynamics : an official publication of the American Association of Anatomists. 2011 Feb; 240(2):365-71. Epub 2011 Jan 11.
- Fu J, Hsu W. "Epidermal Wnt controls hair follicle induction by orchestrating dynamic signaling crosstalk between the epidermis and dermis." The Journal of investigative dermatology. 2013 Apr; 133(4):890-8.
- Maruyama T, Jiang M, Hsu W. "Gpr177, a novel locus for bone mineral density and osteoporosis, regulates osteogenesis and chondrogenesis in skeletal development." Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. 2013 May; 28(5):1150-9.
- Maruyama EO, Yu HM, Jiang M, Fu J, Hsu W. "Gpr177 deficiency impairs mammary development and prohibits Wnt-induced tumorigenesis." PloS one. 2013 8(2):e56644.
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