Anti-FGFR2c antibody
Description
Application Data
Description
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Detects fibroblast growth factor receptor 2c mesenchymal splice variant
Application Data
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FGFR2b-His and FGFR2c-His transfected HEK293 cells.
Lane 1: Conditioned media from non-transfected HEK293 cells
Lane 2: Conditioned media from HEK293 cells stably expressing soluble FGFR2b-His
Lane 3-4: Conditioned media from HEK293 cells stably expressing soluble FGFR2c-His
Western blot image provided courtesy of Dr. Jennet Gummadova
The fibroblast growth factor receptor (FGFR) family consists of four transmembrane receptor tyrosine kinases (FGFR1‐4), which regulate important physiological processes, such as cell proliferation, differentiation, migration and survival throughout the body. FGFR2c is known as the mesenchymal FGFR2 isoform and when aberrantly expressed in epithelial cells it induces epithelial‐mesenchymal transition (EMT) and is involved in cancer progression. FGFR2 signalling is critical for proper craniofacial development. A gain-of-function mutation in the 2c splice variant is associated with Crouzon syndrome, which is characterized by craniosynostosis, the premature fusion of one or more of the cranial vault sutures, leading to craniofacial maldevelopment. FGFR2c-mediated ERK-MAPK signalling is a key mediator of craniofacial growth and coronal suture development.
The fibroblast growth factor receptor (FGFR) family consists of four transmembrane receptor tyrosine kinases (FGFR1‐4), which regulate important physiological processes, such as cell proliferation, differentiation, migration and survival throughout the body. FGFR2c is known as the mesenchymal FGFR2 isoform and when aberrantly expressed in epithelial cells it induces epithelial‐mesenchymal transition (EMT) and is involved in cancer progression. FGFR2 signalling is critical for proper craniofacial development. A gain-of-function mutation in the 2c splice variant is associated with Crouzon syndrome, which is characterized by craniosynostosis, the premature fusion of one or more of the cranial vault sutures, leading to craniofacial maldevelopment. FGFR2c-mediated ERK-MAPK signalling is a key mediator of craniofacial growth and coronal suture development.
| Catalogue number | crb2005090 |
|---|---|
| Antibody | Anti-FGFR2c antibody |
| Antigen Peptide | KLH conjugated synthetic peptide crb1200371e |
| Protein ID | UniProtKB - |
| Aliases | Fibroblast growth factor receptor 2c, FGFR2c |
| Cross-Reactivity | Human |
| Host Species | Anti-Rabbit |
| Antibody Type | Polyclonal |
| Concentration | 1mg/ml |
| Validation | 1:1000 (WB), 1:1000 (ELISA) |
| Target | FGFR2c |
| Disease Area | Signal transduction |
| Specificity | Protein |
| Citations | Pfaff, M., Xue, K., Li, L., Horowitz, M., Steinbacher, D. and Eswarakumar, J. (2016). FGFR2c-mediated ERK–MAPK activity regulates coronal suture development. Dev Biol, 415(2), 242-250. PMID: 27034231
Ranieri, D., Rosato, B., Nanni, M., Belleudi, F. and Torrisi, M. (2017). Expression of the FGFR2c mesenchymal splicing variant in human keratinocytes inhibits differentiation and promotes invasion. Mol Carcinog, 57(2), 272-283. PMID: 29068468 |
| References | Pfaff, M., Xue, K., Li, L., Horowitz, M., Steinbacher, D. and Eswarakumar, J. (2016). FGFR2c-mediated ERK–MAPK activity regulates coronal suture development. Dev Biol, 415(2), 242-250. PMID: 27034231
Ranieri, D., Rosato, B., Nanni, M., Belleudi, F. and Torrisi, M. (2017). Expression of the FGFR2c mesenchymal splicing variant in human keratinocytes inhibits differentiation and promotes invasion. Mol Carcinog, 57(2), 272-283. PMID: 29068468 |
The fibroblast growth factor receptor (FGFR) family consists of four transmembrane receptor tyrosine kinases (FGFR1‐4), which regulate important physiological processes, such as cell proliferation, differentiation, migration and survival throughout the body. FGFR2c is known as the mesenchymal FGFR2 isoform and when aberrantly expressed in epithelial cells it induces epithelial‐mesenchymal transition (EMT) and is involved in cancer progression.
FGFR2 signalling is critical for proper craniofacial development. A gain-of-function mutation in the 2c splice variant is associated with Crouzon syndrome, which is characterized by craniosynostosis, the premature fusion of one or more of the cranial vault sutures, leading to craniofacial maldevelopment. FGFR2c-mediated ERK-MAPK signalling is a key mediator of craniofacial growth and coronal suture development.