PDGFRB (platelet-derived growth factor receptor β) is a type III tyrosine kinase receptor, which exists as a homodimer. This receptor interacts with multiple ligands, but its main physiological ligand is PDGF-BB homodimer. It is located on human chromosome 5q32.
Immunogen
The antiserum was produced against synthesized peptide derived from human PDGFR beta.
Immunogen Range: 991-1040
Biochem/physiol Actions
PDGFRB (platelet-derived growth factor receptor β), upon interaction with PGDFB, regulates multiple processes such as, sclerotic disorders, wound healing and tumor angiogenesis. Gain-of-function mutation in this gene is linked with Penttinen syndrome. Loss-of-function mutation in this gene results in the neurodegenerative disorder primary familial brain calcification (PFBC).
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Attempts have been made to use cell transplantation and biomaterials to promote cell proliferation, differentiation, migration, and survival, as well as angiogenesis, in the context of brain injury. However, whether bioactive materials can repair the damage caused by ischemic stroke
Primary Familial Brain Calcification (PFBC), a neurodegenerative disease characterized by progressive pericapillary calcifications, has recently been linked to heterozygous mutations in PDGFB and PDGFRB genes. Here, we functionally analyzed several of these mutations in vitro. All six analyzed PDGFB mutations
American journal of human genetics, 97(3), 465-474 (2015-08-19)
Penttinen syndrome is a distinctive disorder characterized by a prematurely aged appearance with lipoatrophy, epidermal and dermal atrophy along with hypertrophic lesions that resemble scars, thin hair, proptosis, underdeveloped cheekbones, and marked acro-osteolysis. All individuals have been simplex cases. Exome
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