Go Back NGF R (222 aa) - Fc Chimera

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A DNA sequence encoding the signal peptide and extracellular domain of human NGF R (aa 1-250) was fused to the Fc region of human IgG1 (aa 93-330). The chimeric protein was expressed in modified human 293 cells.

Nerve growth factor receptor (NGF R), also known as p75NTR or CD271 antigen, is a low affinity NGF receptor primarily responsible for modulating the affinity and activity of tyrosine kinases that promote neuronal survival. Ligand binding by neurotrophins, including beta NGF, brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT3) and neurotrophin-5 (NT4/5), to the NGF R can promote either survival or apoptosis of neurons. NGF receptors such as TrkA, B and C, can associate with NGF R to stimulate higher affinity ligand binding, although on its own NGF R binds to all neutrophins within equal affinity. Neurotrophin-NGF R signaling mediates conditions such as pain, depression, obesity, nerve regeneration disorders, learning and memory. Additionally, NGF R is thought to play a role in neuronal death that occurs in disorders of the CNS such as Alzheimer’s disease. NGF R is a type I membrane protein that is synthesized as a 427 amino acid glycoprotein comprised of a 28 amino acid signal peptide, a 222 amino acid extracellular domain that includes four TNFR-Cys repeats (aa31-aa188), a Ser/Thr rich stalk (aa197-aa248), a 22 amino acid transmembrane region, and a 155 amino acid cytoplasmic domain. NGF R is N-glycosylated and phosphorylated on serine residues, and mass spectroscopic analysis of the NGF R stalk identified 7 sites of O-linked glycosylation that may affect the affinity of neurotrophin binding (see Chapman et al., 1996 J. Neurochem. 66, 1707-1716). Symansis Life Sciences’ NGF R (222aa) contains the aforementioned stalk. In contrast to TrkA, B and C, which contain intracellular tyrosine kinase domains, NGF R lacks intracellular enzymatic activity. However NGF R does contain a type II death domain for binding TNF receptor associated factors (TRAFs) that function in mediating the effects of NGF R signaling. For a review of NGF R and Alzheimer’s disease please refer to Salehi A, et al. (2004) J Neural Transm. 111(3): 323-45.