|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||45183 Da|
|Other Names||Tumor necrosis factor receptor superfamily member 16, Gp80-LNGFR, Low affinity neurotrophin receptor p75NTR, Low-affinity nerve growth factor receptor, NGF receptor, p75 ICD, CD271, NGFR, TNFRSF16|
|Target/Specificity||A synthetic peptide corresponding to residues of human NGFR was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||NGFR Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Plays a role in the regulation of the translocation of GLUT4 to the cell surface in adipocytes and skeletal muscle cells in response to insulin, probably by regulating RAB31 activity, and thereby contributes to the regulation of insulin-dependent glucose uptake (By similarity). Low affinity receptor which can bind to NGF, BDNF, NT-3, and NT-4. Can mediate cell survival as well as cell death of neural cells. Necessary for the circadian oscillation of the clock genes ARNTL/BMAL1, PER1, PER2 and NR1D1 in the suprachiasmatic nucleus (SCN) of the brain and in liver and of the genes involved in glucose and lipid metabolism in the liver.|
|Cellular Location||Membrane; Single-pass type I membrane protein|
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Provided below are standard protocols that you may find useful for product applications.
Neurotrophins signal cell survival, differentiation, growth cessation, and apoptosis through two classes of cell surface receptors, the Trks and NGF Receptor (p75NTR). p75NTR, when activated in the absence of a strong Trk signal, induces apoptosis of neurons, while in the presence of Trk it enhances responses to neurotrophin (1). p75NTR, when it is not bound by NGF, may play a role in neuronal selection during embryonic development and suggest that neuroblastomas may arise from immature neuroblasts that escape programmed cell death. Therefore, the loss of p75NTR expression in developing neural crest cells might be a primary event in the genesis of neuroblastoma (2). It has also been suggested that neuronal death in Alzheimer's disease is mediated, at least in part, by the interaction of beta-amyloid with p75NTR, and suggest new targets for therapeutic intervention (3).
1. Kaplan DR, et al. Curr Opin Cell Bio 9(2):213-21, 1997
2. Bunone G, et al. Oncogene 14(12):1463-70, 1997
3. Yaar M, et al. J Clin Invest 100(9):2333-40, 1997
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