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Ngfr  -  nerve growth factor receptor

Rattus norvegicus

Synonyms: Gp80-LNGFR, LNGFR, Low affinity neurotrophin receptor p75NTR, Low-affinity nerve growth factor receptor, NGF receptor, ...
 
 
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Disease relevance of Ngfr

 

Psychiatry related information on Ngfr

  • Reciprocal changes in expression of mRNA for nerve growth factor and its receptors TrkA and LNGFR in brain of aged rats in relation to maze learning deficits [6].
  • Thus, ligand-dependent p75NTR regulation of the ceramide pathway mediates survival in certain neurons and may represent an important target for neuroprotective drugs in degenerative diseases involving p75NTR-expressing neurons, such as Alzheimer's disease [7].
 

High impact information on Ngfr

  • The product of the proto-oncogene trk, p140trk, is a tyrosine kinase receptor that has been identified as a signal-transducing receptor for NGF, while the role of the low affinity NGF receptor, p75NGFR, in signal transduction is less clear [8].
  • We have isolated mammalian neural crest cells using a monoclonal antibody to the low affinity NGF receptor, and established conditions for the serial propagation of these cells in clonal culture to assess their developmental potential [9].
  • Taken together, these results indicate that NGF has the ability to promote cell death in specific cell types through a ligand-dependent signalling mechanism involving the p75 neurotrophin receptor [10].
  • Death of oligodendrocytes mediated by the interaction of nerve growth factor with its receptor p75 [10].
  • The NGF receptor (NGFR) mRNA was found in the Sertoli cells of rat testis [11].
 

Chemical compound and disease context of Ngfr

 

Biological context of Ngfr

  • The mechanisms employed by the p75 neurotrophin receptor (p75NTR) to mediate neurotrophin-dependent apoptosis are poorly defined [17].
  • Our results show that NRAGE contributes to p75NTR-dependent cell death and suggest novel functions for MAGE family proteins [17].
  • Surprisingly, p75NTR increased, rather than decreased, Akt phosphorylation in a variety of cell types, including human Niemann-Pick fibroblasts, which lack acidic sphingomyelinase activity [18].
  • The precursor of BDNF (pro-BDNF) is differentially cleaved in aminoglycoside-deafened cochleae, resulting in a predominant up-regulation of a truncated form of pro-BDNF, which colocalized with p75NTR-expressing SGN fibers [19].
  • Nuclear transcription factors c-Jun and cyclic AMP response element-binding protein phosphorylated by p75NTR- and TrkB-activated signal pathways, respectively, also showed a corresponding differential modulation, suggesting an activation of apoptotic pathways, coupled to a loss of pro-survival neurotrophic support [19].
 

Anatomical context of Ngfr

  • Aminoglycoside-induced degeneration of adult spiral ganglion neurons involves differential modulation of tyrosine kinase B and p75 neurotrophin receptor signaling [19].
  • Truncated TrkB receptor-induced outgrowth of dendritic filopodia involves the p75 neurotrophin receptor [20].
  • p75 and TrkA receptor signaling independently regulate amyloid precursor protein mRNA expression, isoform composition, and protein secretion in PC12 cells [21].
  • Increased Pro-Nerve Growth Factor and p75 Neurotrophin Receptor Levels in Developing Hypothyroid Rat Cerebral Cortex Are Associated with Enhanced Apoptosis [1].
  • Here, we observed that NgR and p75 were colocalized in low-density membrane raft fractions derived from forebrains and cerebella as well as from cerebellar granule cells [22].
 

Associations of Ngfr with chemical compounds

  • The precise mechanism that p75NTR uses to promote cell death is not certain, but one possibility is that p75NTR-dependent ceramide accumulation inhibits phosphatidylinositol 3-kinase-mediated Akt activation [18].
  • However, treatment of PC12 cells with C2-ceramide, an analogue of ceramide, the endogenous product produced by the activity of p75NTR-activated sphingomyelinase, mimicked the effects of NGF on cell morphology and stimulation of both APP mRNA levels and APP secretion [21].
  • Effect of anti-NGF on ovarian expression of alpha1- and beta2-adrenoceptors, TrkA, p75NTR, and tyrosine hydroxylase in rats with steroid-induced polycystic ovaries [23].
  • Here we show that nerve growth factor (NGF) induced a rapid release of glutamate and an increase of Ca2+ in cerebellar neurons through a p75-dependent pathway [24].
  • Nerve growth factor-induced glutamate release is via p75 receptor, ceramide, and Ca(2+) from ryanodine receptor in developing cerebellar neurons [24].
  • The region of p75 that Kalirin9 binds includes its mastoparan-like fifth helix, which was shown to recruit RhoGDI-RhoA [25].
 

Physical interactions of Ngfr

  • NgR interacted with p75 in lipid rafts [22].
  • We found that p75 can directly bind the GTPases Ras and Rho and that the unstimulated p75 inactivates total cellular Ras through a differential influence on the dissociation of GDP and GTP from Ras and an exchange of bound Ras.GDP for free Ras.GTP [26].
  • Brain-derived neurotrophic factor and the anti-p75 monoclonal antibody MC192 have been shown to interfere with the binding of nerve growth factor to p75 [27].
  • These data are consistent with receptor allosterism, and prompted a search for TrkA/p75NTR complexes in the absence of NGF [28].
  • We suggest that BDNF increases production or release of FGF-2 by binding to p75NTR on Müller cells [29].
 

Regulatory relationships of Ngfr

  • The p75NTR is a multifunctional type I membrane protein that promotes neurotrophin-induced neuronal survival and differentiation by forming a heteromeric co-receptor complex with the Trk receptors [30].
  • Soluble NgRECD binds all CNS myelin-derived ligands and thus has the potential to act as an inhibitory signalling antagonist, but the role of TROY and its shed ectodomain in growth cone mobility is unknown. siRNA knockdown of p75NTR also inactivates Rho-A and disinhibits NTF-stimulated RGC neurite outgrowth in cultures with added CNS myelin [31].
  • Additionally, BDNF was expressed in Pax7+ satellite cells where it colocalized with p75NTR [32].
  • Norepinephrine stores were not affected by high salt intake, but tyrosine hydroxylase, and dopamine beta-hydroxylase were elevated in the salt-induced hypertrophied left ventricle in conjunction with increased levels of nerve growth factor and p75 neurotrophin receptor [33].
  • These findings identify NRAGE as a p75NTR interactor capable of inducing caspase activation and cell death through a JNK-dependent mitochondrial apoptotic pathway [34].
 

Other interactions of Ngfr

  • When neurons were initially cultured in 10 ng/ml NGF for 5 d, and then 200 ng/ml NGF was added, LNGF receptor, T alpha 1, and TH mRNAs all increased within 48 h [35].
  • The Akt kinase plays a crucial role in supporting Trk-dependent cell survival, whereas the p75 neurotrophin receptor (p75NTR) facilitates cellular apoptosis [18].
  • Schwann cell-derived factor-induced modulation of the NgR/p75NTR/EGFR axis disinhibits axon growth through CNS myelin in vivo and in vitro [31].
  • TrkC, the high-affinity NT-3 receptor, and trkA, the high-affinity NGF receptor, are both expressed from the early OLP through the mature OL stage [36].
  • Activation of the mitogen-activated protein kinase pathway through p75NTR: a common mechanism for the neurotrophin family [37].
  • We demonstrate that activation of the TrkA receptor upon binding of nerve growth factor (NGF) regulates the metalloprotease-mediated shedding of p75 leaving a membrane-bound p75 C-terminal fragment (p75-CTF) [38].
 

Analytical, diagnostic and therapeutic context of Ngfr

References

  1. Increased Pro-Nerve Growth Factor and p75 Neurotrophin Receptor Levels in Developing Hypothyroid Rat Cerebral Cortex Are Associated with Enhanced Apoptosis. Kumar, A., Sinha, R.A., Tiwari, M., Pal, L., Shrivastava, A., Singh, R., Kumar, K., Kumar Gupta, S., Godbole, M.M. Endocrinology (2006) [Pubmed]
  2. Concomitant up-regulation of astroglial high and low affinity nerve growth factor receptors in the CA1 hippocampal area following global transient cerebral ischemia in rat. Oderfeld-Nowak, B., Orzyłowska-Sliwińska, O., Sołtys, Z., Zaremba, M., Januszewski, S., Janeczko, K., Mossakowski, M. Neuroscience (2003) [Pubmed]
  3. TACE-induced cleavage of NgR and p75NTR in dorsal root ganglion cultures disinhibits outgrowth and promotes branching of neurites in the presence of inhibitory CNS myelin. Ahmed, Z., Mazibrada, G., Seabright, R.J., Dent, R.G., Berry, M., Logan, A. FASEB J. (2006) [Pubmed]
  4. Mechanisms of p75-mediated death of hippocampal neurons. Role of caspases. Troy, C.M., Friedman, J.E., Friedman, W.J. J. Biol. Chem. (2002) [Pubmed]
  5. Mutation of low affinity nerve growth factor receptor gene in spontaneously hypertensive and stroke-prone spontaneously hypertensive rats: one of the promising candidate genes for hypertension. Nemoto, K., Kageyama, H., Hagiwara, T., Tashiro, F., Tomita, T., Tomita, I., Hano, T., Nishio, I., Ueyama, T. Brain Res. (1994) [Pubmed]
  6. Reciprocal changes in expression of mRNA for nerve growth factor and its receptors TrkA and LNGFR in brain of aged rats in relation to maze learning deficits. Hasenöhrl, R.U., Söderstróm, S., Mohammed, A.H., Ebendal, T., Huston, J.P. Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. (1997) [Pubmed]
  7. A novel p75NTR signaling pathway promotes survival, not death, of immunopurified neocortical subplate neurons. DeFreitas, M.F., McQuillen, P.S., Shatz, C.J. J. Neurosci. (2001) [Pubmed]
  8. Disruption of the low affinity receptor-binding site in NGF allows neuronal survival and differentiation by binding to the trk gene product. Ibáñez, C.F., Ebendal, T., Barbany, G., Murray-Rust, J., Blundell, T.L., Persson, H. Cell (1992) [Pubmed]
  9. Isolation of a stem cell for neurons and glia from the mammalian neural crest. Stemple, D.L., Anderson, D.J. Cell (1992) [Pubmed]
  10. Death of oligodendrocytes mediated by the interaction of nerve growth factor with its receptor p75. Casaccia-Bonnefil, P., Carter, B.D., Dobrowsky, R.T., Chao, M.V. Nature (1996) [Pubmed]
  11. Expression of beta-nerve growth factor receptor mRNA in Sertoli cells downregulated by testosterone. Persson, H., Ayer-Le Lievre, C., Söder, O., Villar, M.J., Metsis, M., Olson, L., Ritzen, M., Hökfelt, T. Science (1990) [Pubmed]
  12. Transient association of the phosphotyrosine phosphatase SHP-2 with TrkA is induced by nerve growth factor. Goldsmith, B.A., Koizumi, S. J. Neurochem. (1997) [Pubmed]
  13. Suramin induces phosphorylation of the high-affinity nerve growth factor receptor in PC12 cells and dorsal root ganglion neurons. Gill, J.S., Connolly, D.C., McManus, M.J., Maihle, N.J., Windebank, A.J. J. Neurochem. (1996) [Pubmed]
  14. Colocalization of low- and high-affinity NGF receptors on PC12 cells, C6 glioma cells and dorsal root ganglion neurons. Spoerri, P.E., Petrelli, L., Guidolin, D., Skaper, S.D. Eur. J. Cell Biol. (1993) [Pubmed]
  15. Cholesterol biosynthesis and the pro-apoptotic effects of the p75 nerve growth factor receptor in PC12 pheochromocytoma cells. Yan, C., Mirnics, Z.K., Portugal, C.F., Liang, Y., Nylander, K.D., Rudzinski, M., Zaccaro, C., Saragovi, H.U., Schor, N.F. Brain Res. Mol. Brain Res. (2005) [Pubmed]
  16. Nerve growth factor rescue of cisplatin neurotoxicity is mediated through the high affinity receptor: studies in PC12 cells and p75 null mouse dorsal root ganglia. Fischer, S.J., Podratz, J.L., Windebank, A.J. Neurosci. Lett. (2001) [Pubmed]
  17. NRAGE, a novel MAGE protein, interacts with the p75 neurotrophin receptor and facilitates nerve growth factor-dependent apoptosis. Salehi, A.H., Roux, P.P., Kubu, C.J., Zeindler, C., Bhakar, A., Tannis, L.L., Verdi, J.M., Barker, P.A. Neuron (2000) [Pubmed]
  18. The p75 neurotrophin receptor activates Akt (protein kinase B) through a phosphatidylinositol 3-kinase-dependent pathway. Roux, P.P., Bhakar, A.L., Kennedy, T.E., Barker, P.A. J. Biol. Chem. (2001) [Pubmed]
  19. Aminoglycoside-induced degeneration of adult spiral ganglion neurons involves differential modulation of tyrosine kinase B and p75 neurotrophin receptor signaling. Tan, J., Shepherd, R.K. Am. J. Pathol. (2006) [Pubmed]
  20. Truncated TrkB receptor-induced outgrowth of dendritic filopodia involves the p75 neurotrophin receptor. Hartmann, M., Brigadski, T., Erdmann, K.S., Holtmann, B., Sendtner, M., Narz, F., Lessmann, V. J. Cell. Sci. (2004) [Pubmed]
  21. p75 and TrkA receptor signaling independently regulate amyloid precursor protein mRNA expression, isoform composition, and protein secretion in PC12 cells. Rossner, S., Ueberham, U., Schliebs, R., Perez-Polo, J.R., Bigl, V. J. Neurochem. (1998) [Pubmed]
  22. Segregation of Nogo66 receptors into lipid rafts in rat brain and inhibition of Nogo66 signaling by cholesterol depletion. Yu, W., Guo, W., Feng, L. FEBS Lett. (2004) [Pubmed]
  23. Effect of anti-NGF on ovarian expression of alpha1- and beta2-adrenoceptors, TrkA, p75NTR, and tyrosine hydroxylase in rats with steroid-induced polycystic ovaries. Manni, L., Holmäng, A., Cajander, S., Lundeberg, T., Aloe, L., Stener-Victorin, E. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2006) [Pubmed]
  24. Nerve growth factor-induced glutamate release is via p75 receptor, ceramide, and Ca(2+) from ryanodine receptor in developing cerebellar neurons. Numakawa, T., Nakayama, H., Suzuki, S., Kubo, T., Nara, F., Numakawa, Y., Yokomaku, D., Araki, T., Ishimoto, T., Ogura, A., Taguchi, T. J. Biol. Chem. (2003) [Pubmed]
  25. The role of Kalirin9 in p75/nogo receptor-mediated RhoA activation in cerebellar granule neurons. Harrington, A.W., Li, Q.M., Tep, C., Park, J.B., He, Z., Yoon, S.O. J. Biol. Chem. (2008) [Pubmed]
  26. Inactivation and activation of Ras by the neurotrophin receptor p75. Blöchl, A., Blumenstein, L., Ahmadian, M.R. Eur. J. Neurosci. (2004) [Pubmed]
  27. The anti-p75 antibody, MC192, and brain-derived neurotrophic factor inhibit nerve growth factor-dependent neurite growth from adult sensory neurons. Kimpinski, K., Jelinski, S., Mearow, K. Neuroscience (1999) [Pubmed]
  28. Reciprocal modulation of TrkA and p75NTR affinity states is mediated by direct receptor interactions. Ross, G.M., Shamovsky, I.L., Lawrance, G., Solc, M., Dostaler, S.M., Weaver, D.F., Riopelle, R.J. Eur. J. Neurosci. (1998) [Pubmed]
  29. Role of the low-affinity NGF receptor (p75) in survival of retinal bipolar cells. Wexler, E.M., Berkovich, O., Nawy, S. Vis. Neurosci. (1998) [Pubmed]
  30. Regulated intramembrane proteolysis of the p75 neurotrophin receptor modulates its association with the TrkA receptor. Jung, K.M., Tan, S., Landman, N., Petrova, K., Murray, S., Lewis, R., Kim, P.K., Kim, D.S., Ryu, S.H., Chao, M.V., Kim, T.W. J. Biol. Chem. (2003) [Pubmed]
  31. Schwann cell-derived factor-induced modulation of the NgR/p75NTR/EGFR axis disinhibits axon growth through CNS myelin in vivo and in vitro. Ahmed, Z., Suggate, E.L., Brown, E.R., Dent, R.G., Armstrong, S.J., Barrett, L.B., Berry, M., Logan, A. Brain (2006) [Pubmed]
  32. BDNF is expressed in skeletal muscle satellite cells and inhibits myogenic differentiation. Mousavi, K., Jasmin, B.J. J. Neurosci. (2006) [Pubmed]
  33. Differential effects of high salt intake on neuropeptide Y and adrenergic markers in hearts of Dahl rats. Nyquist-Battie, C., Cochran, P., Chronwall, B.M. Peptides (1998) [Pubmed]
  34. NRAGE, a p75 neurotrophin receptor-interacting protein, induces caspase activation and cell death through a JNK-dependent mitochondrial pathway. Salehi, A.H., Xanthoudakis, S., Barker, P.A. J. Biol. Chem. (2002) [Pubmed]
  35. Concentration-dependent regulation of neuronal gene expression by nerve growth factor. Ma, Y., Campenot, R.B., Miller, F.D. J. Cell Biol. (1992) [Pubmed]
  36. Nerve growth factor and neurotrophin-3 differentially regulate the proliferation and survival of developing rat brain oligodendrocytes. Cohen, R.I., Marmur, R., Norton, W.T., Mehler, M.F., Kessler, J.A. J. Neurosci. (1996) [Pubmed]
  37. Activation of the mitogen-activated protein kinase pathway through p75NTR: a common mechanism for the neurotrophin family. Lad, S.P., Neet, K.E. J. Neurosci. Res. (2003) [Pubmed]
  38. TrkA receptor activation by nerve growth factor induces shedding of the p75 neurotrophin receptor followed by endosomal gamma-secretase-mediated release of the p75 intracellular domain. Urra, S., Escudero, C.A., Ramos, P., Lisbona, F., Allende, E., Covarrubias, P., Parraguez, J.I., Zampieri, N., Chao, M.V., Annaert, W., Bronfman, F.C. J. Biol. Chem. (2007) [Pubmed]
  39. Prevention of apoptotic but not necrotic cell death following neuronal injury by neurotrophins signaling through the tyrosine kinase receptor. Kim, D.H., Zhao, X., Tu, C.H., Casaccia-Bonnefil, P., Chao, M.V. J. Neurosurg. (2004) [Pubmed]
  40. Regulatory elements and transcriptional regulation by testosterone and retinoic acid of the rat nerve growth factor receptor promoter. Metsis, M., Timmusk, T., Allikmets, R., Saarma, M., Persson, H. Gene (1992) [Pubmed]
  41. Differential change in mRNA expression of p75 and Trk neurotrophin receptors in nucleus gracilis after spinal nerve ligation in the rat. Goettl, V.M., Hussain, S.R., Alzate, O., Wirtz, D.J., Stephens, R.L., Hackshaw, K.V. Exp. Neurol. (2004) [Pubmed]
  42. Overexpression of the p75 neurotrophin receptor in the sensori-motor cortex of rats exposed to ethanol during early postnatal life. Toesca, A., Giannetti, S., Granato, A. Neurosci. Lett. (2003) [Pubmed]
 
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