Trends in Neurosciences
p75NTR and apoptosis: Trk-dependent and Trk-independent effects
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Intrinsic receptor effect (IRE) vs ligand-dependent receptor effect (LiRE)
Receptor effects that do not require ligand binding have been described previously: for example, the sky oncogene product[25]functions as a tyrosine kinase in the absence of ligand binding. Perhaps a more appropriately physiological example is that of CD45, which apparently functions as a phosphatase in its monomeric form, but suppresses this activity following dimerization[26].
In general, receptor effects have been defined by comparing the cellular status in the presence and absence of the
p75NTR and Trk: mutual repression?
Over the past few years, several reports have appeared describing interactive effects of p75NTR and TrkA. Taken together, these reports argue for the possibility that p75NTR and TrkA exhibit mutual repression: with coexpression, signaling through one is inhibited by the presence of the other, such that a maximal signal is obtained only by costimulation, which relieves the mutual repression (Fig. 2). Such a proposed relationship would have striking effects on specificity and on signal-to-noise
p75NTR-mediated apoptosis: ligand-dependent, ligand-independent or both?
Several groups have now reported that p75NTR mediates apoptosis, and, interestingly, both ligand-dependent19, 20and ligand-independent7, 21, 23, 36apoptosis induction have been described. The ligand-independent apoptosis induction can occur in cells that do or do not express Trk[21]. As noted above, earlier work from von Bartheld et al.[8]demonstrated enhanced neural cell death in the presence of NGF, in cells that expressed TrkB but not TrkA. Whether mismatched Trk family members are expressed
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2021, Redox BiologyCitation Excerpt :Thus, more in-depth mechanisms studies are required to explore further in order to gain a better understanding of PlsEtn function. p75 neurotrophin receptor (p75NTR), the low-affinity neurotrophins receptor, has been well documented that p75NTR plays a critical role in production of Aβ, neuronal death, neurite degeneration, tau hyperphosphorylation [21–24]. Besides, target p75NTR appears to controls energy expenditure and provide a potential therapeutic intervention for preventing liver steatosis and other metabolic disease [25].
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2019, European Journal of Medicinal ChemistryCitation Excerpt :Among several RTKs linked with cancer, the NGFR is found to be positively correlated with astrocytic gliomas and several reports suggests the role of NGFs in GBM growth [8–10]. NGFRs includes two distinct family of receptor Trks and p75NTR and are found to be differentially expressed in glioblastoma and are identified as effective drugable targets for GBM [8,11–15]. NGFR is a transmembrane receptor for the neurotrophin family.
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