ArticleJournal of molecular neuroscience : MN2000
Neurotrophin dependence domain: a domain required for the mediation of apoptosis by the p75 neurotrophin receptor.
Article in Journal of molecular neuroscience : MN, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 37 citations in OpenAlex.
- EphB3 receptors function as dependence receptors to mediate oligodendrocyte cell death following contusive spinal cord injury.Cell death & disease · 2015Article
- Cerebellar Purkinje cell p75 neurotrophin receptor and autistic behavior.Translational psychiatry · 2014Article
- Neurotrophins induce nitric oxide generation in human pulmonary artery endothelial cells.Cardiovascular research · 2011Article
- Dependence receptors: mechanisms of an announced death.Cell cycle (Georgetown, Tex.) · 2010Article
- Review
- Cardiovascular actions of neurotrophins.Physiological reviews · 2009Review
- Dependence receptors: between life and death.Cellular and molecular life sciences : CMLS · 2004Review
- The p75 neurotrophin receptor can induce autophagy and death of cerebellar Purkinje neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Inhibitor specificity of recombinant and endogenous caspase-9.The Biochemical journal · 2002Article
- Role of p75 neurotrophin receptor in the neurotoxicity by beta-amyloid peptides and synergistic effect of inflammatory cytokines.The Journal of experimental medicine · 2002Article
- PLAIDD, a type II death domain protein that interacts with p75 neurotrophin receptor.Neuromolecular medicine · 2002Article
- The dependence receptor DCC (deleted in colorectal cancer) defines an alternative mechanism for caspase activation.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 8 institutions in 2 countries.
Funding
Abstract
The mechanisms underlying neurotrophin dependence, and cellular dependent states in general, are unknown. We show that a 29 amino acid region in the intracellular domain of the common neurotrophin receptor, p75NTR, is required for the mediation of apoptosis by p75NTR. Furthermore, contrary to results obtained with Fas, monomeric p75NTR is required for apoptosis induction, whereas multimerization inhibits the pro-apoptotic effect. Within the 29-residue domain required for apoptosis induction by p75NTR, a 14-residue region is sufficient as a peptide inducer of apoptosis. This 14-residue peptide requires the positively charged carboxyterminal residues for its effect on cell death, and these same residues are required by the full-length p75NTR. These studies define a novel type of domain that mediates neurotrophin dependence, and suggest that other cellular dependent states may be mediated by proteins displaying similar domains.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.