Attenuation of a Caspase-3 Dependent Cell Death in NT4- and p75-Deficient Embryonic Sensory Neurons
Molecular and Cellular Neuroscience, ISSN: 1044-7431, Vol: 16, Issue: 3, Page: 258-268
2000
- 29Citations
- 15Captures
Metric Options: Counts1 Year3 YearSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations29
- Citation Indexes29
- 29
- CrossRef18
- Captures15
- Readers15
- 15
Article Description
Neuronal survival during the developmental period of naturally occurring cell death is mediated through a successful competition for limiting concentrations of neurotrophic factors, and the deprived neurons will die. New results show that induced death through the p75 neurotrophin receptor (p75 NTR ), a member of the p55TNF/Fas family of cell death receptors, may also influence survival during development. We find that eliminating p75 NTR or neurotrophin 4 (NT4) in mice leads to a marked attenuation of apoptosis during the programmed cell death period of the trigeminal ganglion neurons, suggesting that NT4 can induce the death of these neurons through the p75 NTR. These in vivo findings were reproduced in primary cell cultures, where NT4 was found to induce death in a p75 NTR -dependent pathway. Analysis of p75 deficient and wild-type cells revealed two separate cell death pathways, a p75 NTR - and caspase-3-independent pathway activated by trophic factor deprivation, and a p75 NTR - and caspase-3-dependent pathway initiated by NT4. Crossing in the NT4 null alleles in brain-derived neurotrophic factor (BDNF) null mutant mice led to a rescue of a large proportion of BDNF-dependent neurons from excessive cell death, indicating that trophic factor deprivation is not sufficient for the death of many neurons and that additional death inducing signals might be required. Our results suggest that NT4 competitively signals survival and death of sensory neurons through trkB and p75 NTR, respectively.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1044743100908753; http://dx.doi.org/10.1006/mcne.2000.0875; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0033779336&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/10995552; https://linkinghub.elsevier.com/retrieve/pii/S1044743100908753; https://dx.doi.org/10.1006/mcne.2000.0875
Elsevier BV
Provide Feedback
Have ideas for a new metric? Would you like to see something else here?Let us know