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Phosphorylation events mediated by protein kinase C alpha and epsilon participate in regulation of tau steady-state levels and generation of certain "Alzheimer-like" phospho-epitopes
Boyce JJ, Shea TB.. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 1997-06-01
Topic: Brain proteins, microglia and lab models
Hyperactivation of protein kinase C (PKC) in intact neuroblastoma cells by several methods increases site-specific tau phosphorylation as shown by increases in paired helical filament-I (PHF-I) and ALZ-50 but not AT-8 immunoreactivity. In the present study, the influence of PKC on tau metabolism was further examined by isoform-specific antisense oligonucleotide-mediated PKC downregulation in human SH-SY-5Y neuroblastoma cells and by generation of stably-transfected subclones expressing isoform-specific anti-PKC mRNA sequences. Downregulation of PKC epsilon by both of these methods reduced PHF-I and ALZ-50 immunoreactivity, suggesting that this PKC isoform, perhaps via downstream kinase cascades, regulated tau phosphorylation events that normally generate these epitopes. By contrast, downregulation of either PKC epsilon or PKC alpha reduced immunoreactivity towards the phosphate-independent anti-tau antibodies 5E2 and JM, suggesting that both of these isoforms participated in regulation of tau steady-state levels. Downregulation of PKC beta did not affect any of the above changes. The above roles were apparently unique for PKC epsilon and PKC alpha, since activation of multiple PKC isoforms by phorbol ester treatment and/or other calcium-dependent kinase(s) by ionophore-mediated calcium influx could not compensate for downregulation of PKC alpha or PKC epsilon in maintaining tau steady-state levels or PHF-I/ALZ-50 immunoreactivity, respectively. These findings suggest that hyperactivation of signal transduction pathways, including those regulated by PKC, could evoke changes in neuronal cells reminiscent of those seen in affected neurons in Alzheimer's disease.
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APA 7th
Boyce, J. J., & Shea, T. B. (1997). Phosphorylation events mediated by protein kinase C alpha and epsilon participate in regulation of tau steady-state levels and generation of certain "Alzheimer-like" phospho-epitopes. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience. https://doi.org/10.1016/s0736-5748(97)00010-5
Vancouver
Boyce JJ, Shea TB. Phosphorylation events mediated by protein kinase C alpha and epsilon participate in regulation of tau steady-state levels and generation of certain "Alzheimer-like" phospho-epitopes. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience. 1997. doi:10.1016/s0736-5748(97)00010-5. PMID: 9253654.
BibTeX
@article{boyce1997-9253654,
author = {Boyce, J. J. and Shea, T. B.},
title = {{Phosphorylation events mediated by protein kinase C alpha and epsilon participate in regulation of tau steady-state levels and generation of certain "Alzheimer-like" phospho-epitopes}},
journal = {International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience},
year = {1997},
doi = {10.1016/s0736-5748(97)00010-5},
pmid = {9253654},
url = {https://doi.org/10.1016/s0736-5748(97)00010-5}
}
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Key findings
- Downregulation of PKC epsilon by both of these methods reduced PHF-I and ALZ-50 immunoreactivity, suggesting that this PKC isoform, perhaps via downstream kinase cascades, regulated tau phosphorylation events that normally generate these epitopes.
- By contrast, downregulation of either PKC epsilon or PKC alpha reduced immunoreactivity towards the phosphate-independent anti-tau antibodies 5E2 and JM, suggesting that both of these isoforms participated in regulation of tau steady-state levels.
- These findings suggest that hyperactivation of signal transduction pathways, including those regulated by PKC, could evoke changes in neuronal cells reminiscent of those seen in affected neurons in Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 1997 — older than 20 years, still counted |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 9253654) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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