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Death receptor signaling
Inna N. Lavrik, Alexander Golks, Peter H. Krammer. Journal of Cell Science, 2005-01-14
Topic: Inflammation, microglia and astrocytes
Triggering members of the DR family by death ligands results in the transduction of either apoptotic or survival signals. DISC formation results in the activation of caspase-8, which plays the central role in transduction of the apoptotic signal. The release of Cyt c from mitochondria results in apoptosome formation, followed by the activation of procaspase-9, which in turn cleaves downstream effector caspases (Korsmeyer et al., 2000). TNFR1 stimulation is postulated to result in the formation of two signaling complexes (Micheau and Tschopp, 2003). This would allow the treatment of a number of diseases potentially associated with defects in DR signaling, such as multiple sclerosis and Alzheimer's disease.We would like to thank Karsten Gülow and Martin Sprick for their critical comments and the Wilhem Sander Stiftung, SFB 405, Tumorzentrum Heidelberg/Mannheim for supporting our work.
Key findings
- Triggering members of the DR family by death ligands results in the transduction of either apoptotic or survival signals.
- DISC formation results in the activation of caspase-8, which plays the central role in transduction of the apoptotic signal.
- The release of Cyt c from mitochondria results in apoptosome formation, followed by the activation of procaspase-9, which in turn cleaves downstream effector caspases (Korsmeyer et al., 2000).
- TNFR1 stimulation is postulated to result in the formation of two signaling complexes (Micheau and Tschopp, 2003).
- This would allow the treatment of a number of diseases potentially associated with defects in DR signaling, such as multiple sclerosis and Alzheimer's disease.We would like to thank Karsten Gülow and Martin Sprick for their critical comments and the Wilhem Sander Stiftung, SFB 405, Tumorzentrum Heidelberg/Mannheim for supporting our work.
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 (Journal of Cell Science) |
| 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 | 2005 — 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 15654015) |
| 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 | — |
What each of these 20 components measures, and what this score is not →
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Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Lavrik, I. N., Golks, A., & Krammer, P. H. (2005). Death receptor signaling. Journal of Cell Science. https://doi.org/10.1242/jcs.01610
Vancouver
Lavrik IN, Golks A, Krammer PH. Death receptor signaling. Journal of Cell Science. 2005. doi:10.1242/jcs.01610. PMID: 15654015.
BibTeX
@article{lavrik2005-15654015,
author = {Lavrik, Inna N. and Golks, Alexander and Krammer, Peter H.},
title = {{Death receptor signaling}},
journal = {Journal of Cell Science},
year = {2005},
doi = {10.1242/jcs.01610},
pmid = {15654015},
url = {https://doi.org/10.1242/jcs.01610}
}