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ADAM17 is the main sheddase for the generation of human triggering receptor expressed in myeloid cells (hTREM2) ectodomain and cleaves TREM2 after Histidine 157
Feuerbach D, Schindler P, Barske C, Joller S, Beng-Louka E, Worringer KA, Kommineni S, Kaykas A et al.. Neuroscience letters, 2017-09-18
Topic: Brain proteins, microglia and lab models
Plain-language summary
Triggering receptor expressed in myeloid cells (TREM2) is a member of the immunoglobulin superfamily and is expressed in macrophages, dendritic cells, microglia, and osteoclasts. TREM2 plays a role in phagocytosis, regulates release of cytokine, contributes to microglia maintenance, and its ectodomain is shed from the cell surface. Here, the question was addressed at which position sheddases cleave TREM2 and what are the proteases involved in this process.
What this study adds
Evidence grade: Low
This laboratory work identified ADAM17 as the main protease that releases the TREM2 ectodomain and showed it cleaves TREM2 after Histidine 157. It describes basic TREM2 biology only and provides no evidence about treating, curing or preventing Alzheimer's disease.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Feuerbach, D., Schindler, P., Barske, C., Joller, S., Beng-Louka, E., Worringer, K. A., et al. (2017). ADAM17 is the main sheddase for the generation of human triggering receptor expressed in myeloid cells (hTREM2) ectodomain and cleaves TREM2 after Histidine 157. Neuroscience letters. https://doi.org/10.1016/j.neulet.2017.09.034
Vancouver
Feuerbach D, Schindler P, Barske C, Joller S, Beng-Louka E, Worringer KA, et al. ADAM17 is the main sheddase for the generation of human triggering receptor expressed in myeloid cells (hTREM2) ectodomain and cleaves TREM2 after Histidine 157. Neuroscience letters. 2017. doi:10.1016/j.neulet.2017.09.034. PMID: 28923481.
BibTeX
@article{feuerbach2017-28923481,
author = {Feuerbach, D. and Schindler, P. and Barske, C. and Joller, S. and Beng-Louka, E. and Worringer, K. A. and Kommineni, S. and Kaykas, A. and others},
title = {{ADAM17 is the main sheddase for the generation of human triggering receptor expressed in myeloid cells (hTREM2) ectodomain and cleaves TREM2 after Histidine 157}},
journal = {Neuroscience letters},
year = {2017},
doi = {10.1016/j.neulet.2017.09.034},
pmid = {28923481},
url = {https://doi.org/10.1016/j.neulet.2017.09.034}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- TREM2 plays a role in phagocytosis, regulates release of cytokine, contributes to microglia maintenance, and its ectodomain is shed from the cell surface.
- Here, the question was addressed at which position sheddases cleave TREM2 and what are the proteases involved in this process.
- Using both pharmacological and genetic approaches we report that the main protease contributing to the release of TREM2 ectodomain is ADAM17, (a disintegrin and metalloproteinase domain containing protein, also called TACE, TNFα converting enzyme) while ADAM10 plays a minor role.
- Complementary biochemical experiments reveal that cleavage occurs between histidine 157 and serine 158.
Why it matters
This laboratory work identified ADAM17 as the main protease that releases the TREM2 ectodomain and showed it cleaves TREM2 after Histidine 157. It describes basic TREM2 biology only and provides no evidence about treating, curing or preventing Alzheimer's disease.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 49/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuroscience letters) |
| Journal's citation record | 3 / 4 | Neuroscience Letters: journal h-index 267 (OpenAlex, 2026-10-29) |
| 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 | 2 / 5 | 2017 — within 10 year(s) of the newest study here |
| 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 175 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 15.9 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 3 / 6 | Cited 3.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 36 other studies in this library |
| Still being cited | 3 / 4 | Cited 81 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Ulf Neumann: h-index 39 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California, San Francisco: institution h-index 1,915 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28923481) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 49 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.neulet.2017.09.034
- PubMed: 28923481
- Original source →
- Free full text: bioRxiv (Cold Spring Harbor Laboratory) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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