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The APOL1 protective M1 modifier occurs exclusively with the KIK protein haplotype to suppress channel conductance
Yang, D.; Bartolomeo, K. R.; Liu, S.; Gonzalez-Vicente, A.; Wheeler, N. R.; Benchek, P.; Zhu, X.; Haines et al.. medRxiv (preprint), 2026-09-15
Topic: Brain proteins, microglia and lab models
IntroductionGenetic studies have shown the APOL1 variant p.N264K, also called M1, is associated with markedly lower kidney disease risk when co-inherited with the G2-risk allele. Reported race was compared with genetically inferred ancestry. In vitro thallium flux assays demonstrated that M1 alone and p.Lys150 alone each partially reduced thallium flux but completely abrogated thallium flux when on the same haplotype. These functional interactions highlight the importance of considering the M1 variant in its haplotype context when designing basic research studies and translating results into future approaches for therapeutic intervention.
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APA 7th
Yang, D., Bartolomeo, K. R., Liu, S., Gonzalez-Vicente, A., Wheeler, N. R., Benchek, P., et al. (2026). The APOL1 protective M1 modifier occurs exclusively with the KIK protein haplotype to suppress channel conductance. medRxiv (preprint). https://doi.org/10.64898/2026.09.14.26362999
Vancouver
Yang D, Bartolomeo KR, Liu S, Gonzalez-Vicente A, Wheeler NR, Benchek P, et al. The APOL1 protective M1 modifier occurs exclusively with the KIK protein haplotype to suppress channel conductance. medRxiv (preprint). 2026. doi:10.64898/2026.09.14.26362999.
BibTeX
@article{yang2026-a81a35f6,
author = {Yang, D. and Bartolomeo, K. R. and Liu, S. and Gonzalez-Vicente, A. and Wheeler, N. R. and Benchek, P. and Zhu, X. and Haines and others},
title = {{The APOL1 protective M1 modifier occurs exclusively with the KIK protein haplotype to suppress channel conductance}},
journal = {medRxiv (preprint)},
year = {2026},
doi = {10.64898/2026.09.14.26362999},
url = {https://doi.org/10.64898/2026.09.14.26362999}
}
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
- IntroductionGenetic studies have shown the APOL1 variant p.N264K, also called M1, is associated with markedly lower kidney disease risk when co-inherited with the G2-risk allele.
- Reported race was compared with genetically inferred ancestry.
- In vitro thallium flux assays demonstrated that M1 alone and p.Lys150 alone each partially reduced thallium flux but completely abrogated thallium flux when on the same haplotype.
- These functional interactions highlight the importance of considering the M1 variant in its haplotype context when designing basic research studies and translating results into future approaches for therapeutic intervention.
Why it matters
This laboratory study looked at how two versions of the APOL1 gene affect cell channels when they occur together on the same chromosome. It is basic in-vitro research about kidney disease genetics, not a study of Alzheimer's disease or its treatment.
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Study details
- Participants40,909
- Effect size99.5%
- Evidence strengthLow
How this study scored 16/100
Preprint — not yet peer-reviewed. It scored 32 on the same rubric, but non-peer-reviewed sources are capped at 16, so it shows as 16. Scored zero for study design and randomised / blinded because the record does not state it. We have no data on impact for its field and year, so that was left out: it earned 30 of the 94 points we could judge it on, which is 32 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 2 / 10 | Tier 4 — not a peer-reviewed journal (medRxiv (preprint)) |
| Journal's citation record | 0 / 4 | Not a journal article, so the journal's record does not count |
| 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 | 4 / 10 | Preprint — not yet peer-reviewed. Hosted on a preprint server. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 4 / 4 | 40,909 participants |
| Effect reported | 2 / 3 | Effect reported as a number, without an interval or test |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 0 / 7 | Cited 0 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.0 citations a year over 2 year(s) since 2026 |
| 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 | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author John R. Sedor: h-index 63 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Case Western Reserve University: institution h-index 1,159 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 2 / 2 | Free to read |
| Points | 30 / 94 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 30 of the 94 points we could judge it on is 32 out of 100. |
| Total | 32 / 100 | Capped to 16 because this is not a peer-reviewed article. |
What each of these 20 components measures, and what this score is not →
Read the original
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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