Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI.
James E. Hixson, D.T. Vernier. Journal of Lipid Research, 1990-03-01
Topic: Brain proteins, microglia and lab models
We have used restriction isotyping (restriction enzyme isoform genotyping) for rapid typing of common apolipoprotein E isoforms (E2, E3, E4). ApoE restriction isotyping used oligonucleotides to amplify apolipoprotein E gene sequences containing amino acid positions 112 and 158. The amplification products were digested with HhaI and subjected to electrophoresis on polyacrylamide gels. Each of the isoforms was distinguished by a unique combination of HhaI fragment sizes that enabled unambiguous typing of all homozygotic and heterozygotic combinations. HhaI cleaves at GCGC encoding 112arg (E4) and 158arg (E3, E4), but does not cut at GTGC encoding 112cys (E2, E3) and 158cys (E2).
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APA 7th
Hixson, J. E., & Vernier, D. (1990). Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI. Journal of Lipid Research. https://doi.org/10.1016/s0022-2275(20)43176-1
Vancouver
Hixson JE, Vernier D. Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI. Journal of Lipid Research. 1990. doi:10.1016/s0022-2275(20)43176-1. PMID: 2341813.
BibTeX
@article{hixson1990-2341813,
author = {Hixson, James E. and Vernier, D.T.},
title = {{Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI}},
journal = {Journal of Lipid Research},
year = {1990},
doi = {10.1016/s0022-2275(20)43176-1},
pmid = {2341813},
url = {https://doi.org/10.1016/s0022-2275(20)43176-1}
}
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.
Key findings
- We have used restriction isotyping (restriction enzyme isoform genotyping) for rapid typing of common apolipoprotein E isoforms (E2, E3, E4).
- ApoE restriction isotyping used oligonucleotides to amplify apolipoprotein E gene sequences containing amino acid positions 112 and 158.
- The amplification products were digested with HhaI and subjected to electrophoresis on polyacrylamide gels.
- Each of the isoforms was distinguished by a unique combination of HhaI fragment sizes that enabled unambiguous typing of all homozygotic and heterozygotic combinations.
- HhaI cleaves at GCGC encoding 112arg (E4) and 158arg (E3, E4), but does not cut at GTGC encoding 112cys (E2, E3) and 158cys (E2).
Why it matters
This paper describes a method for rapid typing of apolipoprotein E isoforms (E2, E3, E4) using gene amplification and restriction enzyme digestion. It is a laboratory technique paper and does not directly address treating, curing, or preventing Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 53/100
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 senior author's track record, so that was left out: it earned 51 of the 96 points we could judge it on, which is 53 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of Lipid Research) |
| Journal's citation record | 3 / 4 | Journal of Lipid Research: journal h-index 324 (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 | 1 / 5 | 1990 — 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 / 7 | Cited 2,945 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 77.5 citations a year over 38 year(s) since 1990 |
| Impact for its field and year | 5 / 6 | Cited 30.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 5 / 6 | Cited by 154 other studies in this library |
| Still being cited | 3 / 4 | Cited 94 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | OpenAlex's profile for last-listed author D.T. Vernier holds only 2 work(s), too few to judge a track record — left out of this score |
| Institution's track record | 0 / 3 | Texas Biomedical Research Institute: institution h-index 440 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 2341813) |
| Free to read | 2 / 2 | Free to read |
| Points | 51 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 51 of the 96 points we could judge it on is 53 out of 100. |
| Total | 53 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/s0022-2275(20)43176-1
- PubMed: 2341813
- Original source →
- Free full text: Journal of Lipid Research →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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