Evidence map›Paper›PMID 37469559›Full record

ArticleFrontiers in physiology2023

Protein structural insights into a rare PCSK9 gain-of-function variant (R496W) causing familial hypercholesterolemia in a Saudi family: whole exome sequencing and computational analysis.

Noor Ahmad Shaik, Najla Al-Shehri, Mohammad Athar, Ahmed Awan, Mariam Khalili, Hadiah Bassam Al Mahadi, Gehan Hejazy, Omar I Saadah, Sameer Eida Al-Harthi, Ramu Elango and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 3 countries.

Noor Ahmad ShaikDepartment of Genetic Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Najla Al-ShehriDepartment of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Mohammad AtharDepartment of Medical Genetics, Faculty of Medicine, Umm Al-Qura University, Makkah, Saudi Arabia.
Ahmed AwanDepartment of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Mariam KhaliliDepartment of Pharmacology, College of Medicine, Khalifa University, Abu Dhabi, United Arab Emirates.
Hadiah Bassam Al MahadiDepartment of Research and Development, Al Borg Medical Laboratories, Jeddah, Saudi Arabia.
Gehan HejazyDepartment of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Omar I SaadahDepartment of Pediatrics, Pediatric Gastroenterology Unit, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Sameer Eida Al-HarthiDepartment of Clinical Pharmacology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Ramu ElangoDepartment of Genetic Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Babajan BanaganapalliDepartment of Genetic Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Eman AlefishatDepartment of Pharmacology, College of Medicine, Khalifa University, Abu Dhabi, United Arab Emirates.
Zuhier AwanDepartment of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
King Abdulaziz University · SAKhalifa University of Science and Technology · AEUmm al-Qura University · SAUniversity of Jordan · JO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Familial hypercholesterolemia (FH) is a globally underdiagnosed genetic condition associated with premature cardiovascular death. The genetic etiology data on Arab FH patients is scarce. Therefore, this study aimed to identify the genetic basis of FH in a Saudi family using whole exome sequencing (WES) and multidimensional bioinformatic analysis. Our WES findings revealed a rare heterozygous gain-of-function variant (R496W) in the exon 9 of the

Indexed as

cardiovascular diseasesfamilial hypercholesterolemiapcsk9sanger sequencewhole exome sequence

Identifiers

PMID37469559
PMCPMC10353052
OpenAlexW4383101638

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.