Evidence map›Paper›PMID 37957262›Full record

ArticleScientific reports2023

Induced alternative splicing an opportunity to study PCSK9 protein isoforms at physiologically relevant concentrations.

Jessica M Cale, Kristin A Ham, Dunhui Li, Craig S McIntosh, Gerald F Watts, Steve D Wilton, May T Aung-Htut

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 69% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. Review
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

7 authors at 3 institutions in 1 country.

Jessica M Cale *Centre for Molecular Medicine and Innovative Therapeutics, Health Futures Institute, Murdoch University, 90 South Street, Murdoch, WA, 6150, Australia.
Kristin A Ham *Centre for Molecular Medicine and Innovative Therapeutics, Health Futures Institute, Murdoch University, 90 South Street, Murdoch, WA, 6150, Australia.
Dunhui LiCentre for Molecular Medicine and Innovative Therapeutics, Health Futures Institute, Murdoch University, 90 South Street, Murdoch, WA, 6150, Australia.
Craig S McIntoshCentre for Molecular Medicine and Innovative Therapeutics, Health Futures Institute, Murdoch University, 90 South Street, Murdoch, WA, 6150, Australia.
Gerald F WattsSchool of Medicine, Faculty of Health and Medical Sciences, University of Western Australia, Perth, WA, 6009, Australia.
Steve D WiltonCentre for Molecular Medicine and Innovative Therapeutics, Health Futures Institute, Murdoch University, 90 South Street, Murdoch, WA, 6150, Australia.
May T Aung-HtutCentre for Molecular Medicine and Innovative Therapeutics, Health Futures Institute, Murdoch University, 90 South Street, Murdoch, WA, 6150, Australia. m.aung-htut@murdoch.edu.au.
Murdoch University · AUPerron Institute for Neurological and Translational Science · AUThe University of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Splice modulating antisense oligomers (AOs) are increasingly used to modulate RNA processing. While most are investigated for their use as therapeutics, AOs can also be used for basic research. This study examined their use to investigate internally and terminally truncated proprotein convertase subtilisin/kexin type 9 (PCSK9) protein isoforms. Previous studies have used plasmid or viral-vector-mediated protein overexpression to study different PCSK9 protein isoforms, creating an artificial environment within the cell. Here we designed and tested AOs to remove specific exons that encode for PCSK9 protein domains and produced protein isoforms at more physiologically relevant levels. We evaluated the isoforms' expression, secretion, and subsequent impact on the low-density lipoprotein (LDL) receptor and its activity in Huh-7 cells. We found that modifying the Cis-His-rich domain by targeting exons 10 or 11 negatively affected LDL receptor activity and hence did not enhance LDL uptake although the levels of LDL receptor were increased. On the other hand, removing the hinge region encoded by exon 8, or a portion of the prodomain encoded by exon 2, have the potential as therapeutics for hypercholesterolemia. Our findings expand the understanding of PCSK9 isoforms and their impact on the LDL receptor and its activity at physiologically relevant concentrations.

Indexed as

Proprotein Convertase 9Serine EndopeptidasesAlternative SplicingHumansProprotein ConvertasesProtein IsoformsReceptors, LDLPCSK9 protein, humanProprotein Convertase 9Proprotein ConvertasesProtein IsoformsReceptors, LDLSerine Endopeptidases

Identifiers

PMID37957262
PMCPMC10643364
OpenAlexW4388638860

What Socratic holds

Textmetadata
LicenceCC BY
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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.