Evidence map›Paper›PMID 31980684›Full record

ArticleScientific reports2020

A misprocessed form of Apolipoprotein A-I is specifically associated with recurrent Focal Segmental Glomerulosclerosis.

Conxita Jacobs-Cachá, Natàlia Puig-Gay, Dominic Helm, Mandy Rettel, Joana Sellarès, Anna Meseguer, Mikhail M Savitski, Francesc J Moreso, Maria José Soler, Daniel Seron and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Precision medicine for focal segmental glomerulosclerosis.Kidney research and clinical practice · 2024
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Podocytopathies.Nature reviews. Disease primers · 2020
    Review
  11. 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

11 authors at 2 institutions in 2 countries.

Conxita Jacobs-Cachá *Nephrology Research Group, Hospital Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain. conxita.jacobs@vhir.org.ORCID http://orcid.org/0000-0003-2518-7847
Natàlia Puig-Gay *Renal Physiopathology Group-CIBBIM. Hospital Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain.
Dominic HelmProteomics Core Facility, European Molecular Biology Laboratory, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-9321-2069
Mandy RettelProteomics Core Facility, European Molecular Biology Laboratory, Heidelberg, Germany.
Joana SellarèsNephrology Research Group, Hospital Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain.
Anna MeseguerRenal Physiopathology Group-CIBBIM. Hospital Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain.
Mikhail M SavitskiProteomics Core Facility, European Molecular Biology Laboratory, Heidelberg, Germany.
Francesc J MoresoNephrology Research Group, Hospital Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain.ORCID http://orcid.org/0000-0002-7267-3963
Maria José SolerNephrology Research Group, Hospital Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain.
Daniel SeronNephrology Research Group, Hospital Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain.
Joan Lopez-HellinRenal Physiopathology Group-CIBBIM. Hospital Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain. joalopez@vhebron.net.
Vall d'Hebron Institut de Recerca · ESEuropean Molecular Biology Laboratory · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apolipoprotein A-Ib (ApoA-Ib) is a high molecular weight form of Apolipoprotein A-I (ApoA-I) found specifically in the urine of kidney-transplanted patients with recurrent idiopathic focal segmental glomerulosclerosis (FSGS). To determine the nature of the modification present in ApoA-Ib, we sequenced the whole APOA1 gene in ApoA-Ib positive and negative patients, and we also studied the protein primary structure using mass spectrometry. No genetic variations in the APOA1 gene were found in the ApoA-Ib positive patients that could explain the increase in its molecular mass. The mass spectrometry analysis revealed three extra amino acids at the N-Terminal end of ApoA-Ib that were not present in the standard plasmatic form of ApoA-I. These amino acids corresponded to half of the propeptide sequence of the immature form of ApoA-I (proApoA-I) indicating that ApoA-Ib is a misprocessed form of proApoA-I. The description of ApoA-Ib could be relevant not only because it can allow the automated analysis of this biomarker in the clinical practice but also because it has the potential to shed light into the molecular mechanisms that cause idiopathic FSGS, which is currently unknown.

Indexed as

Protein Processing, Post-TranslationalAmino Acid SequenceAntibody SpecificityApolipoprotein A-IBiomarkersBlotting, WesternElectrophoresis, Gel, Two-DimensionalGlomerulosclerosis, Focal SegmentalHumansMass SpectrometryMolecular WeightPolymorphism, Single NucleotideProtein PrecursorsRecurrenceApolipoprotein A-IBiomarkersProtein Precursors

Identifiers

PMID31980684
PMCPMC6981185
OpenAlexW3001237139

What OpenQuestion 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 OpenQuestion graph.