Evidence map›Paper›PMID 34554924›Full record

ArticleDiabetes2021

Long RNA Sequencing and Ribosome Profiling of Inflamed β-Cells Reveal an Extensive Translatome Landscape.

Sofia Thomaidou, Roderick C Slieker, Arno R van der Slik, Jasper Boom, Flip Mulder, Amadeo Munoz-Garcia, Leen M 't Hart, Bobby Koeleman, Françoise Carlotti, Rob C Hoeben and 3 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 1 institution in 2 countries.

Sofia ThomaidouDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands.
Roderick C SliekerDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands.ORCID 0000-0003-0961-9152
Arno R van der SlikDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands.
Jasper BoomSequencing Analysis Support Core, Department of Biomedical Data Sciences, Leiden University Medical Center, Leiden, the Netherlands.
Flip MulderCenter for Molecular Medicine, Utrecht Medical Center, Utrecht, the Netherlands.
Amadeo Munoz-GarciaDepartment of Internal Medicine, Leiden University Medical Center, Leiden, the Netherlands.
Leen M 't HartDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands.
Bobby KoelemanCenter for Molecular Medicine, Utrecht Medical Center, Utrecht, the Netherlands.
Françoise CarlottiDepartment of Internal Medicine, Leiden University Medical Center, Leiden, the Netherlands.ORCID 0000-0001-7929-8468
Rob C HoebenDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands.
Bart O RoepDepartment of Internal Medicine, Leiden University Medical Center, Leiden, the Netherlands.ORCID 0000-0003-1616-8337
Hailiang MeiSequencing Analysis Support Core, Department of Biomedical Data Sciences, Leiden University Medical Center, Leiden, the Netherlands.
Arnaud ZaldumbideDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands a.zaldumbide@lumc.nl.ORCID 0000-0001-6680-4456
Leiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disease characterized by autoreactive T cell-mediated destruction of the insulin-producing pancreatic β-cells. Increasing evidence suggest that the β-cells themselves contribute to their own destruction by generating neoantigens through the production of aberrant or modified proteins that escape central tolerance. We recently demonstrated that ribosomal infidelity amplified by stress could lead to the generation of neoantigens in human β-cells, emphasizing the participation of nonconventional translation events in autoimmunity, as occurring in cancer or virus-infected tissues. Using a transcriptome-wide profiling approach to map translation initiation start sites in human β-cells under standard and inflammatory conditions, we identify a completely new set of polypeptides derived from noncanonical start sites and translation initiation within long noncoding RNA. Our data underline the extreme diversity of the β-cell translatome and may reveal new functional biomarkers for β-cell distress, disease prediction and progression, and therapeutic intervention in T1D.

Indexed as

InflammationAutoimmunityBiomarkersCells, CulturedDiabetes Mellitus, Type 1Gene Expression ProfilingHumansInsulin-Secreting CellsPancreatitisPeptide Chain Initiation, TranslationalProtein BiosynthesisProtein Processing, Post-TranslationalRibosomesRNA, Long NoncodingSequence Analysis, RNATranscriptomeBiomarkersRNA, Long Noncoding

Identifiers

PMID34554924
OpenAlexW3168903164

What OpenQuestion holds

Textmetadata
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.