Evidence map›Paper›PMID 25061557›Full record

ArticleMolecular metabolism2014

PTBP1 is required for glucose-stimulated cap-independent translation of insulin granule proteins and Coxsackieviruses in beta cells.

Klaus-Peter Knoch, Suchita Nath-Sain, Antje Petzold, Hendryk Schneider, Mike Beck, Carolin Wegbrod, Anke Sönmez, Carla Münster, Anne Friedrich, Merja Roivainen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 48 citations in OpenAlex.

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  7. PTBP1 as a potential regulator of disease.Molecular and cellular biochemistry · 2024
    Review
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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 5 institutions in 2 countries.

Klaus-Peter KnochPaul Langerhans Institute Dresden, TU Dresden Germany ; German Center for Diabetes Research, 01307 Dresden, Germany.
Suchita Nath-SainPaul Langerhans Institute Dresden, TU Dresden Germany ; German Center for Diabetes Research, 01307 Dresden, Germany.
Antje PetzoldPaul Langerhans Institute Dresden, TU Dresden Germany ; German Center for Diabetes Research, 01307 Dresden, Germany.
Hendryk SchneiderPaul Langerhans Institute Dresden, TU Dresden Germany ; German Center for Diabetes Research, 01307 Dresden, Germany.
Mike BeckPaul Langerhans Institute Dresden, TU Dresden Germany ; German Center for Diabetes Research, 01307 Dresden, Germany.
Carolin WegbrodPaul Langerhans Institute Dresden, TU Dresden Germany ; German Center for Diabetes Research, 01307 Dresden, Germany.
Anke SönmezPaul Langerhans Institute Dresden, TU Dresden Germany ; German Center for Diabetes Research, 01307 Dresden, Germany.
Carla MünsterPaul Langerhans Institute Dresden, TU Dresden Germany ; German Center for Diabetes Research, 01307 Dresden, Germany.
Anne FriedrichPaul Langerhans Institute Dresden, TU Dresden Germany ; German Center for Diabetes Research, 01307 Dresden, Germany.
Merja RoivainenNational Institute for Health and Welfare, Helsinki, Finland.
Michele SolimenaPaul Langerhans Institute Dresden, TU Dresden Germany ; Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany.
Technische Universität Dresden · DEDeutsches Diabetes-Zentrum e.V. · DEGerman Center for Diabetes Research · DEPaul Langerhans Institute Dresden · DEFinnish Institute for Health and Welfare · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose and GLP-1 stimulate not only insulin secretion, but also the post-transcriptional induction of insulin granule biogenesis. This process involves the nucleocytoplasmic translocation of the RNA binding protein PTBP1. Binding of PTBP1 to the 3'-UTRs of mRNAs for insulin and other cargoes of beta cell granules increases their stability. Here we show that glucose enhances also the binding of PTBP1 to the 5'-UTRs of these transcripts, which display IRES activity, and their translation exclusively in a cap-independent fashion. Accordingly, glucose-induced biosynthesis of granule cargoes was unaffected by pharmacological, genetic or Coxsackievirus-mediated inhibition of cap-dependent translation. Infection with Coxsackieviruses, which also depend on PTBP1 for their own cap-independent translation, reduced instead granule stores and insulin release. These findings provide insight into the mechanism for glucose-induction of insulin granule production and on how Coxsackieviruses, which have been implicated in the pathogenesis of type 1 diabetes, can foster beta cell failure.

Indexed as

Beta cellsCV, CoxsackievirusDiabeteseIF4E-V5, eIF4E tagged at its C-terminus with a V5-epitopeER, endoplasmic reticulumEV, EnterovirusF, FaulknerFL, firefly luciferaseInsulinIRES, internal ribosomal entry siteITAF, IRES-trans-acting factorMCA, MIN6 cell adaptedmTORC1, mammalian Target Of Rapamycin Complex 1PABP, poly(A)-binding proteinPC, prohormone convertasePolypyrimidine tract-binding proteinPTBP1, polypyrimidine tract-binding protein 1S6K1, p70S6 Kinase 1Secretory granulesT1D, type 1 diabetesTranslationUTR, untranslated regionVirus

Identifiers

PMID25061557
PMCPMC4099505
OpenAlexW2018792810

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.