Evidence map›Paper›PMID 29910119›Full record

ArticleMolecular metabolism2018

Secretagogin protects Pdx1 from proteasomal degradation to control a transcriptional program required for β cell specification.

Katarzyna Malenczyk, Edit Szodorai, Robert Schnell, Gert Lubec, Gábor Szabó, Tomas Hökfelt, Tibor Harkany

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2018. 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
2.4field-weighted citation impact, top 12% 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, 20 citations in OpenAlex.

  1. Review
  2. A hydrophobic groove in secretagogin allows for alternate interactions with SNAP-25 and syntaxin-4 in endocrine tissues.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
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  12. Article
  13. 20 Years of Secretagogin: Exocytosis and Beyond.Frontiers in molecular neuroscience · 2019
    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

7 authors at 3 institutions in 3 countries.

Katarzyna MalenczykDepartment of Molecular Neurosciences, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090, Vienna, Austria; Department of Neuroscience, Karolinska Institutet, Retzius väg 8, SE-17177, Stockholm, Sweden.
Edit SzodoraiDepartment of Molecular Neurosciences, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090, Vienna, Austria; Paracelsus Medical University, Strubergasse 21, A-5020, Salzburg, Austria.
Robert SchnellDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Scheeles väg 2, SE-17177, Stockholm, Sweden.
Gert LubecParacelsus Medical University, Strubergasse 21, A-5020, Salzburg, Austria.
Gábor SzabóInstitute of Experimental Medicine, Hungarian Academy of Sciences, Szigony utca 43, H-1083, Budapest, Hungary.
Tomas HökfeltDepartment of Neuroscience, Karolinska Institutet, Retzius väg 8, SE-17177, Stockholm, Sweden.
Tibor HarkanyDepartment of Molecular Neurosciences, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090, Vienna, Austria; Department of Neuroscience, Karolinska Institutet, Retzius väg 8, SE-17177, Stockholm, Sweden. Electronic address: Tibor.Harkany@meduniwien.ac.at.
Karolinska Institutet · SEParacelsus Medical University · ATHUN-REN Institute of Experimental Medicine · HU

Funding

UCD Mutant Mouse Regional Resource CenterU42OD012210 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KC KENT LLOYD · 2012 to 2026
$29.2M
NIH HHS U42 OD012210
6 · The paper itself

Abstract

objectiveSpecification of endocrine cell lineages in the developing pancreas relies on extrinsic signals from non-pancreatic tissues, which initiate a cell-autonomous sequence of transcription factor activation and repression switches. The steps in this pathway share reliance on activity-dependent Ca

methodsWe used high-resolution histochemistry to explore the coincident expression of secretagogin and transcription factors driving β cell differentiation. Secretagogin promoter activity was tested in response to genetically manipulating Pax6 and Pax4 expression. Secretagogin null mice were produced with their pancreatic islets morphologically and functionally characterized during fetal development. A proteomic approach was utilized to identify the Ca

resultsHere, we show that secretagogin, a Ca

conclusionsIn sum, secretagogin scales the temporal availability of a Ca

Indexed as

ProteolysisAnimalsCalciumCells, CulturedHEK293 CellsHomeodomain ProteinsHumansInsulinInsulin-Secreting CellsInsulin SecretionMice, Inbred C57BLPaired Box Transcription FactorsPAX6 Transcription FactorProteasome Endopeptidase ComplexSecretagoginsTrans-ActivatorsCalciumHomeodomain ProteinsInsulinNkx6-1 protein, mousePaired Box Transcription Factorspancreatic and duodenal homeobox 1 proteinPax4 protein, mousePax6 protein, mousePAX6 Transcription FactorProteasome Endopeptidase ComplexSCGN protein, mouseSecretagoginsTrans-ActivatorsCa(2+) signalingDiabetesDifferentiationβ cell

Identifiers

PMID29910119
PMCPMC6034064
OpenAlexW2806303007

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.