Evidence map›Paper›PMID 24407176›Full record

ArticleCellular signalling2014

Extra-nuclear activity of INSM1 transcription factor enhances insulin receptor signaling pathway and Nkx6.1 expression through RACK1 interaction.

Tao Zhang, Chiachen Chen, Mary B Breslin, Kejing Song, Michael S Lan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular signalling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Function and Transcriptional Regulation of BovineInternational journal of molecular sciences · 2019
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

5 authors at 1 institution in 1 country.

Tao ZhangThe Research Institute for Children, Children's Hospital, New Orleans, LA 70118, USA.
Chiachen ChenThe Research Institute for Children, Children's Hospital, New Orleans, LA 70118, USA.
Mary B BreslinThe Research Institute for Children, Children's Hospital, New Orleans, LA 70118, USA; Department of Pediatrics, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA; Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Kejing SongThe Research Institute for Children, Children's Hospital, New Orleans, LA 70118, USA.
Michael S LanThe Research Institute for Children, Children's Hospital, New Orleans, LA 70118, USA; Department of Pediatrics, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA; Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA. Electronic address: mlan@chnola-research.org.
Children's Hospital of New Orleans · US

Funding

Transcription Factors in Neuroendocrine DifferentiationR01DK061436 · NIDDK · LOUISIANA STATE UNIV HSC NEW ORLEANS · PI LAN, MICHAEL S · 2003 to 2009
$1.5M
NIDDK NIH HHS R01 DK061436NIDDK NIH HHS R01DK061436
6 · The paper itself

Abstract

INSM1 is an islet transcription factor essential for pancreas development. INSM1 functions as a transcriptional repressor of NeuroD/β2 and insulin gene in the pancreas. INSM1 also possesses extra-nuclear activities through binding to multiple cellular regulators such as cyclin D1 and RACK1. In this study, we report that the interaction of INSM1 and RACK1 is essential to enhance the insulin receptor (InR)-mediated signaling pathway. A proline-rich region in the N-terminus of INSM1 is required for RACK1 binding, which interrupts RACK1-InR interaction and enhances InR signal activation. Binding of INSM1 to RACK1 increases AKT phosphorylation. The INSM1-enhanced AKT phosphorylation can be inhibited by the PI3K inhibitor, LY294002. When INSM1 induces AR42J cell trans-differentiation, the Nkx6.1 gene is activated through the InR-mediated signaling pathway and an elevation of the acetyl-H4 modification on the Nkx6.1 gene promoter/enhancer is observed. The PI3K inhibitor interrupts Nkx6.1 and insulin gene expression. Therefore, we conclude that the extra-nuclear activity of INSM1 by enhancing the PI3K/AKT signaling pathway is important for pancreatic cell differentiation.

Indexed as

Signal TransductionAmino Acid SequenceAnimalsCell Line, TumorChlorocebus aethiopsChromonesCOS CellsDNA-Binding ProteinsHomeodomain ProteinsInsulinMiceMolecular Sequence DataMorpholinesNeuropeptidesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase Inhibitors2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesDNA-Binding ProteinsHomeodomain ProteinsInsm1 protein, mouseInsulinMorpholinesNeuropeptidesNkx6-1 protein, mousePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktRACK1 protein, mouseReceptor, InsulinReceptors for Activated C KinaseRepressor ProteinsTranscription FactorsInR signalingINSM1Nkx6.1PI3K/AKTRACK1

Identifiers

PMID24407176
PMCPMC3927318
OpenAlexW1983773589

What OpenQuestion holds

Textmetadata
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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.