Evidence map›Paper›PMID 19246490›Full record

ReviewFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009

Structure, expression, and biological function of INSM1 transcription factor in neuroendocrine differentiation.

Michael S Lan, Mary B Breslin

Open access · greenAbstract readReview
In one paragraph

Review in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.3field-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

62 citing papers in PubMed, 139 citations in OpenAlex.

  1. Article
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  9. New Concepts of Regeneration and Renewal of Adrenal Chromaffin Cells.International journal of molecular sciences · 2025
    Review
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  11. Article
  12. Small cell lung cancer and neuroendocrine tumours.Breathe (Sheffield, England) · 2024
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Michael S LanResearch Institute for Children, Children's Hospital, 200 Henry Clay Ave., Research and Education Bldg., Rm. 2211, New Orleans, LA 70118, USA. mlan@chnola-research.org
Mary B Breslin
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 DK-61436NIDDK NIH HHS R01 DK061436
6 · The paper itself

Abstract

Zinc-finger transcription factors are DNA-binding proteins that are implicated in many diverse biological functions. INSM1 (formerly IA-1) contains five zinc-finger motifs and functions as a transcription factor. INSM1 protein structure is highly conserved in homologues of different species. It is predominantly expressed in developing neuroendocrine tissues and the nervous system in mammals. INSM1 represents an important player in early embryonic neurogenesis. In pancreatic endocrine cell differentiation, Ngn3 first activates INSM1 and subsequently NeuroD/beta2. Conversely, INSM1 exerts a feedback mechanism to suppress NeuroD/beta2 and its own gene expression. INSM1 gene ablation in the mouse results in the impairment of pancreatic endocrine cell maturation. Further, deletion of INSM1 severely impairs catecholamine biosynthesis and secretion from the adrenal gland that results in early embryonic lethality. Genetically, INSM1 acts as a downstream factor of Mash 1 and Phox2b in the differentiation of the sympatho-adrenal lineage. In the developing neocortex, mouse embryos lacking INSM1 expression contain half the number of basal progenitors and show a reduction in cortical plate radial thickness. Cell signaling studies reveal that INSM1 contributes to the induction of cell cycle arrest/exit necessary to facilitate cellular differentiation. INSM1 is highly expressed in tumors of neuroendocrine origin. Hence, its promoter could serve as a tumor-specific promoter that drives a specific targeted cancer gene therapy for the treatment of neuroendocrine tumors. Taken together, all of these features of INSM1 strongly support its role as an important regulator during neuroendocrine differentiation.

Indexed as

Cell DifferentiationCarcinoma, NeuroendocrineDNA-Binding ProteinsHumansNeuroendocrine CellsPancreasRepressor ProteinsTranscription FactorsDNA-Binding ProteinsINSM1 protein, humanRepressor ProteinsTranscription Factors

Identifiers

PMID19246490
PMCPMC2704596
OpenAlexW1970172422

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.