Evidence map›Paper›PMID 23183171›Full record

ArticleEndocrinology2013

IGF-I 3' untranslated region: strain-specific polymorphisms and motifs regulating IGF-I in osteoblasts.

Spenser S Smith, Catherine B Kessler, Vikram Shenoy, Clifford J Rosen, Anne M Delany

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Regulatory Role of MicroRNAs in Muscle Atrophy during Exercise Intervention.International journal of molecular sciences · 2018
    Review
  9. Article
  10. Article
  11. Article
  12. Minireview: mechanisms of growth hormone-mediated gene regulation.Molecular endocrinology (Baltimore, Md.) · 2014
    Review
  13. Article
  14. Review
  15. Article
  16. MicroRNA in myogenesis and muscle atrophy.Current opinion in clinical nutrition and metabolic care · 2013
    Review
  17. 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 2 institutions in 1 country.

Spenser S SmithCenter for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA.
Catherine B Kessler
Vikram Shenoy
Clifford J Rosen
Anne M Delany
UConn Health · USMaine Medical Center Research Institute · US

Funding

Genetics of IGF1 and Bone Density: The Role of NocturninR01AR045433 · NIAMS · MAINEHEALTH · PI ROSEN, CLIFFORD JAMES · 1998 to 2012
$6.8M
Function and Regulation of Osteonectin in BoneR01AR044877 · NIAMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI DELANY, ANNE M · 2003 to 2013
$2.6M
Function and Regulation of Osteonectin in BoneR56AR044877 · NIAMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI DELANY, ANNE M · 2008 to 2008
$319k
FUNCTION AND REGULATION OF OSTEONECTIN IN BONER29AR044877 · NIAMS · ST. FRANCIS HOSPITAL AND MEDICAL CENTER · PI DELANY, ANNE M · 1998 to 2002
$298k
NIAMS NIH HHS AR44877NIAMS NIH HHS AR45433NIAMS NIH HHS R01 AR044877NIAMS NIH HHS R01 AR045433NIAMS NIH HHS R29 AR044877NIAMS NIH HHS R56 AR044877
6 · The paper itself

Abstract

Reduced IGF-I is associated with low bone mass in humans and mice. C3H/He/J (C3H) mice have higher skeletal IGF-I and greater bone mass than C57BL/6J (B6). We hypothesized that strain-related genotypic differences in Igf1 affected skeletal function. The Igf1 coding region is nonpolymorphic, but its 3' untranslated region (UTR) is polymorphic between C3H and B6. Luciferase-Igf1 3' UTR reporter constructs showed that these polymorphic regions did not affect UTR function. IGF-I splice variants give rise to a common mature IGF-I peptide, but different E peptides. We identified two splice products, exon 4+6 (Ea) and exon 4+5+6 (Eb, mechano-growth factor) and found that their abundance was unchanged during osteoblastic differentiation. The Igf1 3' UTR encoded by exon 6 contains alternative polyadenylation sites. Proximal site use produces a short 3' UTR of approximately 195 bases, whereas distal site usage results in an approximately 6300-base UTR. Although Igf1 mRNA levels did not change during osteoblastic differentiation, distal polyadenylation site usage was increased in B6 cells but not in C3H. The resulting long Igf1 RNA isoform is less stable and has decreased translation efficiency, which may be one mechanism contributing to decreased IGF-I in B6 vs. C3H mice. Although the long UTR contains a conserved [GU](18) repeat, which is a positive regulator of UTR activity, it is also targeted by negative regulators, miR-29 and miR-365. These microRNAs are increased in B6 and C3H cells during osteoblastic differentiation. Differential expression of the long Igf1 3' UTR isoform may be a possible mechanism for enhanced IGF-I regulation in B6 vs. C3H mice.

Indexed as

3' Untranslated RegionsAnimalsCell DifferentiationCell LineCells, CulturedExonsInsulin-Like Growth Factor IMiceOsteoblastsPolymorphism, GeneticRNA Splicing3' Untranslated RegionsInsulin-Like Growth Factor I

Identifiers

PMID23183171
PMCPMC3529377
OpenAlexW2023713532

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.