Evidence map›Paper›PMID 22562201›Full record

ArticleThe International journal of developmental biology2012

Akt1 and insulin-like growth factor 2 (Igf2) regulate placentation and fetal/postnatal development.

Lindsey N Kent, Shigeki Ohboshi, Michael J Soares

Open access · bronzeAbstract read
In one paragraph

Article in The International journal of developmental biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Cited2 is a key regulator of placental development and plasticity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. SUV39H2 controls trophoblast stem cell fate.Biochimica et biophysica acta. General subjects · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. SGK1: The Dark Side of PI3K Signaling.Current topics in developmental biology · 2017
    Review
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

3 authors at 1 institution in 1 country.

Lindsey N KentInstitute for Reproductive Health and Regenerative Medicine, Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, USA.
Shigeki Ohboshi
Michael J Soares
The University of Kansas Health System · US

Funding

Research Design and Analysis Core (RDAC)P30HD002528 · NICHD · UNIVERSITY OF KANSAS LAWRENCE · PI FOWLER, STEPHEN CLETIUS · 1985 to 2015
$22.1M
TROPHOBLAST DIFFERENTIATIONR01HD020676 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI MICHAEL J SOARES · 1986 to 2026
$10.1M
NICHD NIH HHS P30 HD002528NICHD NIH HHS R01 HD020676
6 · The paper itself

Abstract

Phenotypic characterization of Akt1 and Igf2 null mice has revealed roles for each in the regulation of placentation, and fetal and postnatal growth. Insulin-like growth factor 2 (IGF2) is encoded by the Igf2 gene and influences cellular function, at least in part, through activation of an intracellular serine/threonine kinase called AKT1. Akt1 and Igf2 null mice were originally characterized on inbred and mixed genetic backgrounds, prohibiting direct comparisons of their phenotypes. The impact of loss of AKT1 or IGF2 on placental, fetal, and postnatal function were examined following transfer of Akt1 and Igf2 null mutations to an outbred CD1 genetic background. Disruption of IGF2 did not affect AKT expression or activation. Both Akt1-/- and Igf2-/- mice exhibited decreased placental weight, fetal weight and viability. Deregulation of placental growth was similar in Akt1 and Igf2 nulls; however, disruption of Igf2 had a more severe impact on prenatal survival and postnatal growth. Placental structure, including organization of junctional and labyrinth zones and development of the interstitial, invasive, trophoblast lineage, were similar in mutant and wild-type mice. Akt1 and Igf2 null mutations affected postnatal growth. The relative impact of each gene differed during pre-weaning versus post-weaning growth phases. AKT1 had a more significant role during pre-weaning growth, whereas IGF2 was a bigger contributor to post-weaning growth. Akt1 and Igf2 null mutations impact placental, fetal and postnatal growth. Placental phenotypes are similar; however, fetal and postnatal growth patterns are unique to each mutation.

Indexed as

AnimalsAnimals, NewbornBlotting, WesternFemaleFetal DevelopmentFetal ViabilityImmunohistochemistryInsulin-Like Growth Factor IIMaleMiceMice, Inbred C57BLMice, KnockoutOrgan SizePlacentaPlacentationPregnancyAkt1 protein, mouseIGF2 protein, mouseInsulin-Like Growth Factor IIProto-Oncogene Proteins c-akt

Identifiers

PMID22562201
PMCPMC3894249
OpenAlexW2023906779

What OpenQuestion holds

Textmetadata
LicenceTDM
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.