Evidence map›Paper›PMID 22275359›Full record

ArticleThe Journal of biological chemistry2012

Insulin-like growth factor receptor-1 and nuclear factor κB are crucial survival signals that regulate caspase-3-mediated lens epithelial cell differentiation initiation.

Subhasree Basu, Suren Rajakaruna, A Sue Menko

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Exploring caspase functions in mouse models.Apoptosis : an international journal on programmed cell death · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Making the head: Caspases in life and death.Frontiers in cell and developmental biology · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Cell Death and Liver Disease.Gut and liver · 2020
    Review
  16. Article
  17. Osteogenic Potential of Caspases Related to Endochondral Ossification.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018
    Article
  18. Article
  19. Caspases and osteogenic markers--in vitro screening of inhibition impact.In vitro cellular & developmental biology. Animal · 2016
    Article
  20. 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

3 authors at 1 institution in 1 country.

Subhasree BasuDepartment of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Suren Rajakaruna
A Sue Menko
Thomas Jefferson University · US

Funding

Tyrosine Phosphorylation in Lens Cell DifferentiationR01EY014258 · NEI · THOMAS JEFFERSON UNIVERSITY · PI MENKO, A. SUE · 2003 to 2015
$3.9M
FUNCTION OF ADHESION MOLECULES IN LENS DEVELOPMENTR01EY010577 · NEI · THOMAS JEFFERSON UNIVERSITY · PI MENKO, A. SUE · 1993 to 2011
$3.9M
NEI NIH HHS EY014258NEI NIH HHS EY10577NEI NIH HHS R01 EY010577NEI NIH HHS R01 EY014258
6 · The paper itself

Abstract

It is now known that the function of the caspase family of proteases is not restricted to effectors of programmed cell death. For example, there is a significant non-apoptotic role for caspase-3 in cell differentiation. Our own studies in the developing lens show that caspase-3 is activated downstream of the canonical mitochondrial death pathway to act as a molecular switch in signaling lens cell differentiation. Importantly, for this function, caspase-3 is activated at levels far below those that induce apoptosis. We now have provided evidence that regulation of caspase-3 for its role in differentiation induction is dependent on the insulin-like growth factor-1 receptor (IGF-1R) survival-signaling pathway. IGF-1R executed this regulation of caspase-3 by controlling the expression of molecules in the Bcl-2 and inhibitor of apoptosis protein (IAP) families. This effect of IGF-1R was mediated through NFκB, demonstrated here to function as a crucial downstream effector of IGF-1R. Inhibition of expression or activation of NFκB blocked expression of survival proteins in the Bcl-2 and IAP families and removed controls on the activation state of caspase-3. The high level of caspase-3 activation that resulted from inhibiting this IGF-1R/NFκB signaling pathway redirected cell fate from differentiation toward apoptosis. These results provided the first evidence that the IGF-1R/NFκB cell survival signal is a crucial regulator of the level of caspase-3 activation for its non-apoptotic function in signaling cell differentiation.

Indexed as

AnimalsAvian ProteinsCaspase 3Cell DifferentiationCells, CulturedCell SurvivalChick EmbryoChickensEnzyme ActivationEpithelial CellsGene Expression RegulationInhibitor of Apoptosis ProteinsLens Capsule, CrystallineNF-kappa BProto-Oncogene Proteins c-bcl-2Receptor, IGF Type 1Avian ProteinsCaspase 3Inhibitor of Apoptosis ProteinsNF-kappa BProto-Oncogene Proteins c-bcl-2Receptor, IGF Type 1

Identifiers

PMID22275359
PMCPMC3381865
OpenAlexW2008877139

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.