Evidence map›Paper›PMID 22354967›Full record

ArticleThe Journal of biological chemistry2012

Transducin-like enhancer of Split-1 (TLE1) combines with Forkhead box protein G1 (FoxG1) to promote neuronal survival.

Somasish Ghosh Dastidar, Sriram Narayanan, Stefano Stifani, Santosh R D'Mello

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. PLP1-Targeting Antisense Oligonucleotides Improve FOXG1 Syndrome Mice.International journal of molecular sciences · 2024
    Article
  2. Article
  3. Sex differences in schizophrenia: a longitudinal methylome analysis.Journal of neural transmission (Vienna, Austria : 1996) · 2022
    Article
  4. Review
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  14. Review
  15. Tle1 tumor suppressor negatively regulates inflammation in vivo and modulates NF-κB inflammatory pathway.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  16. Article
  17. HSF1 protects neurons through a novel trimerization- and HSP-independent mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  18. 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

4 authors at 2 institutions in 2 countries.

Somasish Ghosh DastidarDepartment of Molecular and Cell Biology, University of Texas, Richardson, Texas 75080, USA.
Sriram Narayanan
Stefano Stifani
Santosh R D'Mello
The University of Texas at Dallas · USMontreal Neurological Institute and Hospital · CA

Funding

Signaling Pathways Regulating Neuronal SurvivalR01NS040408 · NINDS · UNIVERSITY OF TEXAS DALLAS · PI D'MELLO, SANTOSH R · 2002 to 2018
$4.8M
Molecular control of HDAC4-mediated neuroprotectionR21NS058462 · NINDS · UNIVERSITY OF TEXAS DALLAS · PI D'MELLO, SANTOSH R · 2008 to 2009
$351k
NINDS NIH HHS NS058462NINDS NIH HHS NS40408NINDS NIH HHS R01 NS040408NINDS NIH HHS R21 NS058462
6 · The paper itself

Abstract

Transducin-like enhancer of split-1 (TLE1) plays a critical role in the regulation of neurogenesis by inhibiting the differentiation of neural progenitor cells into neurons. Although TLE1 is also expressed highly in the postnatal brain and through adulthood, its role in postmitotic neurons is not clear. Using cultures of cerebellar granule neurons, we show that expression of TLE1 is reduced in neurons primed to die. Reestablishment of elevated TLE1 levels by ectopic expression protects neurons from death, whereas suppression of TLE1 expression in otherwise healthy neurons induces cell death. These results show that TLE1 is necessary for the maintenance of neuronal survival. Experiments using pharmacological inhibitors as well as expression of point mutants indicate that phosphorylation of TLE1 by casein kinase-2 (CK2) at Ser-239 and Ser-253 is necessary for its survival-promoting activity. TLE1-mediated survival is also inhibited by pharmacological inhibition of PI3K-Akt signaling but not by inhibitors of Raf-MEK-ERK signaling or other molecules, including histone deacetylases, calcium calmodulin kinase, or CK1. The survival-promoting activity of TLE1 depends critically on interaction with FoxG1, another protein involved in the regulation of neurogenesis and shown previously to promote survival of postmitotic neurons. Likewise, the ability of FoxG1 to promote neuronal survival depends on TLE1. Taken together, our study demonstrates that TLE1 cooperates with FoxG1 to promote neuronal survival in a CK2- and PI3K-Akt-dependent manner.

Indexed as

AnimalsCell DeathCells, CulturedCell SurvivalCerebellumForkhead Box Protein O1Forkhead Transcription FactorsGene Expression RegulationHistone DeacetylasesMAP Kinase Signaling SystemNerve Tissue ProteinsNeuronsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktraf KinasesRatsForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, ratHistone DeacetylasesNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktraf KinasesRepressor Proteins

Identifiers

PMID22354967
PMCPMC3340250
OpenAlexW2030843629

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.