Evidence map›Paper›PMID 17277356›Full record

ArticleThe Journal of biological chemistry2007

Glycogen synthase kinase-3 represses cyclic AMP response element-binding protein (CREB)-targeted immediate early genes in quiescent cells.

John W Tullai, Jie Chen, Michael E Schaffer, Eliza Kamenetsky, Simon Kasif, Geoffrey M Cooper

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

41 citing papers in PubMed, 72 citations in OpenAlex.

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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

John W TullaiDepartment of Biology, Boston University, Boston, Massachusetts 02215.
Jie ChenDepartment of Biology, Boston University, Boston, Massachusetts 02215.
Michael E SchafferBioinformatics Program, Boston University, Boston, Massachusetts 02215.
Eliza KamenetskyDepartment of Biology, Boston University, Boston, Massachusetts 02215.
Simon KasifBioinformatics Program, Boston University, Boston, Massachusetts 02215; Department of Biomedical Engineering, Boston University, Boston, Massachusetts 02215.
Geoffrey M CooperDepartment of Biology, Boston University, Boston, Massachusetts 02215; Bioinformatics Program, Boston University, Boston, Massachusetts 02215. Electronic address: gmcooper@bu.edu.
Boston University · US

Funding

Regulation of apoptosis by PI 3-kinase/Akt signalingR01CA018689 · NCI · DANA-FARBER CANCER INSTITUTE · PI COOPER, GEOFFREY M · 1985 to 2012
$6.2M
Comparative Cross-Species Genomic Analysis SystemR33HG002850 · NHGRI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI KASIF, SIMON · 2004 to 2006
$1.0M
NCI NIH HHS 1R01-CA18689NCI NIH HHS R01 CA018689NHGRI NIH HHS 1R33-HG002850NHGRI NIH HHS R33 HG002850
6 · The paper itself

Abstract

Despite its central role in cell survival and proliferation, the transcriptional program controlled by GSK-3 is poorly understood. We have employed a systems level approach to characterize gene regulation downstream of PI 3-kinase/Akt/GSK-3 signaling in response to growth factor stimulation of quiescent cells. Of 31 immediate-early genes whose induction was dependent on PI 3-kinase signaling, 12 were induced directly by inhibition of GSK-3. Most of the GSK-3-regulated genes encoded transcription factors, growth factors, and signaling molecules. Binding sites for CREB were highly over-represented in the upstream regions of these genes, with 9 genes containing CREB sites that were conserved in mouse orthologs. Binding sites predicted in 6 genes were confirmed by CREB chromatin immunoprecipitation and forskolin induction of CBP binding. Moreover, CREB siRNA substantially blocked induction of 5 genes by forskolin and of 3 genes following inhibition of GSK-3. These results indicate that GSK-3 actively represses gene expression in quiescent cells, with inhibition of CREB playing a key role in this transcriptional response.

Indexed as

Genes, Immediate-EarlyAmino Acid SequenceAnimalsCell Line, TumorCyclic AMP Response Element-Binding ProteinGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3HumansMiceMolecular Sequence DataResting Phase, Cell CycleCREB1 protein, humanCyclic AMP Response Element-Binding ProteinGlycogen Synthase Kinase 3

Identifiers

PMID17277356
PMCPMC1839957
OpenAlexW1969173606

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.