Evidence map›Paper›PMID 17005865›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Role of megakaryoblastic acute leukemia-1 in ERK1/2-dependent stimulation of serum response factor-driven transcription by BDNF or increased synaptic activity.

Katarzyna Kalita, Giorgi Kharebava, Jing-Juan Zheng, Michal Hetman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 24% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. RhoA: a dubious molecule in cardiac pathophysiology.Journal of biomedical science · 2021
    Review
  5. Review
  6. Article
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  8. Article
  9. Nucleoskeletal regulation of transcription: Actin on MRTF.Experimental biology and medicine (Maywood, N.J.) · 2019
    Review
  10. Article
  11. Single-molecule imaging of the transcription factor SRF reveals prolonged chromatin-binding kinetics upon cell stimulation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Article
  13. Review
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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 1 country.

Katarzyna KalitaKentucky Spinal Cord Injury Research Center and Department of Neurological Surgery, University of Louisville, Louisville, Kentucky 40292, USA.
Giorgi Kharebava
Jing-Juan Zheng
Michal Hetman
Neurological Surgery · USUniversity of Louisville · US

Funding

Signaling pathways in neuronal susceptibility to hypoxiaP20RR015576 · NCRR · UNIVERSITY OF LOUISVILLE · PI HUBSCHER, CHARLES H. · 2000 to 2009
$18.5M
Survival signaling in CNS neurons exposed to DNA damageR01NS047341 · NINDS · UNIVERSITY OF LOUISVILLE · PI HETMAN, MICHAL · 2004 to 2008
$1.3M
NCRR NIH HHS P20 RR015576NCRR NIH HHS RR015576-06NINDS NIH HHS NS047341-01NINDS NIH HHS R01 NS047341
6 · The paper itself

Abstract

Serum response factor (SRF)-mediated transcription contributes to developmental and adult brain plasticity. Therefore, we investigated the role of a newly identified SRF coactivator, MKL1, in the regulation of SRF-driven transcription in rat forebrain neurons. MKL1 expression was found in newborn rat cortical or hippocampal neurons in culture as well as in adult rat forebrain. Immunostaining demonstrated constitutive nuclear localization of MKL1 in the CA1 region of the hippocampus, in the deep layers of the neocortex, and in cultured neurons. Overexpression of MKL1 in primary cortical neurons elevated SRF-driven transcription and enhanced its stimulation by BDNF. In addition, inhibition of endogenous MKL1 by overexpression of a dominant-negative MKL1 mutant or by small interfering RNA reduced BDNF activation of SRF-driven transcription. In neurons, endogenous MKL1 was associated with SRF-regulated chromatin regions of several endogenous genes including c-fos, JunB, Srf, and Cyr61. BDNF activation of MKL1/SRF-driven transcription was dependent on the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, which also led to MKL1 phosphorylation. Finally, synaptic activity stimulation of SRF-driven transcription was reduced by inhibition of endogenous MKL1. Conversely, synaptic activity enhanced transcription by overexpressed MKL1. MKL1 regulation by synaptic activity was mediated through the NMDA receptor-activated ERK1/2. These results suggest that neuronal MKL1 contributes to SRF-regulated gene expression induced by BDNF or synaptic activity. In addition, MKL1 appears as a novel mediator of the signaling between ERK1/2 and SRF. Moreover, MKL1 is a likely regulator of SRF-driven transcription programs that underlie neuronal plasticity.

Indexed as

4-AminopyridineAmidesAnimalsAnimals, NewbornBicucullineBrain-Derived Neurotrophic FactorButadienesCells, CulturedCerebral CortexChlorocebus aethiopsChromonesCOS CellsCysteine-Rich Protein 61Gene Expression RegulationGenes, fosHippocampus2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one4-AminopyridineAmidesBicucullineBrain-Derived Neurotrophic FactorButadienesCCN1 protein, ratChromonesCysteine-Rich Protein 61Immediate-Early ProteinsIntercellular Signaling Peptides and ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MorpholinesNitrilesN-MethylaspartatePotassium ChlorideProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junPyridinesSerum Response FactorTranscription FactorsU 0126Y 27632

Identifiers

PMID17005865
PMCPMC6674463
OpenAlexW2006938902

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.