Evidence map›Paper›PMID 16537533›Full record

ArticleThe Journal of biological chemistry2006

Identification of T-cadherin as a novel target of DNA methyltransferase 3B and its role in the suppression of nerve growth factor-mediated neurite outgrowth in PC12 cells.

Shoumei Bai, Kalpana Ghoshal, Samson T Jacob

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  8. Epigenetic regulation of axon and dendrite growth.Frontiers in molecular neuroscience · 2012
    Article
  9. Review
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  11. T-cadherin structures reveal a novel adhesive binding mechanism.Nature structural & molecular biology · 2010
    Article
  12. Article
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  15. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Shoumei BaiDepartment of Molecular and Cellular Biochemistry, College of Medicine, Ohio State University, Columbus, Ohio 43210.
Kalpana GhoshalDepartment of Molecular and Cellular Biochemistry, College of Medicine, Ohio State University, Columbus, Ohio 43210.
Samson T JacobDepartment of Molecular and Cellular Biochemistry, College of Medicine, Ohio State University, Columbus, Ohio 43210. Electronic address: jacob.42@osu.edu.
The Ohio State University · US

Funding

MOLECULAR MECHANISMS OF DIET-INDUCED CARCINOGENESISR01CA086978 · NCI · OHIO STATE UNIVERSITY · PI GHOSHAL, KALPANA, JACOB, SAMSON T · 2002 to 2018
$4.9M
DNA METHYLATION AND GENE EXPRESSION IN CANCER CELLSR01ES010874 · NIEHS · OHIO STATE UNIVERSITY · PI JACOB, SAMSON T · 2000 to 2004
$1.6M
NCI NIH HHS CA 86978NCI NIH HHS R01 CA086978NIEHS NIH HHS ES 10874NIEHS NIH HHS R01 ES010874
6 · The paper itself

Abstract

Previously we showed that DNA methyltransferase 3b (Dnmt3b) is required for nerve growth factor (NGF)-induced differentiation of PC12 cells to neuronal phenotype. The present study identified T-cadherin (T-Cad) as one of the targets of Dnmt3b by chromatin immunoprecipitation (ChIP) assay. Combined bisulfite restriction analysis and bisulfite sequencing showed that T-Cad promoter was sparsely methylated in PC12 cells. ChIP-CHOP analysis demonstrated that Dnmt3b is associated with T-Cad promoter irrespective of its methylation status. The mRNA and protein levels of T-Cad were markedly elevated in cells depleted of Dnmt3b by antisense or small interfering RNA. Suppression of T-Cad promoter activity by Dnmt3b was independent of its catalytic activity, which was consistent with the insignificant change in T-Cad promoter methylation status in Dnmt3b-depleted cells. In contrast, deletion of its N-terminal ATRX and PWWP domain abolished its repressor function. Association of histone deacetylase 2 (Hdac2) with T-Cad promoter and restoration of the promoter activity from Dnmt3b-mediated suppression upon treatment with Hdac inhibitor indicated involvement of histone deacetylation in this process. NGF-induced neurite outgrowth was inhibited in a dose dependent manner upon ectopic expression of T-Cad in PC12 cells. Immunofluorescence studies showed that T-Cad was redistributed upon NGF treatment, as evident from its concentration in axon growth cones as opposed to its localization at cell-cell contact region in undifferentiated cells. These results demonstrate a novel role of T-Cad in the NGF-mediated differentiation of PC12 cells to neuronal phenotype.

Indexed as

AnimalsCadherinsCell DifferentiationDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BDown-RegulationGene Expression Regulation, EnzymologicNerve Growth FactorNeuritesPC12 CellsRatsSubstrate SpecificityCadherinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BH-cadherinNerve Growth Factor

Identifiers

PMID16537533
PMCPMC2241734
OpenAlexW2000182236

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.