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Soichi Kojima

Researcher at Jikei University School of Medicine

Publications -  178
Citations -  9488

Soichi Kojima is an academic researcher from Jikei University School of Medicine. The author has contributed to research in topics: Hepatic stellate cell & Retinoic acid. The author has an hindex of 47, co-authored 173 publications receiving 8492 citations. Previous affiliations of Soichi Kojima include Gifu University & Memorial Sloan Kettering Cancer Center.

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A promoter-level mammalian expression atlas

Alistair R. R. Forrest, +280 more
- 27 Mar 2014 - 
TL;DR: For example, the authors mapped transcription start sites (TSSs) and their usage in human and mouse primary cells, cell lines and tissues to produce a comprehensive overview of mammalian gene expression across the human body.
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An atlas of human long non-coding RNAs with accurate 5′ ends

TL;DR: This work integrates multiple transcript collections to generate a comprehensive atlas of 27,919 human lncRNA genes with high-confidence 5′ ends and expression profiles across 1,829 samples from the major human primary cell types and tissues, identifying 19,175 potentially functional lncRNAs in the human genome.
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Transcribed enhancers lead waves of coordinated transcription in transitioning mammalian cells

Erik Arner, +108 more
- 27 Feb 2015 - 
TL;DR: The data support a highly generalizable model in which enhancer transcription is the earliest event in successive waves of transcriptional change during cellular differentiation or activation.
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Requirement for transglutaminase in the activation of latent transforming growth factor-beta in bovine endothelial cells.

TL;DR: Results indicate that type II TGase is a component required for cell surface, plasmin-mediated LTGF-beta activation process and that increased expression of TGase accompanies retinoid-induced activation ofLTGF- beta.
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Lipoprotein (a) inhibits the generation of transforming growth factor beta: an endogenous inhibitor of smooth muscle cell migration.

TL;DR: Results suggest that high plasma levels of Lp(a) might enhance smooth muscle cell migration by decreasing the levels of the migration inhibitor TGF-beta thus contributing to generation of the atheromatous lesions.