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Tae-Don Kim

Researcher at Korea Research Institute of Bioscience and Biotechnology

Publications -  74
Citations -  2626

Tae-Don Kim is an academic researcher from Korea Research Institute of Bioscience and Biotechnology. The author has contributed to research in topics: Interleukin 21 & Interleukin 12. The author has an hindex of 31, co-authored 64 publications receiving 2116 citations. Previous affiliations of Tae-Don Kim include Korea University of Science and Technology & Pohang University of Science and Technology.

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Heterogeneous nuclear ribonucleoprotein C modulates translation of c-myc mRNA in a cell cycle phase-dependent manner

Jong Heon Kim, +6 more
- 15 Jan 2003 - 
TL;DR: Findings suggest that hnRNP C, via IRES binding, modulates translation of c-myc mRNA in a cell cycle phase-dependent manner.
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Mouse period 2 mRNA circadian oscillation is modulated by PTB–mediated rhythmic mRNA degradation

Kyung-Chul Woo, +6 more
- 01 Jan 2009 - 
TL;DR: It is proposed that post-transcriptional mRNA decay mediated by PTB is a fine-tuned regulatory mechanism that includes dampening-down effects during circadian mRNA oscillations.
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Human microRNA-27a* targets Prf1 and GzmB expression to regulate NK-cell cytotoxicity

Tae-Don Kim, +11 more
- 17 Nov 2011 - 
TL;DR: It is shown that human microRNA (miR)- 27a* is a negative regulator of NK-cell cytotoxicity by silencing Prf1 and GzmB expression, and modulating endogenous miR-27a* levels in NK cells represents a potential immunotherapeutic strategy.
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TXNIP maintains the hematopoietic cell pool by switching the function of p53 under oxidative stress.

Haiyoung Jung, +25 more
- 02 Jul 2013 - 
TL;DR: Data indicate that TXNIP is a regulator of p53 and plays a pivotal role in the maintenance of the hematopoietic cells by regulating intracellular ROS during oxidative stress.
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Prostaglandin E2 Secreted by Thyroid Cancer Cells Contributes to Immune Escape Through the Suppression of Natural Killer (NK) Cell Cytotoxicity and NK Cell Differentiation.

Arum Park, +10 more
- 09 Aug 2018 - 
TL;DR: Prostaglandin E2 produced by thyroid cancer cells suppressed the cytolytic activity of NK cells by inhibiting the expression of the natural cytotoxicity receptors NKp44 and NKp30 and the death receptor tumor necrosis factor-related apoptosis-inducing ligand.