Sung-Keum Seo

发表

Activating transcription factor 4 and CCAAT/enhancer-binding protein-beta negatively regulate the mammalian target of rapamycin via Redd1 expression in response to oxidative and endoplasmic reticulum stress.

C. Rhee, Su-Jae Lee, S. An, 2009, Free radical biology & medicine.

SP600125 negatively regulates the mammalian target of rapamycin via ATF4‐induced Redd1 expression

I. Park, T. Choe, Jong-Il Kim, 2009, FEBS letters.

Alteration of miRNA profiles by ionizing radiation in A549 human non-small cell lung cancer cells.

In-Chul Park, Su-Jae Lee, S. An, 2009, International journal of oncology.

Specific proteolysis of the A-kinase-anchoring protein 149 at the Asp582 residue by caspases during apoptosis.

Su-Jae Lee, K. Yang, Y. Jin, 2008, Oncology reports.

Nuclear protein 1 induced by ATF4 in response to various stressors acts as a positive regulator on the transcriptional activation of ATF4

I. Park, T. Choe, Jong-Il Kim, 2009, IUBMB life.

A combination of sulindac and arsenic trioxide synergistically induces apoptosis in human lung cancer H1299 cells via c-Jun NH2-terminal kinase-dependent Bcl-xL phosphorylation.

C. Rhee, Su-Jae Lee, S. An, 2008, Lung cancer.

Redd1 inhibits the invasiveness of non-small cell lung cancer cells.

I. Park, T. Choe, W. Noh, 2011, Biochemical and biophysical research communications.

A Truncated Form of p23 Down-regulates Telomerase Activity via Disruption of Hsp90 Function*

C. Rhee, S. An, I. Park, 2009, The Journal of Biological Chemistry.

Combined Effects of Sulindac and Suberoylanilide Hydroxamic Acid on Apoptosis Induction in Human Lung Cancer Cells

C. Rhee, Su-Jae Lee, S. An, 2008, Molecular Pharmacology.

Ginkgetin induces cell death in breast cancer cells via downregulation of the estrogen receptor.

Hyunggee Kim, I. Park, T. Choe, 2017, Oncology letters.

Hypoxic condition- and high cell density-induced expression of Redd1 is regulated by activation of hypoxia-inducible factor-1alpha and Sp1 through the phosphatidylinositol 3-kinase/Akt signaling pathway.

C. Rhee, Su-Jae Lee, H. Um, 2007, Cellular signalling.

Implications of caspase-dependent proteolytic cleavage of cyclin A1 in DNA damage-induced cell death.

S. An, I. Park, T. Choe, 2014, Biochemical and biophysical research communications.

Sorafenib induces apoptotic cell death in human non-small cell lung cancer cells by down-regulating mammalian target of rapamycin (mTOR)-dependent survivin expression.

Su-Jae Lee, S. An, I. Park, 2011, Biochemical pharmacology.

Selective inhibition of histone deacetylase 2 induces p53-dependent survivin downregulation through MDM2 proteasomal degradation

Sang-Gu Hwang, I. Park, T. Choe, 2014, Oncotarget.

Histone Deacetylase Inhibitors Sensitize Human Non-small Cell Lung Cancer Cells to Ionizing Radiation Through Acetyl p53-Mediated c-myc Down-Regulation

S. An, I. Park, T. Choe, 2011, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

Sulindac-derived reactive oxygen species induce apoptosis of human multiple myeloma cells via p38 mitogen activated protein kinase-induced mitochondrial dysfunction

C. Rhee, Su-Jae Lee, S. An, 2006, Apoptosis.

Synergistic induction of apoptosis by sulindac and arsenic trioxide in human lung cancer A549 cells via reactive oxygen species-dependent down-regulation of survivin.

In-Chul Park, Myung-Jin Park, Tae-Boo Choe, 2006, Biochemical pharmacology.

Dichloroacetate potentiates tamoxifen-induced cell death in breast cancer cells via downregulation of the epidermal growth factor receptor

Sang-Gu Hwang, Jie-Young Song, I. Park, 2016, Oncotarget.

Activation of Epidermal Growth Factor Receptor and Its Downstream Signaling Pathway by Nitric Oxide in Response to Ionizing Radiation

C. Rhee, Su-Jae Lee, I. Park, 2008, Molecular Cancer Research.

Knockdown of TWIST1 enhances arsenic trioxide- and ionizing radiation-induced cell death in lung cancer cells by promoting mitochondrial dysfunction.

Sang-Gu Hwang, I. Park, T. Choe, 2014, Biochemical and biophysical research communications.