Merck Young Scientist Award for ... - AHK Korea

Merck Young Scientist Award for Bioscience
1. Background
Merck Young Scientist Award was established globally in 2007 as
an investment in the next generation of scientific research and
recognizes outstanding young scientists in several countries in the
Asia-Pacific region, including Malaysia, Japan and the Philippines
as well as USA.
Merck Korea created the ‘Merck Young Scientist Award for
Bioscience’ together with the Korean Society of Medical
Biochemistry and Molecular Biology (KSMBMB). The first award ceremony and lectures were
held on October 29, 2009 at the international conference of KSMBMB.
2. Purpose
The award goes to scientists who have performed excellent research in the field of life
science, which is egarded as a future growth engine, and is intended to encourage young
scientists to focus on their research and raise up prospective researchers who will play a
pivotal role in the development of the field.
to support young researchers at the start of their academic career
to raise up potential researchers who will play a important role in life science.
3. Winners
First-Place Winner: Inha HEO
Ph.D. candidate / Seoul National University, Seoul, Korea
Advisor: Prof. Narry Kim
Second-Place Winner: Dr. Shin-Young Park
Ph.D. / College of Medicine, Hanyang University, Seoul, Korea
Advisor: Prof. Joong-Soo Han

: The House Dust Mite Allergen Der f 2-induced Phospholipase D1 Activation is Critical for the
Production of Interleukin-13 through Activating Transcription Factor-2 Activation in Human
Bronchial Epithelial Cells
Abstract
The purpose of this study was to identify the role of phospholipase D1 (PLD1) in Der f 2-induced I
nterleukin (IL)-13 production. The major house dust mite allergen, Der f 2, increased PLD activity in
human bronchial epithelial cells (BEAS-2B), and dominant negative (DN)-PLD1 or PLD1 siRNA dec
reased Der f 2-induced IL-13 expression and production. Treatment of Der f 2 activated phospholip
ase Cγ (PLCγ) / protein kinase Cα (PKCα) / p38 mitogen activated protein kinases (MAPK) pathwa
y, respectively. Der f 2-induced PLD activation was attenuated by PLCγ inhibitor (U73122 and PAO
), PKCα inhibitor (RO320432 and GO6976), and p38 MAPK inhibitor (SB203580 and SB202190). T
hese results indicated that PLCγ, PKCα, and p38 MAPK act as upstream activators of PLD in Der f
2-treated BEAS-2B cells. Furthermore, expression and production of IL-13 increased by Der f 2 wer
e also blocked by inhibition of PLCγ, PKCα, or p38 MAPK, respectively, indicating that IL-13 expres
sion and production were related to a PLCγ / PKCα / p38 MAPK pathway. We found that activating
transcription factor-2 (ATF-2) was activated by Der f 2 in BEAS-2B cells, and activation of ATF-2 wa
s controlled by PLD1. When the ATF-2 activity was blocked with ATF-2 siRNA, Der f 2-induced IL-
13 expression and production were decreased. Thus, ATF-2 might be one of the transcriptional fact
ors for the expression of IL-13 in Der f 2 treated BEAS-2B cells. Taken together, PLD1 acts as an i
mportant regulator in Der f 2-induced expression and production of IL-13 through activation of ATF-
2 in BEAS-2B cells.
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