Dae Won Kim
Yonsei University · 生化学・遺伝学・分子生物学
研究室紹介
Professor Dae Won Kim's research lab focuses on the molecular mechanisms underlying developmental biology, particularly in skeletal and neural systems. The lab investigates transcriptional regulation, signaling pathways such as BMP, Ihh, and NF-κB, and their roles in cell fate determination, chondrocyte differentiation, and developmental plasticity. A central theme is the interplay between transcription factors like Nkx3.2 and co-regulators (e.g., HDAC1, NEMO) in controlling cell survival, differentiation, and disease-relevant processes. The lab also explores behavioral and psychological aspects of clinical training, particularly in counseling and early termination in therapeutic relationships.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15We have previously shown that Nkx3.2, a transcriptional repressor that is expressed in the sclerotome and developing cartilage, can activate the chondrocyte differentiation program in somitic mesoderm in a bone morphogenetic protein (BMP)-dependent manner. In this work, we elucidate how BMP signaling modulates the transcriptional repressor activity of Nkx3.2. We have found that Nkx3.2 forms a complex, in vivo, with histone deacetylase 1 (HDAC1) and Smad1 and -4 in a BMP-dependent manner. The hom
ASB9 interacts with the creatine kinase system and negatively regulates cell growth. The differential expression and function of ASB9 and ASB9DeltaSOCS may be a key factor in the growth of human cell lines and primary cells.
본 연구에서는 조기종결을 경험한 초심 상담수련생과 내담자들이 왜 상담이 조기에 종결되었는가에 대해 지각하는 차별적 특징을 개념도(concept mapping) 방법으로 알아보았다. 이를 위해 수련생 7명과 내담자 9명을 대상으로 조기종결 경험에 관한 면접을 실시한 후 핵심문장을 추출하여 다차원척도법과 군집분석을 실시하였다. 연구결과 상담수련생이 지각한 조기종결 이유는 ‘상담자-내담자 요인’과 ‘독립성-상호관계성’의 두 개 차원으로 나누어 졌으며, ‘상담역량부족’, ‘내담자의 저항’, ‘상담자․내담자 간 부조화’, ‘상담자의 방어적 반응’ 등 총 네 개의 군집으로 나타났다. 반면 내담자의 조기종결 이유는 ‘상담자-내담자 요인’과 ‘상담과정-상담효과성 기대’의 두 가지 차원으로 구분되었으며, 두 개의 차원 상에 위치한 네 개의 군집은 ‘초기문제 해소 및 상황변화’, ‘상담자의 공감부족’, ‘상담자의 전문성에 대한 불신’, ‘자기공개에 대한 불편감’ 등 이었다. 본 연구는 조기종결의 이유
The Ihh (Indian Hedgehog) pathway plays an essential role in facilitating chondrocyte hypertrophy and bone formation during skeletal development. Nkx3.2 (NK3 homeobox 2) is initially induced in chondrocyte precursor cells, maintained in early-stage chondrocytes and down-regulated in terminal-stage chondrocytes. Consistent with these expression patterns, Nkx3.2 has been shown to enhance chondrocyte differentiation and cell survival, while inhibiting chondrocyte hypertrophy and apoptosis. Thus, in
Animals can adapt to dynamic environmental conditions by modulating their developmental programs. Understanding the genetic architecture and molecular mechanisms underlying developmental plasticity in response to changing environments is an important and emerging area of research. Here, we show a novel role of cAMP response element binding protein (CREB)-encoding crh-1 gene in developmental polyphenism of C. elegans. Under conditions that promote normal development in wild-type animals, crh-1 mu
NF-κB is a multifunctional transcription factor involved in diverse biological processes. It has been well documented that NF-κB can be activated in response to various stimuli. While signal-inducible NF-κB activation mechanisms have been extensively characterized, exogenous signal-independent intrinsic NF-κB activation processes remain poorly understood. Here we show that IκB kinase β (IKKβ) can be intrinsically activated in the nucleus by a homeobox protein termed Nkx3.2 in the absence of exog
Transfusion-related acute lung injury (TRALI) is a serious adverse transfusion reaction that is presented as acute hypoxemia and non-cardiogenic pulmonary edema, which develops during or within 6 hr of transfusion. Major pathogenesis of TRALI is known to be related with anti-HLA class I, anti-HLA class II, or anti-HNA in donor's plasma. However, anti-HLA or anti-HNA in recipient against transfused donor's leukocyte antigens also cause TRALI in minor pathogenesis and which comprises about 10% of
Nkx3.2, the vertebrate homologue of Drosophila bagpipe, has been implicated as playing a role in chondrogenic differentiation. In brief, Nkx3.2 is initially expressed in chondrocyte precursor cells and later during cartilage maturation, its expression is diminished in hypertrophic chondrocytes. In addition to Nkx3.2 expression analyses, previous studies using ex vivo chick embryo cultures and in vitro cell cultures have suggested that Nkx3.2 can suppress chondrocyte hypertrophy. However, it has