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Dohyun Lee,Changhyun Kim,Hunhee Lee,Suhyeong Lee,Hongjeon Kang,Hyunwoo Kim,Hui Kyung Park,Jaeyeong Heo,Hyeong Joon Kim IEEE 2014 IEEE electron device letters Vol.35 No.8
<P>We improved the characteristics of 4H-SiC Schottky barrier diodes (SBDs) by post-oxidation annealing in nitric oxide ambient (NO POA). Unlike the sacrificial oxidized SBDs, the SBDs with added NO POA exhibited highly uniform Schottky barrier height and nearly ideal breakdown voltage of 1990 V. Time-of-flight secondary ion mass spectroscopy revealed nitrogen pileup at the sacrificially oxidized SiC surface after NO POA. We believe that NO POA electrically passivated the detrimental residual carbon at the SiC surface by forming C-N bonds, improving the performance of the SBDs.</P>
Dysregulated CREB3 cleavage at the nuclear membrane induces karyoptosis-mediated cell death
Lee Ga-Eun,Bang Geul,Byun Jiin,Lee Cheol-Jung,Chen Weidong,Jeung Dohyun,An Hyun-Jung,Kang Han Chang,Lee Joo Young,Lee Hye Suk,Hong Young-Soo,Kim Dae Joon,Keniry Megan,Kim Jin Young,Choi Jin-Sung,Fanto 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-
Cancer cells often exhibit resistance to apoptotic cell death, but they may be vulnerable to other types of cell death. Elucidating additional mechanisms that govern cancer cell death is crucial for developing new therapies. Our research identified cyclic AMP-responsive element-binding protein 3 (CREB3) as a crucial regulator and initiator of a unique cell death mechanism known as karyoptosis. This process is characterized by nuclear shrinkage, deformation, and the loss of nuclear components following nuclear membrane rupture. We found that the N-terminal domain (aa 1-230) of full-length CREB3 (CREB3-FL), which is anchored to the nuclear inner membrane (INM), interacts with lamins and chromatin DNA. This interaction maintains a balance between the outward force exerted by tightly packed DNA and the inward constraining force, thereby preserving INM integrity. Under endoplasmic reticulum (ER) stress, aberrant cleavage of CREB3-FL at the INM leads to abnormal accumulation of the cleaved form of CREB3 (CREB3-CF). This accumulation disrupts the attachment of CREB3-FL to the INM, resulting in sudden rupture of the nuclear membrane and the onset of karyoptosis. Proteomic studies revealed that CREB3-CF overexpression induces a DNA damage response akin to that caused by UVB irradiation, which is associated with cellular senescence in cancer cells. These findings demonstrated that the dysregulation of CREB3-FL cleavage is a key factor in karyoptotic cell death. Consequently, these findings suggest new therapeutic strategies in cancer treatment that exploit the process of karyoptosis.
Room-temperature growth of Mg on Si(111): stepwise versus continuous deposition
Lee, Dohyun,Lee, Geunseop,Kim, Sehun,Hwang, Chanyong,Koo, Ja-Yong,Lee, Hangil IOP Pub 2007 Journal of physics, an Institute of Physics journa Vol.19 No.26
<P>Using low-energy electron diffraction and scanning tunnelling microscopy, we studied the formation of Mg silicide and metallic Mg islands on a Si(111)-7 ? 7 surface at room temperature as a function of Mg coverage. We found that the mechanism by which Mg islands grew on the Si(111)-7 ? 7 surface, and the morphology of the islands that formed, depended on whether the Mg deposition was performed in a stepwise or continuous manner. When Mg was deposited in a stepwise manner, with 1?h between deposition events, an amorphous Mg silicide overlayer formed on the Si(111)-7 ? 7 surface during the initial stage of deposition (up to 2.0?ML Mg coverage), as shown by the observation of δ7 ? 7 and 1 ? 1 low-energy electron diffraction patterns. Upon further stepwise Mg deposition, round-shaped Mg islands grew on the amorphous Mg silicide layer, as shown by scanning tunnelling microscopy and the emergence of a 1 ? 1 low-energy electron diffraction pattern. If, on the other hand, the Mg was deposited continuously in a single step, hexagonal Mg islands formed on the flat Mg silicide layers, and a <img SRC='http://ej.iop.org/images/0953-8984/19/26/266004/cm243037ieqn1.gif' ALIGN='MIDDLE' ALT='({{2 \over 3} \sqrt {3}} \times {{2 \over 3} \sqrt {3}})\mathrm {R}30 ^{\circ } '/> and 1 ? 1 mixed phase was observed. Moreover, using scanning tunnelling spectroscopy, we confirmed the semiconducting and metallic nature of the Mg silicide layer and hexagonal Mg islands on the Si(111)-7 ? 7 surface depending on their Mg coverage, respectively. </P>
Ga-Eun Lee,Dohyun Jeung,Weidong Chen,Jiin Byun,Joo Young Lee,Han Chang Kang,Hye Suk Lee,Dae Joon Kim,Jin-Sung Choi,Cheol-Jung Lee,Hyun-Jung An,Yong-Yeon Cho 대한약학회 2023 Archives of Pharmacal Research Vol.46 No.1
E2F 1, 2, and 3a, (refer to as E2Fs) are a subfamily of E2F transcription factor family that play essential roles in cell-cycle progression, DNA replication, DNA repair, apoptosis, and differentiation. Although the transcriptional regulation of E2Fs has focused on pocket protein retinoblastoma protein complex, recent studies indicate that post-translational modification and stability regulation of E2Fs play key roles in diverse cellular processes. In this study, we found that FBXO1, a component of S-phase kinase-associated protein 1 (SKP1)-cullin 1-F-box protein (SCF) complex, is an E2Fs binding partner. Furthermore, FBXO1 to E2Fs binding induced K48 ubiquitination and subsequent proteasomal degradation of E2Fs. Binding domain analysis indicated that the Arg (R)/Ile (I) and R/Val (V) motifs, which are located in the dimerization domain of E2Fs, of E2F 1 and 3a and E2F2, respectively, acted as degron motifs (DMs) for FBXO1. Notably, RI/AA or RV/AA mutation in the DMs reduced FBXO1-mediated ubiquitination and prolonged the half-lives of E2Fs. Importantly, the stabilities of E2Fs were affected by phosphorylation of threonine residues located near RI and RV residues of DMs. Phosphorylation prediction database analysis and specific inhibitor analysis revealed that MEK/ERK signaling molecules play key roles in FBXO1/E2Fs’ interaction and modulate E2F protein turnover. Moreover, both elevated E2Fs protein levels by knockdown of FBXO1 and decreased E2Fs protein levels by sh-E2F3a delayed G1/S cell cycle transition, resulting in inhibition of cancer cell proliferation. These results demonstrated that FBXO1-E2Fs axis-mediated precise E2Fs stability regulation plays a key role in cell proliferation via G1/S cell cycle transition.
Microfluidic-based vascularized microphysiological systems
Lee, Somin,Ko, Jihoon,Park, Dohyun,Lee, Seung-Ryeol,Chung, Minhwan,Lee, Younggyun,Jeon, Noo Li The Royal Society of Chemistry 2018 Lab on a chip Vol.18 No.18
<P>Microphysiological systems have emerged in the last decade to provide an alternative to <I>in vivo</I> models in basic science and pharmaceutical research. In the field of vascular biology, in particular, there has been a lack of a suitable <I>in vitro</I> model exhibiting a three-dimensional structure and the physiological function of vasculature integrated with organ-on-a-chip models. The rapid development of organ-on-a-chip technology is well positioned to fulfill unmet needs. Recently, functional integration of vasculature with diverse microphysiological systems has been increasing. This recent trend corresponds to emerging research interest in how the vascular system contributes to various physiological and pathological conditions. This innovative platform has undergone significant development, but adoption of this technology by end-users and researchers in biology is still a work in progress. Therefore, it is critical to focus on simplification and standardization to promote the distribution and acceptance of this technology by the end-users. In this review, we will introduce the latest developments in vascularized microphysiological systems and summarize their outlook in basic research and drug screening applications.</P>