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Dual-specificity protein phosphatases Cdc25 are required to maintain meiotic arrest in mouse oocytes
Hyoeun Kang,Seok Chul Hwang,Jeong Su Oh 한국발생생물학회 2013 한국발생생물학회 학술발표대회 Vol.2013 No.8
In oocytes from different species, MPF, a complex of Cdk1 and cyclin B, is the master regulator of cell cycle. The activity of MPF is regulated by the phosphorylations mediated by Wee1B kinase and Cdc25B phosphatase. Although a regulation of MPF activity by these inhibitory phosphorylations are well established, a dogma in the cell cycle is that MPF activity is regulated by the dynamics of cyclin B during the metaphase II (MII) arrest (also known as CSF arrest). However, growing evidences suggest that Wee1B-mediated Cdk1 phosphorylation is also critical to trigger the progression of cell cycle during the onset of anaphase. Therefore, in the present study, we investigated the role of Cdc25B phosphatase during MII arrest. Cdc25B is present in MII arrested oocytes as a hyperphosphorylated form and disruption of its function either by antibody or siRNA injection induces the progression of cell cycle to interphase. Moreover, the hyperphosphorylated form, which has been known as an active form of Cdc25B, is dephosphorylated during the anaphase onset. Interestingly, this dephosphrylation occurred ahead of cyclin B degradation. Conversely, overexpression of Cdc25B prevents metaphase to anaphase transition induced by calcium stimulation. Therefore, our findings provide novel paradigm in cell cycle that MPF activity during metaphase arrest is regulated by the balance between Cdk1 inhibitory kinases, Wee1, and the counteracting phosphatases, Cdc25. When cells exit from metaphase, Cdc25 is inactivated and Wee1 is reactivated and thereby Cdk1 kinase activity is rapidly and transiently decreased. This initial decrease of Cdk1 activity is further promoted by the proteolytic degradation of cyclin B, which ensures irreversible progression of cell cycle to interphase. Thus, the concerted effort of phosphorylation/dephosphorylation of Cdk1 and synthesis/degradation of cyclin B play roles in fine-tuning the activity of Cdk1 during metaphase to anaphase transition.
Accelerated Evolution of the Regulatory Sequences of Brain Development in the Human Genome
Lee, Kang Seon,Bang, Hyoeun,Choi, Jung Kyoon,Kim, Kwoneel Korean Society for Molecular and Cellular Biology 2020 Molecules and cells Vol.43 No.4
Genetic modifications in noncoding regulatory regions are likely critical to human evolution. Human-accelerated noncoding elements are highly conserved noncoding regions among vertebrates but have large differences across humans, which implies human-specific regulatory potential. In this study, we found that human-accelerated noncoding elements were frequently coupled with DNase I hypersensitive sites (DHSs), together with monomethylated and trimethylated histone H3 lysine 4, which are active regulatory markers. This coupling was particularly pronounced in fetal brains relative to adult brains, non-brain fetal tissues, and embryonic stem cells. However, fetal brain DHSs were also specifically enriched in deeply conserved sequences, implying coexistence of universal maintenance and human-specific fitness in human brain development. We assessed whether this coexisting pattern was a general one by quantitatively measuring evolutionary rates of DHSs. As a result, fetal brain DHSs showed a mixed but distinct signature of regional conservation and outlier point acceleration as compared to other DHSs. This finding suggests that brain developmental sequences are selectively constrained in general, whereas specific nucleotides are under positive selection or constraint relaxation simultaneously. Hence, we hypothesize that human- or primate-specific changes to universally conserved regulatory codes of brain development may drive the accelerated, and most likely adaptive, evolution of the regulatory network of the human brain.
Cardiac-specific delivery by cardiac tissue-targeting peptide-expressing exosomes
Kim, Hyoeun,Yun, Nuri,Mun, Dasom,Kang, Ji-Young,Lee, Seung-Hyun,Park, Hyelim,Park, Hyewon,Joung, Boyoung Elsevier 2018 Biochemical and biophysical research communication Vol.499 No.4
<P><B>Abstract</B></P> <P>Naturally occurring RNA carriers such as exosomes might be an untapped source of effective delivery vehicles. However, if exosomes are to be exploited for therapeutic applications, they must target specific tissues or cell types to avoid off-target effects. This study evaluated whether genetic modification of exosomes could enhance exosome delivery to heart cells and heart tissue without toxicity. Exosomes expressing cardiac-targeting peptide (CTP)-Lamp2b on the exosomal membrane (CTP-Exo) were generated by introducing vectors encoding CTP-Lamp2b into HEK 293 cells. The expression of CTP-Lamp2b peptide on exosomes was stabilized by attaching glycosylation sequences. Exosomes expressing only Lamp2b on exosomal membranes (CTL-Exo) were generated as a control. The <I>in vitro</I> and <I>in vivo</I> uptake of CTL-Exo and CTP-Exo was evaluated in cell lines and mice. Both exosomes were delivered to HEK 293 and H9C2 cells. The delivery of the exosome was not different between CTP-Exo and CTL-Exo in HEK 293 cells, whereas the delivery of CTP-Exo was 16% greater than that of CTL-Exo in H9C2 cells (P = 0.047). Cell viability was maintained at almost 100% with different dosages of both CTL-Exo and CTP-Exo. Moreover, compared with CTL-Exo, the <I>in vivo</I> delivery of exosomes to the hearts of mice was increased by 15% with CTP-Exo (P = 0.035). The delivery to livers and spleens was not different between the two exosomes. Genetic modification of exosomes by expressing CTP-Lamp2b on the exosomal membrane enhanced exosome delivery to heart cells and the heart tissue. These results suggested that CTP-Exo might be used as a therapeutic tool for heart disease.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Genetic modification of exosomes could enhance exosome delivery to heart. </LI> <LI> CTP-Exo did not show toxic effects <I>in vitro</I> or <I>in vivo.</I> </LI> <LI> CTP-Exo might be used as a therapeutic tool for heart disease. </LI> </UL> </P>
김효은,조희수,강현아,임소희,조대철 순천향대학교 산업기술연구소 2022 순천향 산업기술연구소논문집 Vol.28 No.2
Appropriate reduction of food waste targets to its volume. The decrease of the volume is subject to disappearance of the smaller shredded particles. We constructed three mathematical models for expressing the volumetric reduction of waste particles. The formulated sets of relevant differential equations were translated in MATLAB format so as to be solved numerically. All three models simulated ‘volume reduction of food waste’quite well so that use of the models could enhance our understanding about plausible mechanism(s) for that biochemical degradation.
다중 사용자 환경에서 효과적인 키 교환을 위한 GPU 기반의 NTRU 고속구현
성효은(Hyoeun Seong),김예원(Yewon Kim),염용진(Yongjin Yeom),강주성(Ju-Sung Kang) 한국정보보호학회 2021 정보보호학회논문지 Vol.31 No.3
대규모 양자컴퓨팅 기술의 실현을 앞둔 현재 공개키 암호 시스템을 양자내성을 가진 암호 시스템으로 전환하는 것은 필수적이다. 미국 국립표준기술연구소 NIST는 양자내성암호(Post-Quantum Cryptography, PQC)를 표준화하기 위한 공모사업을 추진하고 있으며 인터넷 통신 보안에 주로 사용되는 TLS(Transport Layer Security) 프로토콜에 이러한 양자내성암호를 적용하기 위한 차원의 연구도 활발히 진행되고 있다. 본 논문에서는 병렬화된 양자내성암호 NTRU를 활용하여 TLS 상에서 서버와 다수의 사용자가 세션키를 공유하기 위한 키 교환(key exchange) 시나리오를 제시한다. 또한, GPU를 이용하여 NTRU를 병렬화 및 연산을 고속화하는 방법을 제시하고 서버가 대규모 데이터를 처리해야 하는 환경에서 그 효율성을 분석한다. It is imperative to migrate the current public key cryptosystem to a quantum-resistance system ahead of the realization of large-scale quantum computing technology. The National Institute of Standards and Technology, NIST, is promoting a public standardization project for Post-Quantum Cryptography(PQC) and also many research efforts have been conducted to apply PQC to TLS(Transport Layer Security) protocols, which are used for Internet communication security. In this paper, we propose a scenario in which a server and multi-clients share session keys on TLS by using the parallelized NTRU which is PQC in the key exchange process. In addition, we propose a method of accelerating NTRU using GPU and analyze its efficiency in an environment where a server needs to process large-scale data simultaneously.