http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
International Lawyer Interview with Professor Jerome A. Cohen
Jerome A. Cohen (사) 이준국제법연구원 2022 Journal of East Asia and International Law Vol.15 No.1
Dr. Jerome Cohen (孔傑榮/柯恩) is Professor Emeritus at New York University School of Law, Founder and Faculty Director Emeritus of its US-Asia Law Institute, and Adjunct Senior Fellow for Asia at the Council on Foreign Relations. Professor Cohen was born in Elizabeth, New Jersey as the son of a local government attorney. After graduating from Linden High School, he received his B.A. and J.D. degree from prestigious Yale University and its Law School in 1951 and 1955, respectively. As a law student, he served as the Editor-in-Chief of the Yale Law Journal. From 1955–56 he clerked at the Supreme Court under Chief Justice Earl Warren and then under Justice Felix Frankfurter. Professor Cohen joined the faculty of University of California- Berkeley School of Law in 1959. Then, Professor Cohen was asked to recommend a candidate for a four-year grant to study China offered by the Rockefeller Foundation. When there was no clear candidate, however, he decided to pursue the opportunity himself.
A Comparison of the Effects of Canadian and U.S. Policy Shocks on Canadian Flow-of-Funds Variables
Cohen, Jacob,Husted, Steven 세종대학교 국제경제연구소 1987 Journal of Economic Integration Vol.2 No.1
By means of an integrated, two-country flow-of-funds matrix for Canada and the United States, the impacts on the endogenous Canadian variables of four Canadian and U.S. shock variables were compared. The selected exogenous variables were rest of the world gross saving, gross saving of the federal government, financial sources of funds of the central bank and the financial sources of funds of commercial banks. The endogenous variables for thirteen Canadian sectors included gross saving, capital expenditures, net increases in financial assets and increases in liabilities. Perhaps out most valuable finding is that it is not the current account surplus that sparks the Canadian economy but rather capital inflows.
Cohen, Max L.,Kim, Sunhong,Morita, Kiyokazu,Kim, Seong Heon,Han, Min Public Library of Science 2015 PLoS genetics Vol.11 No.3
<▼1><P>Postembryonic development in <I>Caenorhabditis elegans</I> is a powerful model for the study of the temporal regulation of development and for the roles of microRNAs in controlling gene expression. Stable switch-like changes in gene expression occur during development as stage-specific microRNAs are expressed and subsequently down-regulate other stage-specific factors, driving developmental progression. Key genes in this regulatory network are phylogenetically conserved and include the post-transcriptional microRNA repressor LIN-28; the nuclear hormone receptor DAF-12; and the microRNAs LIN-4, LET-7, and the three LET-7 family miRNAs (miR-48, miR-84, and miR-241). DAF-12 is known to regulate transcription of miR-48, miR-84 and miR-241, but its contribution is insufficient to account for all of the transcriptional regulation implied by the mutant phenotypes. In this work, the GATA-family transcription factor ELT-1 is identified from a genetic enhancer screen as a regulator of developmental timing in parallel to DAF-12, and is shown to do so by promoting the expression of the LET-7, miR-48, miR-84, and miR-241 microRNAs. The role of ELT-1 in developmental timing is shown to be separate from its role in cell-fate maintenance during post-embryonic development. In addition, analysis of Chromatin Immnoprecipitation (ChIP) data from the modENCODE project and this work suggest that the contribution of ELT-1 to the control of <I>let-7</I> family microRNA expression is likely through direct transcription regulation.</P></▼1><▼2><P><B>Author Summary</B></P><P>In the nematode roundworm <I>C</I>. <I>elegans</I>, seam cells, a type of adult stem cell, divide in a completely predictable manner throughout post-embryonic development. Study of the control of the timing of these cells’ division and differentiation led to the discovery of the first microRNAs, which are small non-coding RNAs that regulate the expression of protein-coding mRNAs, but knowledge of the regulation of expression of microRNAs themselves within <I>C</I>. <I>elegans</I> stem cells remains incomplete. In this study, the GATA-family transcription factor <I>elt-1</I>, known to be important for the formation and maintenance of tissues during embryonic and post-embryonic development, is found to regulate the expression of <I>let-7</I> family microRNAs in stem cells during late developmental stages. It is found to do so redundantly with <I>daf-12</I>, the only other transcription factor previously known to directly regulate microRNA expression in <I>C</I>. <I>elegans</I>. In addition, the presence of ELT-1 <I>in vivo</I> binding near microRNA coding DNA sequences suggests that its contribution to the regulation of microRNA expression is likely through direct regulation of transcription. Stem cells are important in development, tissue homeostasis, and malignancy, so additional knowledge of the mechanisms underlying their maintenance, renewal, and differentiation is of broad interest.</P></▼2>
HDAC4 Regulates Muscle Fiber Type-Specific Gene Expression Programs
Cohen, Todd J.,Choi, Moon-Chang,Kapur, Meghan,Lira, Vitor A.,Yan, Zhen,Yao, Tso-Pang Korean Society for Molecular and Cellular Biology 2015 Molecules and cells Vol.38 No.4
Fiber type-specific programs controlled by the transcription factor MEF2 dictate muscle functionality. Here, we show that HDAC4, a potent MEF2 inhibitor, is predominantly localized to the nuclei in fast/glycolytic fibers in contrast to the sarcoplasm in slow/oxidative fibers. The cytoplasmic localization is associated with HDAC4 hyper-phosphorylation in slow/oxidative-fibers. Genetic reprogramming of fast/glycolytic fibers to oxidative fibers by active CaMKII or calcineurin leads to increased HDAC4 phosphorylation, HDAC4 nuclear export, and an increase in markers associated with oxidative fibers. Indeed, HDAC4 represses the MEF2-dependent, PGC-$1{\alpha}$-mediated oxidative metabolic gene program. Thus differential phosphorylation and localization of HDAC4 contributes to establishing fiber type-specific transcriptional programs.
p62- and ubiquitin-dependent stress-induced autophagy of the mammalian 26S proteasome
Cohen-Kaplan, Victoria,Livneh, Ido,Avni, Noa,Fabre, Bertrand,Ziv, Tamar,Kwon, Yong Tae,Ciechanover, Aaron National Academy of Sciences 2016 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.113 No.47
<P>The ubiquitin-proteasome system and autophagy are the two main proteolytic systems involved in, among other functions, the maintenance of cell integrity by eliminating misfolded and damaged proteins and organelles. Both systems remove their targets after their conjugation with ubiquitin. An interesting, yet incompletely understood problem relates to the fate of the components of the two systems. Here we provide evidence that amino acid starvation enhances polyubiquitination on specific sites of the proteasome, a modification essential for its targeting to the autophagic machinery. The uptake of the ubiquitinated proteasome is mediated by its interaction with the ubiquitin-associated domain of p62/SQSTM1, a process that also requires interaction with LC3. Importantly, deletion of the PB1 domain of p62, which is important for the targeting of ubiquitinated substrates to the proteasome, has no effect on stress-induced autophagy of this proteolytic machinery, suggesting that the domain of p62 that binds to the proteasome determines the function of p62 in either targeting substrates to the proteasome or targeting the proteasome to autophagy.</P>