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1. HyperCLOVA X Technical Report

Author

Yoo, Kang Min, Han, Jaegeun, In, Sookyo, Jeon, Heewon, Jeong, Jisu, Kang, Jaewook, Kim, Hyunwook, Kim, Kyung-Min, Kim, Munhyong, Kim, Sungju, Kwak, Donghyun, Kwak, Hanock, Kwon, Se Jung, Lee, Bado, Lee, Dongsoo, Lee, Gichang, Lee, Jooho, Park, Baeseong, Shin, Seongjin, Yu, Joonsang, Baek, Seolki, Byeon, Sumin, Cho, Eungsup, Choe, Dooseok, Han, Jeesung, Jin, Youngkyun, Jun, Hyein, Jung, Jaeseung, Kim, Chanwoong, Kim, Jinhong, Kim, Jinuk, Lee, Dokyeong, Park, Dongwook, Sohn, Jeong Min, Han, Sujung, Heo, Jiae, Hong, Sungju, Jeon, Mina, Jung, Hyunhoon, Jung, Jungeun, Jung, Wangkyo, Kim, Chungjoon, Kim, Hyeri, Kim, Jonghyun, Kim, Min Young, Lee, Soeun, Park, Joonhee, Shin, Jieun, Yang, Sojin, Yoon, Jungsoon, Lee, Hwaran, Bae, Sanghwan, Cha, Jeehwan, Gylleus, Karl, Ham, Donghoon, Hong, Mihak, Hong, Youngki, Hong, Yunki, Jang, Dahyun, Jeon, Hyojun, Jeon, Yujin, Jeong, Yeji, Ji, Myunggeun, Jin, Yeguk, Jo, Chansong, Joo, Shinyoung, Jung, Seunghwan, Kim, Adrian Jungmyung, Kim, Byoung Hoon, Kim, Hyomin, Kim, Jungwhan, Kim, Minkyoung, Kim, Minseung, Kim, Sungdong, Kim, Yonghee, Kim, Youngjun, Kim, Youngkwan, Ko, Donghyeon, Lee, Dughyun, Lee, Ha Young, Lee, Jaehong, Lee, Jieun, Lee, Jonghyun, Lee, Jongjin, Lee, Min Young, Lee, Yehbin, Min, Taehong, Min, Yuri, Moon, Kiyoon, Oh, Hyangnam, Park, Jaesun, Park, Kyuyon, Park, Younghun, Seo, Hanbae, Seo, Seunghyun, Sim, Mihyun, Son, Gyubin, Yeo, Matt, Yeom, Kyung Hoon, Yoo, Wonjoon, You, Myungin, Ahn, Doheon, Ahn, Homin, Ahn, Joohee, Ahn, Seongmin, An, Chanwoo, An, Hyeryun, An, Junho, An, Sang-Min, Byun, Boram, Byun, Eunbin, Cha, Jongho, Chang, Minji, Chang, Seunggyu, Cho, Haesong, Cho, Youngdo, Choi, Dalnim, Choi, Daseul, Choi, Hyoseok, Choi, Minseong, Choi, Sangho, Choi, Seongjae, Choi, Wooyong, Chun, Sewhan, Go, Dong Young, Ham, Chiheon, Han, Danbi, Han, Jaemin, Hong, Moonyoung, Hong, Sung Bum, Hwang, Dong-Hyun, Hwang, Seongchan, Im, Jinbae, Jang, Hyuk Jin, Jang, Jaehyung, Jang, Jaeni, Jang, Sihyeon, Jang, Sungwon, Jeon, Joonha, Jeong, Daun, Jeong, Joonhyun, Jeong, Kyeongseok, Jeong, Mini, Jin, Sol, Jo, Hanbyeol, Jo, Hanju, Jo, Minjung, Jung, Chaeyoon, Jung, Hyungsik, Jung, Jaeuk, Jung, Ju Hwan, Jung, Kwangsun, Jung, Seungjae, Ka, Soonwon, Kang, Donghan, Kang, Soyoung, Kil, Taeho, Kim, Areum, Kim, Beomyoung, Kim, Byeongwook, Kim, Daehee, Kim, Dong-Gyun, Kim, Donggook, Kim, Donghyun, Kim, Euna, Kim, Eunchul, Kim, Geewook, Kim, Gyu Ri, Kim, Hanbyul, Kim, Heesu, Kim, Isaac, Kim, Jeonghoon, Kim, Jihye, Kim, Joonghoon, Kim, Minjae, Kim, Minsub, Kim, Pil Hwan, Kim, Sammy, Kim, Seokhun, Kim, Seonghyeon, Kim, Soojin, Kim, Soong, Kim, Soyoon, Kim, Sunyoung, Kim, Taeho, Kim, Wonho, Kim, Yoonsik, Kim, You Jin, Kim, Yuri, Kwon, Beomseok, Kwon, Ohsung, Kwon, Yoo-Hwan, Lee, Anna, Lee, Byungwook, Lee, Changho, Lee, Daun, Lee, Dongjae, Lee, Ha-Ram, Lee, Hodong, Lee, Hwiyeong, Lee, Hyunmi, Lee, Injae, Lee, Jaeung, Lee, Jeongsang, Lee, Jisoo, Lee, Jongsoo, Lee, Joongjae, Lee, Juhan, Lee, Jung Hyun, Lee, Junghoon, Lee, Junwoo, Lee, Se Yun, Lee, Sujin, Lee, Sungjae, Lee, Sungwoo, Lee, Wonjae, Lee, Zoo Hyun, Lim, Jong Kun, Lim, Kun, Lim, Taemin, Na, Nuri, Nam, Jeongyeon, Nam, Kyeong-Min, Noh, Yeonseog, Oh, Biro, Oh, Jung-Sik, Oh, Solgil, Oh, Yeontaek, Park, Boyoun, Park, Cheonbok, Park, Dongju, Park, Hyeonjin, Park, Hyun Tae, Park, Hyunjung, Park, Jihye, Park, Jooseok, Park, Junghwan, Park, Jungsoo, Park, Miru, Park, Sang Hee, Park, Seunghyun, Park, Soyoung, Park, Taerim, Park, Wonkyeong, Ryu, Hyunjoon, Ryu, Jeonghun, Ryu, Nahyeon, Seo, Soonshin, Seo, Suk Min, Shim, Yoonjeong, Shin, Kyuyong, Shin, Wonkwang, Sim, Hyun, Sim, Woongseob, Soh, Hyejin, Son, Bokyong, Son, Hyunjun, Son, Seulah, Song, Chi-Yun, Song, Chiyoung, Song, Ka Yeon, Song, Minchul, Song, Seungmin, Wang, Jisung, Yeo, Yonggoo, Yi, Myeong Yeon, Yim, Moon Bin, Yoo, Taehwan, Yoo, Youngjoon, Yoon, Sungmin, Yoon, Young Jin, Yu, Hangyeol, Yu, Ui Seon, Zuo, Xingdong, Bae, Jeongin, Bae, Joungeun, Cho, Hyunsoo, Cho, Seonghyun, Cho, Yongjin, Choi, Taekyoon, Choi, Yera, Chung, Jiwan, Han, Zhenghui, Heo, Byeongho, Hong, Euisuk, Hwang, Taebaek, Im, Seonyeol, Jegal, Sumin, Jeon, Sumin, Jeong, Yelim, Jeong, Yonghyun, Jiang, Can, Jiang, Juyong, Jin, Jiho, Jo, Ara, Jo, Younghyun, Jung, Hoyoun, Jung, Juyoung, Kang, Seunghyeong, Kim, Dae Hee, Kim, Ginam, Kim, Hangyeol, Kim, Heeseung, Kim, Hyojin, Kim, Hyojun, Kim, Hyun-Ah, Kim, Jeehye, Kim, Jin-Hwa, Kim, Jiseon, Kim, Jonghak, Kim, Jung Yoon, Kim, Rak Yeong, Kim, Seongjin, Kim, Seoyoon, Kim, Sewon, Kim, Sooyoung, Kim, Sukyoung, Kim, Taeyong, Ko, Naeun, Koo, Bonseung, Kwak, Heeyoung, Kwon, Haena, Kwon, Youngjin, Lee, Boram, Lee, Bruce W., Lee, Dagyeong, Lee, Erin, Lee, Euijin, Lee, Ha Gyeong, Lee, Hyojin, Lee, Hyunjeong, Lee, Jeeyoon, Lee, Jeonghyun, Lee, Jongheok, Lee, Joonhyung, Lee, Junhyuk, Lee, Mingu, Lee, Nayeon, Lee, Sangkyu, Lee, Se Young, Lee, Seulgi, Lee, Seung Jin, Lee, Suhyeon, Lee, Yeonjae, Lee, Yesol, Lee, Youngbeom, Lee, Yujin, Li, Shaodong, Liu, Tianyu, Moon, Seong-Eun, Moon, Taehong, Nihlenramstroem, Max-Lasse, Oh, Wonseok, Oh, Yuri, Park, Hongbeen, Park, Hyekyung, Park, Jaeho, Park, Nohil, Park, Sangjin, Ryu, Jiwon, Ryu, Miru, Ryu, Simo, Seo, Ahreum, Seo, Hee, Seo, Kangdeok, Shin, Jamin, Shin, Seungyoun, Sin, Heetae, Wang, Jiangping, Wang, Lei, Xiang, Ning, Xiao, Longxiang, Xu, Jing, Yi, Seonyeong, Yoo, Haanju, Yoo, Haneul, Yoo, Hwanhee, Yu, Liang, Yu, Youngjae, Yuan, Weijie, Zeng, Bo, Zhou, Qian, Cho, Kyunghyun, Ha, Jung-Woo, Park, Joonsuk, Hwang, Jihyun, Kwon, Hyoung Jo, Kwon, Soonyong, Lee, Jungyeon, Lee, Seungho, Lim, Seonghyeon, Noh, Hyunkyung, Choi, Seungho, Lee, Sang-Woo, Lim, Jung Hwa, and Sung, Nako

Subjects
Computer Science - Computation and Language, Computer Science - Artificial Intelligence
Abstract

We introduce HyperCLOVA X, a family of large language models (LLMs) tailored to the Korean language and culture, along with competitive capabilities in English, math, and coding. HyperCLOVA X was trained on a balanced mix of Korean, English, and code data, followed by instruction-tuning with high-quality human-annotated datasets while abiding by strict safety guidelines reflecting our commitment to responsible AI. The model is evaluated across various benchmarks, including comprehensive reasoning, knowledge, commonsense, factuality, coding, math, chatting, instruction-following, and harmlessness, in both Korean and English. HyperCLOVA X exhibits strong reasoning capabilities in Korean backed by a deep understanding of the language and cultural nuances. Further analysis of the inherent bilingual nature and its extension to multilingualism highlights the model's cross-lingual proficiency and strong generalization ability to untargeted languages, including machine translation between several language pairs and cross-lingual inference tasks. We believe that HyperCLOVA X can provide helpful guidance for regions or countries in developing their sovereign LLMs., Comment: 44 pages; updated authors list and fixed author names

Published
2024

3. Identification of XPR-1, a progesterone receptor required for Xenopus oocyte activation

Author

Tian, Jingdon, Kim, Sammy, Heilig, Elizabeth, and Ruderman, Joan V.

Subjects
Progesterone -- Receptors, Xenopus -- Physiological aspects, Oocytes -- Physiological aspects, Meiosis -- Physiological aspects, Mitogens -- Physiological aspects, Cell cycle -- Physiological aspects, Protein kinases -- Physiological aspects, Science and technology
Abstract

Quiescent full-grown Xenopus oocytes remain arrested at the [G.sub.2]/M border of meiosis I until exposed to progesterone, their natural mitogen. Progesterone triggers rapid, nontranscriptional responses that lead to the translational activation of stored mRNAs, resumption of the meiotic cell cycles, and maturation of the oocyte into a fertilizable egg. It has long been presumed that progesterone activates the oocyte through a novel nontranscriptional signaling receptor. Here, we provide evidence that a conventional transcriptional progesterone receptor cloned from Xenopus oocytes, XPR-1, is required for oocyte activation, Overexpression of XPR-1 through mRNA injection increases sensitivity to progesterone and accelerates progesterone-activated cell cycle reentry. Injection of XPR-1 antisense oligonucleotides blocks the ability of oocytes to respond to progesterone; these oocytes are rescued by subsequent injection of XPR-1 or the human progesterone receptor PR-B. Antisense-treated oocytes can be activated in response to inhibition of protein kinase A, one of the earliest known changes occurring downstream of progesterone stimulation. These results argue that the conventional progesterone receptor also functions as the signaling receptor that is responsible for the rapid nontranscriptional activation of frog oocytes.

Published
2000

4. Loved the Michael Jai white cover!

Author

Kim, Sammy

Subjects
General interest, Sports and fitness
Abstract

Yes, I loved seeing my favorite martial arts action star on the cover of the October/ November 2014 issue. Yes, I loved reading his thoughts on fitness and filmmaking. But [...]

Published
2014

8. Identification of XPR-1, a progesterone receptor required for Xenopus oocyte activation.

Author

Jingdong Tian and Kim, Sammy

Subjects
*PROGESTERONE receptors, *OOGENESIS
Abstract

Provides evidence that a conventional transcriptional progesterone receptor cloned from Xenopus oocytes, XPR-1, is required for oocyte activation. Isolation of cDNA encoding XPR-1; Sequences in the hormone-binding and DNA-binding domains; Effect of its overexpression and ablation on factors involved in oocyte activation and meiosis.

Published
2000
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9. BMP-2/ALK3 and HGF signal in parallel to regulate renal collecting duct morphogenesis

Author

Gupta, Indra R., Macias-Silva, Marina, Kim, Sammy, Zhou, Xiaopeng, Piscione, Tino D., Whiteside, Catharine, Wrana, Jeffrey L., and Rosenblum, Norman D.

Abstract

Bone morphogenetic protein (BMP)-2 and hepatocyte growth factor (HGF) exert antagonistic effects on renal collecting duct formation during embryogenesis. A current model proposes HGF inhibits BMP-2 signaling at the level of Smad1 in a common target cell. Here, we show that BMP-2 and HGF control collecting duct formation via parallel pathways. We examined the interactions between BMP-2 and HGF in the mIMCD-3 model of collecting duct morphogenesis. During tubule formation, HGF rescued the inhibitory effects of BMP-2 and of a constitutive active form of the BMP-2 receptor, ALK3, stably expressed in mIMCD-3 cells. To determine whether the effect of HGF occurs through known mediators which act downstream of the BMP-2/ALK3 complex, we examined the effect of HGF on BMP-2-induced Smad1 phosphorylation, Smad1/Smad4 complex formation, and Smad1 nuclear translocation. Neither HGF nor other receptor tyrosine kinase ligands (EGF, FGF-4) induced phosphorylation of endogenous Smad1 in mIMCD-3 cells or in Mv1Lu, MC3T3-E1 or P19 cells. Furthermore, none of these ligands blocked induction of the BMP-responsive promoter, Tlx2. Thus, HGF overcomes the inhibitory effects of BMP-2 on collecting duct morphogenesis without interrupting any of the known signaling events in the BMP-2 dependent Smad1 signaling pathway. We conclude that BMP-2/ALK3 and HGF function to control parallel pathways downstream of their respective cell surface receptors. Integration of these signals likely occurs at the level of transcriptional or post-transcriptional events.

Published
2000
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10. MAILBOX.

Author

Kim, Sammy, Tesmer, Dan, Milloy, Steve, Slater, Kerry, and Perets, Thom

Abstract

Several letters to the editor are presented in response to articles in previous issues including hapkido master Bong Soo Han in the October-November 2014 issue, “Kill or Be Killed" by Scot Conway in the October-November 2014 issue, and “I am aware." by Erynn Young in the June-July 2014 issue.

Published
2014

11. Usp7 Regulates Glial Lineage Cell-Specific Transcription Factors by Modulating Histone H2B Monoubiquitination.

Author

Kim DH, Kim SL, Singh V, and Ramakrishna S

Abstract

Histone H2B monoubiquitination (H2Bub1) is a dynamic posttranslational modification which are linked to DNA damage and plays a key role in a wide variety of regulatory transcriptional programs. Cancer cells exhibit a variety of epigenetic changes, particularly any aberrant H2Bub1 has frequently been associated with the development of tumors. Nevertheless, our understanding of the mechanisms governing the histone H2B deubiquitination and their associated functions during stem cell differentiation remain only partially understood. In this study, we wished to investigate the role of deubiquitinating enzymes (DUBs) on H2Bub1 regulation during stem cell differentiation. In a search for potential DUBs for H2B monoubiquitination, we identified Usp7, a ubiquitin-specific protease that acts as a negative regulator of H2B ubiquitination during the neuronal differentiation of mouse embryonic carcinoma cells. Loss of function of the Usp7 gene by a CRISPR/Cas9 system during retinoic acid-mediated cell differentiation contributes to the increase in H2Bub1. Furthermore, knockout of the Usp7 gene particularly elevated the expression of neuronal differentiation related genes including astryocyte-specific markers and oligodendrocyte-specific markers. In particular, glial lineage cell-specific transcription factors including oligodendrocyte transcription factor 2, glial fibrillary acidic protein, and SRY-box transcription factor 10 was significantly upregulated during neuronal differentiation. Thus, our findings suggest a novel role of Usp7 in gliogenesis in mouse embryonic carcinoma cells.

Published
2024
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