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2. Regulation of BRCA1 stability through the tandem UBX domains of isoleucyl-tRNA synthetase 1

Author

Chung, Scisung, Kang, Mi-Sun, Alimbetov, Dauren S, Mun, Gil-Im, Yunn, Na-Oh, Kim, Yunjin, Kim, Byung-Gyu, Wie, Minwoo, Lee, Eun A, Ra, Jae Sun, Oh, Jung-Min, Lee, Donghyun, Lee, Keondo, Kim, Jihan, Han, Seung Hyun, Kim, Kyong-Tai, Chung, Wan Kyun, Nam, Ki Hyun, Park, Jaehyun, Lee, ByungHoon, Kim, Sunghoon, Zhao, Weixing, Ryu, Sung Ho, Lee, Yun-Sil, Myung, Kyungjae, and Cho, Yunje

Subjects
Biochemistry and Cell Biology, Biological Sciences, 1.1 Normal biological development and functioning, Underpinning research, Isoleucine-tRNA Ligase, Amino Acyl-tRNA Synthetases, Glutamate-tRNA Ligase, RNA, Transfer
Abstract

Aminoacyl-tRNA synthetases (ARSs) have evolved to acquire various additional domains. These domains allow ARSs to communicate with other cellular proteins in order to promote non-translational functions. Vertebrate cytoplasmic isoleucyl-tRNA synthetases (IARS1s) have an uncharacterized unique domain, UNE-I. Here, we present the crystal structure of the chicken IARS1 UNE-I complexed with glutamyl-tRNA synthetase 1 (EARS1). UNE-I consists of tandem ubiquitin regulatory X (UBX) domains that interact with a distinct hairpin loop on EARS1 and protect its neighboring proteins in the multi-synthetase complex from degradation. Phosphomimetic mutation of the two serine residues in the hairpin loop releases IARS1 from the complex. IARS1 interacts with BRCA1 in the nucleus, regulates its stability by inhibiting ubiquitylation via the UBX domains, and controls DNA repair function.

Published
2022

3. Contributors

Author

Adefegha, Stephen A., primary, Ajiboye, Itunu O., additional, Ambi, Senthil Visaga, additional, Anandakumar, Pandi, additional, Atale, Neha, additional, Bae, Geon Ho, additional, Bae, Yoe-Sik, additional, Bagchi, Angshuman, additional, Baisakhiya, Shreya, additional, Bali, Moses, additional, Banerjee, Antara, additional, Benitez, Sonia, additional, Bhagat, Gaurav Kumar, additional, Bhagya, N., additional, Bhattacharyya, Sankar, additional, Boeno, Charles Nunes, additional, Chaudhuri, Rupa, additional, Correa, Fernando, additional, Coward, Kevin, additional, da Silva Setubal, Sulamita, additional, Dahiya, Kiran, additional, Dalal, Deepika, additional, Das, Simita, additional, Das, Undurti N., additional, De Laurentiis, Andrea, additional, Delgado-Bermúdez, Ariadna, additional, Dhananjaya, G., additional, Diniz-Sousa, Rafaela, additional, Ejike, Uju Dorathy Iliemene, additional, Esmeeta, Akanksha, additional, Gangadharan, Gireesh, additional, Ghosh, Sukanya, additional, Gopal, Gayathri, additional, Hegde, Kshema Umesh, additional, Jones, Celine, additional, Kamalakkannan, Abishek, additional, Kang, Ji Hyeon, additional, Krishnaswami, Venkateshwaran, additional, Krushnamurthy, P.H., additional, Liman, Mubarak Labaran, additional, Lopes, Jéssica Amaral, additional, Loushambam, Borish, additional, Mahanta, Nilkamal, additional, Maiti, Amit K., additional, Malik, Ashish Kumar, additional, Mehak, Sonam Fathima, additional, Molehin, Olorunfemi R., additional, Muralidar, Shibi, additional, Nagarajan, Devipriya, additional, Natarajan, Balakrishnan, additional, Naveenkumar, Chandrashekar, additional, Ogunleye, Tiwalola M., additional, Olonishuwa, Paul T., additional, Padmanabhan, Praviene, additional, Parashar, Soumya, additional, Park, Seon Hyang, additional, Pathak, Surajit, additional, Pillai, Vikram Gopalakrishna, additional, Prakash, Diwahar, additional, Puig, Nuria, additional, Rani, Vibha, additional, Rojas, Karen, additional, Ryu, Sung Ho, additional, Saha, Priyanka, additional, Samanta, Anurima, additional, Sánchez-Quesada, José Luis, additional, Sarkar, Debanjan, additional, Shruthi, N.R., additional, Singh, Harshita, additional, Singhal, Shivani, additional, Sinha, Dona, additional, Spandana, K.J., additional, Sunnagatta Nagaraja, Sunilgowda, additional, Valdivia-Najar, Jason, additional, Vallejo-Cardona, Alba Adriana, additional, Velázquez-Fernández, Jesús Bernardino, additional, Verdugo-Molinares, Maritza Guadalupe, additional, Vijayaraghavalu, Sivakumar, additional, Wolfson, Manuel L., additional, Yeste, Marc, additional, Zabel, Brian A., additional, Zamuner, Stella Regina, additional, Zhu, Chao, additional, and Zuliani, Juliana Pavan, additional

Published
2023
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7. Recruiting and Hiring a Diverse and Talented Public-Sector Workforce. Research Report. RR-A1255-1

Author

RAND Education and Labor, Goldman, Charles A., Piquado, Tepring, Irwin, J. Luke, Allen, Daniel, Zhou, Ying, and Ryu, Sung Ho

Abstract

Although there is great interest in attracting talented and underrepresented individuals into public-sector careers, there is also concern that graduates of colleges and universities may not be considering the public sector and that government agencies are not doing all they could to attract the next generation of workers. This report seeks to help bridge these gaps by identifying the most promising strategies that public-sector agencies, colleges and universities, and community organizations can pursue to increase the flow of talented and underrepresented workers into public-sector careers. This report examines one regional public-sector workforce, that of Southern California, but many of the issues and strategies that the authors identify are broadly applicable to other regions. These strategies focus on two fundamental goals -- increasing underrepresented students' awareness of rewarding opportunities in the public sector and making public-sector organizations more diverse -- that should reinforce each other. [Additional support for this study was provided by Southern California Association of Governments (SCAG).]

Published
2021
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9. Phospholipase Signaling in Breast Cancer

Author

Lee, Yu Jin, Shin, Kyeong Jin, Jang, Hyun-Jun, Noh, Dong-Young, Ryu, Sung Ho, Suh, Pann-Ghill, Crusio, Wim E., Series Editor, Dong, Haidong, Series Editor, Radeke, Heinfried H., Series Editor, Rezaei, Nima, Series Editor, Xiao, Junjie, Series Editor, Noh, Dong-Young, editor, Han, Wonshik, editor, and Toi, Masakazu, editor

Published
2021
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15. Osteoclast-secreted SLIT3 coordinates bone resorption and formation

Author

Kim, Beom-Jun, Lee, Young-Sun, Lee, Sun-Young, Baek, Wook-Young, Choi, Young Jin, Moon, Sung Ah, Lee, Seung Hun, Kim, Jung-Eun, Chang, Eun-Ju, Kim, Eun-Young, Yoon, Jin, Kim, Seung-Whan, Ryu, Sung Ho, Lee, Sun-Kyeong, Lorenzo, Joseph A., Ahn, Seong Hee, Kim, Hyeonmok, Lee, Ki-Up, Kim, Ghi Su, and Koh, Jung-Min

Subjects
Bone resorption -- Physiological aspects -- Research, Cell adhesion molecules -- Physiological aspects -- Health aspects, Medical research, Osteogenesis -- Research, Health care industry
Abstract

Coupling is the process that links bone resorption to bone formation in a temporally and spatially coordinated manner within the remodeling cycle. Several lines of evidence point to the critical roles of osteoclast-derived coupling factors in the regulation of osteoblast performance. Here, we used a fractionated secretomic approach and identified the axon-guidance molecule SLIT3 as a clastokine that stimulated osteoblast migration and proliferation by activating [beta]-catenin. SLIT3 also inhibited bone resorption by suppressing osteoclast differentiation in an autocrine manner. Mice deficient in Slit3 or its receptor, Robo1, exhibited osteopenic phenotypes due to a decrease in bone formation and increase in bone resorption. Mice lacking Slit3 specifically in osteoclasts had low bone mass, whereas mice with either neuron-specific Slit3 deletion or osteoblast-specific Slit3 deletion had normal bone mass, thereby indicating the importance of SLIT3 as a local determinant of bone metabolism. In postmenopausal women, higher circulating SLIT3 levels were associated with increased bone mass. Notably, injection of a truncated recombinant SLIT3 markedly rescued bone loss after an ovariectomy. Thus, these results indicate that SLIT3 plays an osteoprotective role by synchronously stimulating bone formation and inhibiting bone resorption, making it a potential therapeutic target for metabolic bone diseases., Introduction Bone is a highly dynamic tissue that constantly undergoes changes and regeneration throughout adult life through a process called remodeling. This consists of 3 consecutive phases: the initiation of [...]

Published
2018
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27. Spiraeoside inhibits mast cells activation and IgE-mediated allergic responses by suppressing phospholipase C-γ-mediated signaling

Author

Kim, Jung Kuk, Seo, Young-Kyo, Park, Sehoon, Park, Soo-Ah, Lim, Seyoung, Lee, Susie, Kwon, Ohman, Seo, Jeong Kon, Choi, Ung-Kyu, Ryu, Sung Ho, and Suh, Pann-Ghill

Subjects
Immunoglobulins -- Health aspects, Materia medica, Vegetable -- Health aspects, Allergic reaction -- Physiological aspects, Mast cells -- Health aspects, Phospholipases -- Health aspects, Allergy -- Physiological aspects, Plant extracts -- Health aspects, Biological sciences
Abstract

Abstract: Mast cells are responsible for IgE-mediated allergic responses through the secretion of various inflammatory cytokines and mediators. Therefore, the pharmacological regulation of mast cell activation is an important goal [...]

Published
2015
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32. Structural Basis for the Antibiotic Resistance of Eukaryotic Isoleucyl-tRNA Synthetase

Author

Chung, Scisung, Kim, Sulhee, Ryu, Sung Ho, Hwang, Kwang Yeon, and Cho, Yunje

Subjects
mupirocin, Isoleucine-tRNA Ligase, Models, Molecular, crystal structure, aminoacyl-tRNA synthetases, Eukaryota, anti-infective agents, Amino Acid Sequence, active site closure, Research Article
Abstract

Pathogenic aminoacyl-tRNA synthetases (ARSs) are attractive targets for anti-infective agents because their catalytic active sites are different from those of human ARSs. Mupirocin is a topical antibiotic that specifically inhibits bacterial isoleucyl-tRNA synthetase (IleRS), resulting in a block to protein synthesis. Previous studies on Thermus thermophilus IleRS indicated that mupirocin-resistance of eukaryotic IleRS is primarily due to differences in two amino acids, His581 and Leu583, in the active site. However, without a eukaryotic IleRS structure, the structural basis for mupirocin-resistance of eukaryotic IleRS remains elusive. Herein, we determined the crystal structure of Candida albicans IleRS complexed with Ile-AMP at 2.9 Å resolution. The largest difference between eukaryotic and prokaryotic IleRS enzymes is closure of the active site pocket by Phe55 in the HIGH loop; Arg410 in the CP core loop; and the second Lys in the KMSKR loop. The Ile-AMP product is lodged in a closed active site, which may restrict its release and thereby enhance catalytic efficiency. The compact active site also prevents the optimal positioning of the 9-hydroxynonanoic acid of mupirocin and plays a critical role in resistance of eukaryotic IleRS to anti-infective agents.

Published
2020

33. IgGs from patients with amyotrophic lateral sclerosis and diabetes target CaVα2δ1 subunits impairing islet cell function and survival

Author

Shi, Yue, Park, Kyoung Sun, Kim, Seung Hyun, Yu, Jia, Zhao, Kaixuan, Yu, Lina, Oh, Ki Wook, Lee, Kayoung, Kim, Jaeyoon, Chaggar, Kanchan, Li, Yuxin, Dolphin, Annette C., Catterall, William A., Ryu, Sung Ho, Yang, Shao-Nian, and Berggren, Per-Olof

Subjects
amyotrophic lateral sclerosis, Medical Sciences, diabetes, cytosolic free Ca2+ concentration, calcium channel, Biological Sciences, immunoglobulin
Abstract

Significance We provide evidence of a mechanistic link between ALS and T2DM. Our data show that a subgroup of ALS-T2DM patients have sera that enhance CaV1 channel-mediated Ca2+ influx and exaggerate [Ca2+]i. These effects occur because the sera accommodate cytotoxic IgG autoantibodies that immunocapture CaVα2δ1 subunits. As a consequence, impairments in [Ca2+]i dynamics, mitochondrial function, insulin secretion, and cell viability appear. We could clarify not only the identity of this serum factor but also the molecular mechanisms underlying its effects on the islet cells. Our findings may lay the foundation for a treatment strategy for this complex and severe group of diabetic patients., Patients with amyotrophic lateral sclerosis (ALS) often show hallmarks of type 2 diabetes mellitus (T2DM). However, the causal link between ALS and T2DM has remained a mystery. We now demonstrate that 60% of ALS patients with T2DM (ALS-T2DM) have sera that exaggerated K+-induced increases in cytosolic free Ca2+ concentration ([Ca2+]i) in mouse islet cells. The effect was attributed to the presence of pathogenic immunoglobulin Gs (IgGs) in ALS-T2DM sera. The pathogenic IgGs immunocaptured the voltage-dependent Ca2+ (CaV) channel subunit CaVα2δ1 in the plasma membrane enhancing CaV1 channel-mediated Ca2+ influx and [Ca2+]i, resulting in impaired mitochondrial function. Consequently, impairments in [Ca2+]i dynamics, insulin secretion, and cell viability occurred. These data reveal that patients with ALS-T2DM carry cytotoxic ALS-T2DM-IgG autoantibodies that serve as a causal link between ALS and T2DM by immunoattacking CaVα2δ1 subunits. Our findings may lay the foundation for a pharmacological treatment strategy for patients suffering from a combination of these diseases.

Published
2019

35. Targeting PLD2 in adipocytes augments adaptive thermogenesis by improving mitochondrial quality and quantity in mice

Author

Kim, Hyung Sik, primary, Park, Min Young, additional, Yun, Nam Joo, additional, Go, Hye Sun, additional, Kim, Mi Young, additional, Seong, Je Kyung, additional, Lee, Minyoung, additional, Kang, Eun Seok, additional, Ghim, Jaewang, additional, Ryu, Sung Ho, additional, Zabel, Brian A., additional, Koh, Ara, additional, and Bae, Yoe-Sik, additional

Published
2021
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