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4,528 results on '"Cho, In Hee"'

11. Suppression of Dexter transfer by covalent encapsulation for efficient matrix-free narrowband deep blue hyperfluorescent OLEDs

Author

Cho, Hwan-Hee, Congrave, Daniel G., Gillett, Alexander J., Montanaro, Stephanie, Francis, Haydn E., Riesgo-Gonzalez, Víctor, Ye, Junzhi, Chowdury, Rituparno, Zeng, Weixuan, Etherington, Marc K., Royakkers, Jeroen, Millington, Oliver, Bond, Andrew D., Plasser, Felix, Frost, Jarvist M., Grey, Clare P., Rao, Akshay, Friend, Richard H., Greenham, Neil C., and Bronstein, Hugo

Published
2024
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23. Author Correction: Importance of dialysis specialists in early mortality in elderly hemodialysis patients: a multicenter retrospective cohort study

Author

Park, Yohan, Lee, Ji Won, Yoon, Se-Hee, Yun, Sung-Ro, Kim, Hyunsuk, Bae, Eunjin, Hyun, Young Youl, Chung, Sungjin, Kwon, Soon Hyo, Cho, Jang-Hee, Yoo, Kyung Don, Park, Woo Yeong, Sun, In O, Yu, Byung Chul, Ko, Gang-Jee, Yang, Jae Won, Song, Sang Heon, Shin, Sung Joon, Hong, Yu Ah, and Hwang, Won Min

Published
2024
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35. Regulation of beige adipocyte thermogenesis by the cold-repressed ER protein NNAT

Author

Choi, Kyung-Mi, Ko, Christopher Y, An, Sung-Min, Cho, Seung-Hee, Rowland, Douglas J, Kim, Jung Hak, Fasoli, Anna, Chaudhari, Abhijit J, Bers, Donald M, and Yoon, John C

Subjects
Biochemistry and Cell Biology, Biological Sciences, Obesity, Animals, Mice, Adipocytes, Adipocytes, Beige, Adipose Tissue, Adipose Tissue, White, Membrane Proteins, Nerve Tissue Proteins, Thermogenesis, Ubiquitin-Protein Ligases, Endoplasmic Reticulum, NNAT, SERCA2, NHLRC1, Beige fat, Physiology, Biochemistry and cell biology
Abstract

ObjectiveCold stimuli trigger the conversion of white adipose tissue into beige adipose tissue, which is capable of non-shivering thermogenesis. However, what process drives this activation of thermogenesis in beige fat is not well understood. Here, we examine the ER protein NNAT as a regulator of thermogenesis in adipose tissue.MethodsWe investigated the regulation of adipose tissue NNAT expression in response to changes in ambient temperature. We also evaluated the functional role of NNAT in thermogenic regulation using Nnat null mice and primary adipocytes that lack or overexpress NNAT.ResultsCold exposure or treatment with a β3-adrenergic agonist reduces the expression of adipose tissue NNAT in mice. Genetic disruption of Nnat in mice enhances inguinal adipose tissue thermogenesis. Nnat null mice exhibit improved cold tolerance both in the presence and absence of UCP1. Gain-of-function studies indicate that ectopic expression of Nnat abolishes adrenergic receptor-mediated respiration in beige adipocytes. NNAT physically interacts with the ER Ca2+-ATPase (SERCA) in adipocytes and inhibits its activity, impairing Ca2+ transport and heat dissipation. We further demonstrate that NHLRC1, an E3 ubiquitin protein ligase implicated in proteasomal degradation of NNAT, is induced by cold exposure or β3-adrenergic stimulation, thus providing regulatory control at the protein level. This serves to link cold stimuli to NNAT degradation in adipose tissue, which in turn leads to enhanced SERCA activity.ConclusionsOur study implicates NNAT in the regulation of adipocyte thermogenesis.

Published
2023

36. CFTR regulates brown adipocyte thermogenesis via the cAMP/PKA signaling pathway

Author

Choi, Kyung-Mi, Cho, Sung-Hee, Kim, Jung Hak, Kim, Ae-Rhee Lilian, Kong, Xiangmudong, and Yoon, John C

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Rare Diseases, Nutrition, Cystic Fibrosis, Obesity, Lung, 2.1 Biological and endogenous factors, Aetiology, Metabolic and endocrine, Congenital, Animals, Mice, Adipocytes, Brown, Cystic Fibrosis Transmembrane Conductance Regulator, Energy Metabolism, Signal Transduction, Thermogenesis, Cyclic AMP-Dependent Protein Kinases, CFTR, thermogenesis, brown adipocyte, cAMP-PKA pathway, Clinical Sciences, Respiratory System, Clinical sciences
Abstract

BackgroundCystic fibrosis (CF) is characterized by reduced growth and lower body weight, which are multifactorial. CF mouse models lack key disease characteristics that predispose to a negative energy balance, such as pulmonary infections or exocrine pancreatic insufficiency, and yet they still exhibit a growth defect and an abnormally increased energy expenditure. Whether adipocyte thermogenesis contributes to the elevated resting energy expenditure in CF mice is unknown.MethodsWe examined the expression of CFTR in thermogenic brown adipose tissue (BAT) and investigated a functional role for CFTR using BAT-specific CFTR null mice (CFTRBATKO).ResultsThe CFTR protein is expressed in mouse BAT at levels comparable to those in the lungs. BAT-specific inactivation of CFTR in mice increases whole-body energy expenditure associated with sympathetic stimulation by cold exposure. Weight gain on a high-fat diet is attenuated in these mice. However, CFTR-deficient brown adipocytes themselves have impaired, rather than enhanced, thermogenic responses. These cells feature decreased lipolysis and blunted activation of the cAMP/PKA signaling pathway in response to adrenergic stimulation. This suggests that compensatory heat production in other tissues likely accounts for the increased systemic energy expenditure seen in CFTRBATKO mice.ConclusionsOur data reveal a new role for CFTR in the regulation of adipocyte thermogenesis.

Published
2023

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