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Your search keyword '"Sho Morioka"' showing total 3 results
Start Over Author "Sho Morioka" Journal journal of cell science
3 results on '"Sho Morioka"'

1. TAK1 determines susceptibility to endoplasmic reticulum stress and hypothalamic leptin resistance

Author

Hiroshi Hanafusa, Sho Morioka, H. Troy Ghashghaei, Nagendran Muthusamy, Kazuhito Sai, Kunihiro Matsumoto, Jun Ninomiya-Tsuji, and Giichi Takaesu

Subjects
0301 basic medicine, medicine.medical_specialty, MAP kinase kinase kinase, Endoplasmic reticulum, Cellular homeostasis, Cell Biology, Biology, MAP3K7, 03 medical and health sciences, 030104 developmental biology, Endocrinology, Downregulation and upregulation, Internal medicine, medicine, Unfolded protein response, ASK1, Protein kinase A
Abstract

Sustained endoplasmic reticulum (ER) stress disrupts normal cellular homeostasis and leads to the development of many types of human diseases, including metabolic disorders. TAK1 (also known as MAP3K7) is a member of the mitogen-activated protein kinase kinase kinase (MAP3K) family and is activated by a diverse set of inflammatory stimuli. Here, we demonstrate that TAK1 regulates ER stress and metabolic signaling through modulation of lipid biogenesis. We found that deletion of Tak1 increased ER volume and facilitated ER-stress tolerance in cultured cells, which was mediated by upregulation of sterol-regulatory-element-binding protein (SREBP)-dependent lipogenesis. In the in vivo setting, central nervous system (CNS)-specific Tak1 deletion upregulated SREBP-target lipogenic genes and blocked ER stress in the hypothalamus. Furthermore, CNS-specific Tak1 deletion prevented ER-stress-induced hypothalamic leptin resistance and hyperphagic obesity under a high-fat diet (HFD). Thus, TAK1 is a crucial regulator of ER stress in vivo, which could be a target for alleviation of ER stress and its associated disease conditions.

Published
2016

2. TAK1 determines susceptibility to endoplasmic reticulum stress and leptin resistance in the hypothalamus

Author

Kazuhito, Sai, Sho, Morioka, Giichi, Takaesu, Nagendran, Muthusamy, H Troy, Ghashghaei, Hiroshi, Hanafusa, Kunihiro, Matsumoto, and Jun, Ninomiya-Tsuji

Subjects
Leptin, Mice, Knockout, Sterol Regulatory Element Binding Proteins, Mice, Hypothalamus, Animals, Obesity, Hyperphagia, Endoplasmic Reticulum Stress, MAP Kinase Kinase Kinases, Dietary Fats, Research Article
Abstract

Sustained endoplasmic reticulum (ER) stress disrupts normal cellular homeostasis and leads to the development of many types of human diseases, including metabolic disorders. TAK1 (also known as MAP3K7) is a member of the mitogen-activated protein kinase kinase kinase (MAP3K) family and is activated by a diverse set of inflammatory stimuli. Here, we demonstrate that TAK1 regulates ER stress and metabolic signaling through modulation of lipid biogenesis. We found that deletion of Tak1 increased ER volume and facilitated ER-stress tolerance in cultured cells, which was mediated by upregulation of sterol-regulatory-element-binding protein (SREBP)-dependent lipogenesis. In the in vivo setting, central nervous system (CNS)-specific Tak1 deletion upregulated SREBP-target lipogenic genes and blocked ER stress in the hypothalamus. Furthermore, CNS-specific Tak1 deletion prevented ER-stress-induced hypothalamic leptin resistance and hyperphagic obesity under a high-fat diet (HFD). Thus, TAK1 is a crucial regulator of ER stress in vivo, which could be a target for alleviation of ER stress and its associated disease conditions.

Published
2015

3. TAK1 determines susceptibility to endoplasmic reticulum stress and leptin resistance in the hypothalamus.

Author

Kazuhito Sai, Sho Morioka, Giichi Takaesu, Muthusamy, Nagendran, Ghashghaei, H. Troy, Hiroshi Hanafusa, Kunihiro Matsumoto, and Jun Ninomiya-Tsuji

Subjects
*ENDOPLASMIC reticulum, *ORGANELLES, *HYPOTHALAMUS, *OBESITY, *METABOLIC disorders
Abstract

Sustained endoplasmic reticulum (ER) stress disrupts normal cellular homeostasis and leads to the development of many types of human diseases, including metabolic disorders. TAK1 (also known as MAP3K7) is a member of the mitogen-activated protein kinase kinase kinase (MAP3K) family and is activated by a diverse set of inflammatory stimuli. Here, we demonstrate that TAK1 regulates ER stress and metabolic signaling through modulation of lipid biogenesis. We found that deletion of Tak1 increased ER volume and facilitated ER-stress tolerance in cultured cells, which was mediated by upregulation of sterol-regulatory-element-binding protein (SREBP)- dependent lipogenesis. In the in vivo setting, central nervous system (CNS)-specific Tak1 deletion upregulated SREBP-target lipogenic genes and blocked ER stress in the hypothalamus. Furthermore, CNS-specific Tak1 deletion prevented ER-stress-induced hypothalamic leptin resistance and hyperphagic obesity under a high-fat diet (HFD). Thus, TAK1 is a crucial regulator of ER stress in vivo, which could be a target for alleviation of ER stress and its associated disease conditions. [ABSTRACT FROM AUTHOR]

Published
2016
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