Identification of cis-regulatory elements and trans-acting proteins of the rat carbohydrate response element binding protein gene

Satoh, S.; Masatoshi, Sakie; Shou, Zhangfei; Yamamoto, Taichi; Ishigure, Tatsuya; Semii, Atsushi; Yamada, Kazuya; Noguchi, T.

doi:10.1016/j.abb.2007.02.028

Cited by 13 publications

(4 citation statements)

References 39 publications

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“…BAT expression of Chrebpß was also SCAPdependent (SI Appendix, Fig. S7A), consistent with the conclusion that SREBP regulated Chrebpß expression as previously described (35). In absence of SREBP, BAT mass was decreased (Fig.…”

Section: Fatty Acid Oxidationsupporting

confidence: 90%

“…Wild-type C57BL/6J male mice were obtained from Jackson Labs Technologies, Inc. Scap Flox/Flox mice (25) were backcrossed to the C57BL/6J genetic background for at least 7 generations (kindly provided by Tim Osborne, Johns Hopkins All Children's Hospital, St. Petersburg, FL). Scap Flox/Flox mice were bred to Ucp1-CreER mice on a C57BL/6J background [kindly provided by David Guertin, University of Massachusetts Medical School, Worcester, MA with generous permission from Christian Wolfrum, ETH Zürich, Zürich, Switzerland (35)]. To induce the expression of the Ucp1-CreER, 6-wk-old mice were injected i.p.…”

Section: Methodsmentioning

confidence: 99%

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Circadian lipid synthesis in brown fat maintains murine body temperature during chronic cold

Adlanmérini

Carpenter

Remsberg

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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Ambient temperature influences the molecular clock and lipid metabolism, but the impact of chronic cold exposure on circadian lipid metabolism in thermogenic brown adipose tissue (BAT) has not been studied. Here we show that during chronic cold exposure (1 wk at 4 °C), genes controlling de novo lipogenesis (DNL) includingSrebp1, the master transcriptional regulator of DNL, acquired high-amplitude circadian rhythms in thermogenic BAT. These conditions activated mechanistic target of rapamycin 1 (mTORC1), an inducer ofSrebp1expression, and engaged circadian transcriptional repressors REV-ERBα and β as rhythmic regulators ofSrebp1in BAT. SREBP was required in BAT for the thermogenic response to norepinephrine, and depletion of SREBP prevented maintenance of body temperature both during circadian cycles as well as during fasting of chronically cold mice. By contrast, deletion of REV-ERBα and β in BAT allowed mice to maintain their body temperature in chronic cold. Thus, the environmental challenge of prolonged noncircadian exposure to cold temperature induces circadian induction of SREBP1 that drives fuel synthesis in BAT and is necessary to maintain circadian body temperature during chronic cold exposure. The requirement for BAT fatty acid synthesis has broad implications for adaptation to cold.

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Section: Fatty Acid Oxidationsupporting

confidence: 90%

Section: Methodsmentioning

confidence: 99%

Circadian lipid synthesis in brown fat maintains murine body temperature during chronic cold

Adlanmérini

Carpenter

Remsberg

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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“…This may reflect the presence of a sterol-response element in the promoter of the ChREBP gene. 22 In addition to this induction of ChREBP by ethanol, our study provides additional mechanisms for increased ChREBP transcriptional activity. These mechanisms appear to involve the ability of ethanol to activate PP2A, because okadaic acid partially reversed this effect.…”

Section: Discussionmentioning

confidence: 72%

Activation of Carbohydrate Response Element-Binding Protein by Ethanol

Liangpunsakul

Ross

Crabb

2013

Journal of Investigative Medicine

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Carbohydrate response element binding protein (ChREBP) is a transcription factor involved in hepatic lipogenesis. Its function is in part under the control of AMP-activated protein kinase (AMPK) and protein phosphatase 2A (PP2A). Given known effects of ethanol on AMPK and PP2A, it is plausible that ethanol might enhance fatty acid synthesis by increasing the activity of ChREBP. We hypothesized that another potential pathway of ethanol-induced hepatic steatosis is mediated by activation of ChREBP. Methods The effects of ethanol on ChREBP were assessed in hepatoma cells and in C57BL/6J mice fed with the Lieber-DeCarli diet. Results When the cells were exposed to ethanol (50 mM) for 24 hrs, the activity of a liver pyruvate kinase (LPK) promoter-luciferase reporter was increased by ~4-fold. Ethanol feeding of mice resulted in the translocation of ChREBP from cytosol to the nucleus. PP2A activity was increased in the liver of ethanol-fed mice by 22%. We found no difference in the levels of hepatic Xu-5-P between ethanol-fed mice and controls. Transfection of a constitutively active AMPK expression plasmid suppressed the basal activity of the LPK luciferase reporter and abolished the effect of ethanol on the reporter activity. However, transfection of rat hepatoma cells with a dominant negative AMPK expression plasmid induced basal LPK luciferase activity by only ~20%. The effect of ethanol on ChREBP was attenuated in the presence of okadaic acid, an inhibitor of PP2A. Conclusions The effects of ethanol on AMPK and PP2A may result in activation of ChREBP, providing another potential mechanism for ethanol-induced hepatic steatosis. However, additional okadaic acid-insensitive effects appear to be important as well.

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“…Besides post‐translational modifications, ChREBP transcriptional activity at the ChoRE of its target genes can be modulated by various co‐activators, co‐repressors and other co‐localised transcription factors . ChREBP mRNA expression can also be regulated by various transcription factors that can bind to the ChREBP promoter, including LXR, TR‐β1, NF‐Y, SREBP‐1a, Sp1, HNF4α, Foxa1 and Foxa2, which increase ChREBP gene transcription, and Oct‐1, which represses ChREBP gene transcription. Detailed descriptions of all ChREBP modifications have been reviewed previously and are not discussed in detail here.…”

Section: Chrebp Regulationmentioning

confidence: 99%

The regulation and role of carbohydrate response element‐binding protein in metabolic homeostasis and disease

Jois

Sleeman

2017

J Neuroendocrinology

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The transcription factor carbohydrate response element‐binding protein (ChREBP) is a member of the basic helix‐loop‐helix leucine zipper transcription factor family. Under high‐glucose conditions, it has a role in regulating the expression of key genes involved in various pathways, including glycolysis, gluconeogenesis and lipogenesis. It does this by forming a tetrameric complex made up of two ChREBP/Mlx heterodimers, which enables it to bind to the carbohydrate response element (ChoRE) in the promoter region of its target genes to regulate transcription. Because ChREBP plays a key role in glucose signalling and metabolism, and aberrations in glucose homeostasis are often present in metabolic diseases, this transcription factor presents itself as an enticing target with respect to further understanding metabolic disease mechanisms and potentially uncovering new therapeutic targets.

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Identification of cis-regulatory elements and trans-acting proteins of the rat carbohydrate response element binding protein gene

Cited by 13 publications

References 39 publications

Circadian lipid synthesis in brown fat maintains murine body temperature during chronic cold

Circadian lipid synthesis in brown fat maintains murine body temperature during chronic cold

Activation of Carbohydrate Response Element-Binding Protein by Ethanol

The regulation and role of carbohydrate response element‐binding protein in metabolic homeostasis and disease

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