Identification of functional glucocorticoid response elements in the mouse FoxO1 promoter

Qin, Weiping; Pan, Jiangping; Qin, Yu; Lee, David N.; Bauman, William A.; Cardozo, Christopher P.

doi:10.1016/j.bbrc.2014.06.080

Cited by 33 publications

(31 citation statements)

References 22 publications

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“…Thus, Castillero et al (29) reported that peroxisome proliferator-activator (PPAR) β/δ up-regulates muscle FOXO1 expression with downstream up-regulation of ubiquitin ligases atrogin 1 and MuRF 1, which initiate muscle wasting and that the muscle wasting can be blocked by inhibition of PPAR β/δ. Moreover, a functional glucocorticoid response element has been identified in the mouse FOXO1 promoter (30), and the administration of an anti-oxidant, resveratrol, prevents dexamethasone stimulation of muscle atrophy-related ubiquitin ligases, the downstream signals from FOXO transcription factors, in vitro (31). The timing of the muscle atrophy induced by steroids is relatively rapid.…”

Section: Is There a Common Mechanism By Which Glucocorticoids Affect mentioning

confidence: 99%

The effect of glucocorticoids on bone and muscle

Klein

2015

Osteoporosis and Sarcopenia

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This article examines the current knowledge of the effects of both exogenous and endogenous glucocorticoids on bone and muscle. It demonstrates the similarity of effects of supraphysiologic loads of glucocorticoids regardless of whether they enter the body in the form of medication or are manufactured by the body in response to stimuli such as inflammation. The effects of endogenous glucocorticoids and the systemic inflammatory response resulting from pediatric burn injury are compared and the difficulty in sorting out which of the two factors is responsible for the ultimate effects on bone and muscle is pointed out. The focus then switches to the body’s response to the influence of both glucocorticoids and inflammatory cytokines and evidence supporting a common pathway of response to oxidative damage caused by both is discussed. Current recommended medical management of glucocorticoid-induced bone and muscle loss is discussed and the failure to reconcile current management with known mechanisms is highlighted.

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Section: Is There a Common Mechanism By Which Glucocorticoids Affect mentioning

confidence: 99%

The effect of glucocorticoids on bone and muscle

Klein

2015

Osteoporosis and Sarcopenia

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“…FoxOs are under the control of neurotransmitters (Liang et al, 2006) and glucocorticoids (Qin et al, 2014). FoxOs also regulate signals for cellular atrophy (Jaitovich et al, 2015), cellular morphology (Aranha et al, 2009) and adult neurogenesis and all of these physiological or pathological conditions contribute to the development of depression (Borre et al, 2014;Mahar et al, 2014;Anacker et al, 2013).…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Forkhead box O transcription factors as possible mediators in the development of major depression

et al. 2015

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“…There were 32 types of TFBSs within the first intron fragment, including the enhancers, i.e., CCAAT/enhancer binding protein beta (CEBPB), CCAAT/enhancer binding protein alpha (CEBP), cAMP activated protein (CAP), GATA binding elements (GATA1), LIM-only protein 2 (LMO2COM), myeloid zinc finger 1 (MZF1), simian-virus-40-protein-1 (SP1), basic helix–loop–helix transcription factors (USF), the repressor, acute myeloid leukemia-1 (AML1), and the enhancers or repressor GRE [17,31]. There were also some elements with unclear functions, i.e., AP1, replication initiator 1 (AP4), AP1FJ, c-Ets-1 (CETS1P54), c-Rel (CREL), caudal type homeobox 1 (CDXA), DELTAEF1, cyclin E/E2F (E2F), E47, GATA3, GATA2, hepatocyte nuclear factor 3β (HNF3β), ikappa B kinase-like 2 (IK2), c-Myb (MYB), MYOD, cardiac-specific homeobox protein (NKX25), OCT1, P53, sex-determining region Y (SRY), STAT, TATA, and TST1 [32,33,34,35,36] (Table S1).…”

Section: Resultsmentioning

confidence: 99%

Negative Glucocorticoid Response-Like Element from the First Intron of the Chicken Growth Hormone Gene Represses Gene Expression in the Rat Pituitary Tumor Cell Line

Lang

Qiu

et al. 2016

IJMS

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The effects of introns, especially the first intron, on the regulation of gene expression remains unclear. Therefore, the objective of the present study was to investigate the transcriptional regulatory function of intron 1 on the chicken growth hormone (cGH) gene in the rat pituitary tumor cell line (GH4-C1). Transient transfection using first-intron-inserted cGH complete coding sequences (CDSs) and non-intron-inserted cGH CDS plasmids, quantitative RT-PCR (qRT-PCR) and western blot assays were used to detect the expression of cGH. The reporter gene assay was also used to investigate the effect of a series of fragments in the first intron of cGH on gene expression in GH4-C1. All of the results revealed that a 200-bp fragment located in the +485/+684 region of intron 1 was essential for repressing the expression of cGH. Further informatics analysis showed that there was a cluster of 13 transcriptional factor binding sites (TFBSs) in the +485/+684 region of the cGH intron 1. Disruption of a glucocorticoid response-like element (the 19-nucleotide sequence 5′-AGGCTTGACAGTGACCTCC-3′) containing a T-box motif (TGACCT) located within this DNA fragment increased the expression of the reporter gene in GH4-C1. In addition, an electrophoretic mobility shift assay (EMSA) revealed a glucocorticoid receptor (GR) protein of rat binding to the glucocorticoid response-like element. Together, these results indicate that there is a negative glucocorticoid response-like element (nGRE) located in the +591/+609 region within the first intron of cGH, which is essential for the down-regulation of cGH expression.

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Identification of functional glucocorticoid response elements in the mouse FoxO1 promoter

Cited by 33 publications

References 22 publications

The effect of glucocorticoids on bone and muscle

The effect of glucocorticoids on bone and muscle

Forkhead box O transcription factors as possible mediators in the development of major depression

Negative Glucocorticoid Response-Like Element from the First Intron of the Chicken Growth Hormone Gene Represses Gene Expression in the Rat Pituitary Tumor Cell Line

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