Binding and activation of the human aldehyde dehydrogenase 2 promoter by hepatocyte nuclear factor 4

Stewart, Mark J.; Dipple, Katrina M.; Estonius, Mats; Nakshatri, Harikrishna; Everett, Lynn M.; Crabb, David W.

doi:10.1016/s0167-4781(98)00115-8

Cited by 35 publications

(18 citation statements)

References 39 publications

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“…factors (Stewart et al, 1996(Stewart et al, , 1998. The A and G alleles occur within an element previously identified in DNAse footprinting assays as the FP330-5' site (Stewart et al, 1998).…”

Section: 56mentioning

confidence: 98%

“…Electrophoretic mobility shift assays (EMSA) were performed by radiolabeling double-stranded oligonucleotides corresponding to the FP330-5' footprint (Stewart et al, 1998) with either A or G at position -361. Reticuloqte lysates (1-2 pl) containing COUP-TFI or ARP-1 were incubated with 1-2 pg of nonspecific competitor DNA (poly (dIC)) in binding buffer containing 10 mM HEPES, p H 7.9, 60 m M KCI, 1 mM EDTA, and 7% (v/v) glycerol on ice for 15 min.…”

Section: Dna Binding Assaysmentioning

confidence: 99%

“…We found that ARP-1 and COUP-TFI affect the expression of several luciferase plasmids (L. Everett and D. Crabb, unpublished data) and therefore initially normalized the CAT activity to the amount of protein in the nuclear extract. Subsequent experiments were normalized to luciferase activity as previously described (Stewart et al, 1998).…”

Section: Transfection Of Cultured Cellsmentioning

confidence: 99%

“…The A and G alleles occur within an element previously identified in DNAse footprinting assays as the FP330-5' site (Stewart et al, 1998). Methylation interference assays had shown the contact points for transcription factors to correspond to a direct repeat (DR) of the motif common to binding sites for the members of the nuclear receptor family (Mangelsdorf et al, 1995).…”

Section: 56mentioning

confidence: 99%

“…The CCAAT box is a binding site for the ubiquitous factor NF-Y (Stewart et al, 1996). Further upstream is a complex nuclear receptor response element that has been found to bind a number of nuclear receptors (Stewart et al, 1998), and to be activated by hepatocyte nuclear factor 4 (HNF-4) and retinoid X receptor (RXR). At the 5' end of this region is an element bound by the orphan receptors apolipoprotein A regulatory protein 1 (ARP-1) and chicken ovalbumin upstream promoter-transcription factor (COUP-TF).…”

mentioning

confidence: 99%

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An A/G Polymorphism in the Promoter of Mitochondrial Aldehyde Dehydrogenase (ALDH2): Effects of the Sequence Variant on Transcription Factor Binding and Promoter Strength

Chou

Stewart

Carr

et al. 1999

Alcoholism Clin & Exp Res

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Section: 56mentioning

confidence: 98%

Section: Dna Binding Assaysmentioning

confidence: 99%

Section: Transfection Of Cultured Cellsmentioning

confidence: 99%

Section: 56mentioning

confidence: 99%

mentioning

confidence: 99%

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An A/G Polymorphism in the Promoter of Mitochondrial Aldehyde Dehydrogenase (ALDH2): Effects of the Sequence Variant on Transcription Factor Binding and Promoter Strength

Chou

Stewart

Carr

et al. 1999

Alcoholism Clin & Exp Res

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Changes in DNA methylation persist over time in males with severe alcohol use disorder—A longitudinal follow‐up study

Soundararajan

Agrawal

Purushottam

et al. 2021

American J of Med Genetics Pt B

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Treatment strategies for alcohol use disorder (AUD) aim for abstinence or harm reduction. While deranged biochemical parameters reverse with alcohol abstinence, whether molecular changes at the epigenetic level reverse is not clearly understood.We investigated whether the reduction from high alcohol use reflects DNA methylation at the gene-specific and global level. In subjects seeking treatment for severe AUD, we assessed gene-specific (aldehyde dehydrogenase [ALDH2]/methylene tetrahydrofolate reductase [MTHFR]) and global (long interspersed elements [LINE-1]) methylation across three-time points (baseline, after detoxification and at an early remission period of 3 months), in peripheral blood leukocytes. We observed that both gene-specific and global DNA methylation did not change over time, irrespective of the drinking status at 3 months (52% abstained from alcohol). Further, we also compared DNA methylation in AUD subjects with healthy controls. At baseline, there was a significantly higher gene-specific DNA methylation (ALDH2: p < .001 and MTHFR: p = .001) and a significant lower global methylation (LINE-1: p = .014) in AUD as compared to controls. Our results suggest that epigenetic changes at the DNA methylation level associated with severe AUD persist for at least 3 months of treatment. K E Y W O R D Salcohol abstinence, alcohol use disorder, DNA methylation, long interspersed nucleotide elements, pyrosequencing | INTRODUCTIONAlcohol use accounts for 13.5% of total deaths among young adults worldwide (WHO, 2018). About 29% of men aged 15-54 years consume alcohol in India, with significant numbers using it daily (12%) or weekly (41%) (NFHS-4, 2015(NFHS-4, -2016. alcohol use disorder (AUD) is a chronic relapsing disorder, with only 15-16% of former users in India abstaining from alcohol over the past year (WHO, 2018). With the focus on abstinence and harm reduction approaches in treating AUD, whether molecular adaptations associated with chronic alcohol use reverse with alcohol abstinence poses an intriguing question.Among the molecular adaptations associated with chronic alcohol use, epigenetic changes are significant because of the associated downstream effects on gene expression (Ponomarev, Wang, Zhang, Harris, & Mayfield, 2012). These epigenetic changes are associated with onset, progression to, and persistence of dependence states (Cecil, Walton, & Viding, 2016;Jangra et al., 2016). It is well established that epigenome-wide, global, and gene-specific studies indicate differential methylation related to alcohol consumption

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Effect of rosiglitazone on the differential expression of obesity and insulin resistance associated proteins in lep/lep mice

et al. 2003

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Peroxisome proliferator-activated receptors (PPARs) participate in the molecular mechanism of pathologies with altered lipid homeostasis such as type 2 diabetes or obesity. The insulin sensitizer drug, rosiglitazone, has been shown to bind and activate PPAR-gamma1 in adipocytes and PPAR-gamma2 in hepatocytes. The identification of new molecular targets associated with fatty acid oxidation and PPAR-gamma nuclear receptor regulation in insulin resistance tissues is a key research goal. In the present study, we have used a proteomic approach to identify such targets. Lean and obese C57 Bl/6J lep/lep mice were given BRL49653, rosiglitazone, 10 mg/kg diet, by dietary admixture for 7 days. Rosiglitazone normalized the impaired glucose tolerance and dyslipidemia in lep/lep mice but had no significant effect in the lean mice. Samples of liver, white and brown adipose tissue, and muscle proteins were obtained and 100 microg of proteins was arrayed by two-dimensional gel electrophoresis. Thirty-four polypeptides were differentially expressed (p < 0.05) between lep/lep and lean mice and eleven were significantly (p < 0.05) modulated by rosiglitazone treatment of the obese mice. None of the proteins was modulated by rosiglitazone treatment of the lean mice. The identity of these differentially expressed proteins was made using tandem mass spectrometric analysis and revealed components of fatty acid and carbohydrate metabolism as well as proteins with unknown function.

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Binding and activation of the human aldehyde dehydrogenase 2 promoter by hepatocyte nuclear factor 4

Cited by 35 publications

References 39 publications

An A/G Polymorphism in the Promoter of Mitochondrial Aldehyde Dehydrogenase (ALDH2): Effects of the Sequence Variant on Transcription Factor Binding and Promoter Strength

An A/G Polymorphism in the Promoter of Mitochondrial Aldehyde Dehydrogenase (ALDH2): Effects of the Sequence Variant on Transcription Factor Binding and Promoter Strength

Changes in DNA methylation persist over time in males with severe alcohol use disorder—A longitudinal follow‐up study

Effect of rosiglitazone on the differential expression of obesity and insulin resistance associated proteins in lep/lep mice

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