Association of the dioxin receptor with the Mr 90,000 heat shock protein: A structural kinship with the glucocorticoid receptor

Denis, Marc G.; Cuthill, Scott; Wikström, Ann Charlotte; Poellinger, Lorenz; Gustafsson, Jan‐Åke

doi:10.1016/s0006-291x(88)80566-7

Cited by 230 publications

(103 citation statements)

References 34 publications

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“…51,52 The generation of antibodies capable of immunoprecipitating the glucocorticoid receptor-associated hsp90 53-55 and the AhR helped identify the hsp90 as part of the unliganded AhR complex with two different approaches. 56,57 Before the cloning of the AhR, a subunit of the liganded complex was identified and thought to be required for the translocation of the AhR into the nucleus. 58,59 Briefly, a cell line expressing a "functional" AhR but uninducible for P 1 -450 (CYP1A1) was systematically transfected with a cDNA library.…”

Section: Identification and Cloning Of The Ahrmentioning

confidence: 99%

The Aryl Hydrocarbon Receptor Complex and the Control of Gene Expression

Beischlag

Morales

Hollingshead

et al. 2008

Crit Rev Eukar Gene Expr

632

587

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The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that controls the expression of a diverse set of genes. The toxicity of the potent AhR ligand 2,3,7,8-tetrachlorodibenzop-dioxin is almost exclusively mediated through this receptor. However, the key alterations in gene expression that mediate toxicity are poorly understood. It has been established through characterization of AhR-null mice that the AhR has a required physiological function, yet how endogenous mediators regulate this orphan receptor remains to be established. A picture as to how the AhR/ARNT heterodimer actually mediates gene transcription is starting to emerge. The AhR/ ARNT complex can alter transcription both by binding to its cognate response element and through tethering to other transcription factors. In addition, many of the coregulatory proteins necessary for AhR-mediated transcription have been identified. Cross talk between the estrogen receptor and the AhR at the promoter of target genes appears to be an important mode of regulation. Inflammatory signaling pathways and the AhR also appear to be another important site of cross talk at the level of transcription. A major focus of this review is to highlight experimental efforts to characterize nonclassical mechanisms of AhR-mediated modulation of gene transcription.

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Section: Identification and Cloning Of The Ahrmentioning

confidence: 99%

The Aryl Hydrocarbon Receptor Complex and the Control of Gene Expression

Beischlag

Morales

Hollingshead

et al. 2008

Crit Rev Eukar Gene Expr

632

587

View full text Add to dashboard Cite

show abstract

“…Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that residents in the cytoplasm as an inactive form by binding of chaperon proteins such as 90 kDa heat shock protein [14,15] and forms heterodimer with AHR nuclear translocator (ARNT) [16] to activate xenobiotic response element located upstream of the target genes such as CYP1A1 due to activation of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-related ligands binding and translocation into the nucleus [17,18]. Nevertheless, AHR is postulated to play important roles not only in the regulation of xenobiotic metabolism but also in the regulation of differentiation in pro-inflammatory T cells [19], ketarinocytes [20], myeloblastic leukemia cells [21], and Neuro2a cells [22].…”

Section: Introductionmentioning

confidence: 99%

Silencing of miR-124 induces neuroblastoma SK-N-SH cell differentiation, cell cycle arrest and apoptosis through promoting AHR

Huang¹,

Chang²,

Chen³

et al. 2011

FEBS Letters

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a b s t r a c tNeuroblastoma is the most common extracranial solid tumor in children. We investigate whether miR-124, the abundant neuronal miRNA, plays a pivotal role in neuroblastoma. Knockdown of miR-124 promotes neuroblastoma SK-N-SH cell differentiation, cell cycle arrest and apoptosis. Further miR-124 is predicted to target aryl hydrocarbon receptor (AHR) which may promote neuroblastoma cell differentiation. We validate that miR-124 may suppress the expression of AHR by targeting its 3 0 -UTR. These results suggest that miR-124 could serve as a potential therapeutic target of neuroblastoma.

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“…Ah receptor (AhR) is clarified as functioning as a mediator of the action of TCDD in this process, and is a member of a family of transcription factors which carry basic helix-loop-helix and PAS (a conserved region among Per, Arnt/AhR and Sim) domains in the N-terminal half (Swanson & Bradfield 1993;Hankinson 1995). In response to the binding of TCDD, AhR-which is present in the cytoplasm in association with HSP90 (Denis et al 1988;Perdew 1988)-translocates to the nucleus upon dissociation from HSP90 (Whitelaw et al 1993) and dimerizes with another bHLH/PAS protein, Arnt (Ah receptor nuclear translocator). This heterodimer recognizes and binds the XRE sequence upstream of the target genes encoding a group of xenobiotic-metabolizing enzymes to activate their transcription (Reyes et al 1992;Matsushita et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Loss of teratogenic response to 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) in mice lacking the Ah (dioxin) receptor

et al. 1997

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Background: The aryl hydrocarbon receptor (AhR or dioxin receptor) is a ligand-activated transcription factor that is considered to mediate pleiotropic biological responses such as teratogenesis, tumour promotion, epithelial hyperplasia and the induction of drug-metabolizing enzymes to environmental contaminants usually represented by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In contrast to the role of AhR in the regulatory mechanism of xenobiotic-metabolizing enzymes, there is no direct proof that the AhR is involved in the teratogenic effects of TCDD.

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Association of the dioxin receptor with the Mr 90,000 heat shock protein: A structural kinship with the glucocorticoid receptor

Cited by 230 publications

References 34 publications

The Aryl Hydrocarbon Receptor Complex and the Control of Gene Expression

The Aryl Hydrocarbon Receptor Complex and the Control of Gene Expression

Silencing of miR-124 induces neuroblastoma SK-N-SH cell differentiation, cell cycle arrest and apoptosis through promoting AHR

Loss of teratogenic response to 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) in mice lacking the Ah (dioxin) receptor

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