AGP/EBP(LAP) expressed in rat hepatoma cells interacts with multiple promoter sites and is necessary for maximal glucocorticoid induction of the rat alpha-1 acid glycoprotein gene.

Williams, P. Mickey; Ratajczak, Thomas; Lee, S. C.; Ringold, Gordon M.

doi:10.1128/mcb.11.10.4959

Cited by 45 publications

(16 citation statements)

References 36 publications

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“…The mechanism for the enhancement of the glucocorticoid response by RAP is unknown but could involve strengthening of the GR interaction with its DNA-binding site or tethering of a protein(s) to allow the formation of a bridge to the basal transcription machinery. Interestingly, similar to findings for the GS gene expressed in chick neural retina, it was recently shown that collaboration of the C/EBP family member LAP (liver-activating protein) is required for maximal glucocorticoid induction of the rat alpha-1 acid glycoprotein gene (76). A C/EBP protein is also involved in glucocorticoid activation of the angiotensinogen gene (10).…”

Section: Discussionmentioning

confidence: 62%

“…Furthermore, a cis-regulatory sequence just 5' to the GR-binding site was shown to be required for the glucocorticoid response in the responsive E10 neural retina (82). This finding suggests that GS expression, similar to the case for several other glucocorticoidcontrolled genes (10,20,21,29,34,76), is controlled by a "composite" GRE (53), alternatively defined as glucocorticoid-responsive unit (34). These composite GREs require non-steroid-binding proteins in addition to the GR for eliciting the glucocorticoid response.…”

mentioning

confidence: 64%

“…2A). The transactivation function of GR may be limited or repressed in more complex glucocorticoid-responsive promoters containing composite GREs, depending on the availability of various factors that act cooperatively with GR (10,20,21,29,34,65,69,75,76,82) or antagonize GR activity (1,53,64,83). This is indeed the case for the retinal endogenous GS gene.…”

Section: Discussionmentioning

confidence: 99%

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Involvement of a C/EBP-like protein in the acquisition of responsiveness to glucocorticoid hormones during chick neural retina development.

Ben-Or¹,

Okret²

1993

Mol. Cell. Biol.

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The glucocorticoid receptor in chicken embryonic neural retina is expressed early in ontogeny, yet the tissue's response to the glucocorticoid hormone, i.e., induction of glutamine synthetase (GS), develops later, only during week 2 of ontogeny. Transient transfection of embryonic day 7 (E7) retinal cells, which are nonresponsive to glucocorticoids, with chimeric plasmids containing the chloramphenicol acetyltransferase reporter gene under the control of glucocorticoid-responsive promoters demonstrated that GR in E7 cells is a functional transactivating factor. We show that the limiting transcription factor that controls the developmental acquisition of responsiveness to glucocorticoids is similar to a CCAAT enhancer-binding protein (C/EBP). This protein recognizes a sequence in the promoter of the chick GS gene, which is required for eliciting the glucocorticoid response. Retinal C/EBP-like protein was not detected in the glucocorticoid-nonresponsive (E7) proliferating glioblasts but was found to be present in the glucocorticoid-responsive (E12) postmitotic cells.

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Section: Discussionmentioning

confidence: 62%

mentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

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Involvement of a C/EBP-like protein in the acquisition of responsiveness to glucocorticoid hormones during chick neural retina development.

Ben-Or¹,

Okret²

1993

Mol. Cell. Biol.

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“…In addition to C/EBP␤-binding motifs, a glucocorticoid-responsive element (GRE) also exists between Ϫ120 and Ϫ107 in the 5Ј-flanking region of the agp gene (8,18). Previous reports showed that maximal induction of the agp gene by glucocorticoids also requires another C/EBP␤-binding element located downstream of GRE (34,50,60). The synergistic interaction between cytokines and glucocorticoids has been attributed to protein-protein interactions between C/EBP␤ and the glucocorticoid receptor (GR) (45).…”

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confidence: 99%

“…Previous studies indicated that maximal induction of the agp gene by glucocorticoid requires the downstream C/EBP␤-binding sequences (34,50,60). To further study the TIF1␤-mediated GR induction of the agp gene, we performed transfection assays using agp promoters containing mutated C/EBP␤-binding sites or mutated GRE.…”

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confidence: 99%

Coactivator TIF1β Interacts with Transcription Factor C/EBPβ and Glucocorticoid Receptor To Induce α1-Acid Glycoprotein Gene Expression

Chang

Chen

Lee

1998

Molecular and Cellular Biology

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The transcription of the ␣1-acid glycoprotein gene is induced by inflammatory cytokines and glucocorticoids. C/EBP␤ is a major transcription factor involved in the induction of the agp gene by some cytokines. In this report, we have identified a novel transcriptional intermediary factor, TIF1␤, which could enhance the transcription of the agp gene by the glucocorticoid receptor (GR) and C/EBP␤. TIF1␤ belongs to a subgroup of RING (really interesting new gene) finger proteins that contain a RING finger preceding two B box-type fingers and a putative coiled-coil domain (RBCC domain). Immunoprecipitation experiments showed that the interaction between GR and TIF1␤ is ligand independent. The overexpression of the TIF1␤ gene enhances GR-regulated expression in a ligand-and glucocorticoid-responsive element (GRE)-dependent manner. TIF1␤ can also augment C/EBP␤-mediated activity on wild-type and GRE-mutated agp genes, but this augmentation is diminished when all three C/EBP␤-binding elements are mutated. Functional and biochemical characterizations indicated that the bZIP domain of C/EBP␤ and the RBCC domain, plant homeodomain finger, and bromodomain of TIF1␤ are crucial for the interactions of these proteins. Taken together, these results suggest that TIF1␤ serves as a converging mediator of signal transduction pathways of glucocorticoids and some inflammatory cytokines.

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Carbon tetrachloride induction of rapid changes in liver nuclear protein factors capable of sequence‐specific binding to regulatory elements in the long terminal repeat of polytropic‐class endogenous murine leukemia virus—related proviruses

Wang

Henley

Yang

et al. 1993

Molecular Carcinogenesis

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Treatment of mice with hepatic carcinogens, including CCl4, has been shown to rapidly enhance the transcription of endogenous murine leukemia virus-related proviral sequences in the liver. To understand the mechanism for this transcriptional stimulation, we used nuclear protein preparations from mouse livers to perform DNase I protection analyses and identified nuclear protein binding on approximately 20 individual sequences within the regulatory regions of the long terminal repeat (LTR) of a polytropic-class endogenous provirus clone. From 3 to 144 h after treatment with CCl4, the livers of FVB/N mice were analyzed for specific nuclear protein binding to the LTR DNA. Three to nine hours after CCl4 treatment, decreased protection was seen at potential regulatory cis-elements throughout the LTR, including specific sites within the putative negative regulatory element (located 5' of the consensus enhancer sequences) and the 3' terminal portion of the polytropic class-specific enhancer-like inserted sequence element and around the CCAA(C/T) box in the promoter region. In addition, by 3-6 h after treatment, a transient increase in protection activity for the transcription initiation site occurred. The loss of cis-element protection expanded to other binding sites and became most marked by 48 h after treatment. As the regenerating liver recovered, the nuclear protein binding activities for these LTR sequences also recovered, but protection at the TATAA and transcription initiation sites remained deprotected at 144 h after treatment. Nuclear protein protection of other sites, particularly in the conserved LTR enhancer sequences, was minimally affected by CCl4 treatment. Three nuclear protein binding sites that showed rapid CCl4-induced kinetic changes were homologous to the consensus sequence for the binding of the transcription factor families MEF-2, HNF-1, and C/EBP. The complex kinetic changes in factors that may contribute to the rapid and transient induction of endogenous retroviral gene expression in the liver after CCl4 exposure are discussed.

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AGP/EBP(LAP) expressed in rat hepatoma cells interacts with multiple promoter sites and is necessary for maximal glucocorticoid induction of the rat alpha-1 acid glycoprotein gene.

Cited by 45 publications

References 36 publications

Involvement of a C/EBP-like protein in the acquisition of responsiveness to glucocorticoid hormones during chick neural retina development.

Involvement of a C/EBP-like protein in the acquisition of responsiveness to glucocorticoid hormones during chick neural retina development.

Coactivator TIF1β Interacts with Transcription Factor C/EBPβ and Glucocorticoid Receptor To Induce α1-Acid Glycoprotein Gene Expression

Carbon tetrachloride induction of rapid changes in liver nuclear protein factors capable of sequence‐specific binding to regulatory elements in the long terminal repeat of polytropic‐class endogenous murine leukemia virus—related proviruses

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