Genetic complementation of a glucocorticoid receptor deficiency by expression of cloned receptor cDNA

Miesfeld, Roger L.; Rusconi, Sandro; Godowski, Paul J.; Maler, Bonnie A.; Okret, Sam; Wikström, Ann Charlotte; Gustafsson, Jan Åke; Yamamoto, Keith R.

doi:10.1016/0092-8674(86)90659-8

Cited by 679 publications

(278 citation statements)

References 34 publications

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“…For local administration of the antisense oligodeoxynucleotide to glucocorticoid receptor mRNA, scrambled sequence, sense or vehicle, cannulae were placed (under ether anaesthesia) bilaterally into the dentate gyrus of the hippocampus; AP = -3.6 mm from the bregma; L = + 1.4; DV = -3.3 from the dura mater (according to the Paxinos stereotaxic rat brain map). Antisense (5'-GGA-TTC-TTT-GGA-GTC-CAT-3') was targeted at the codons immediately downstream of the initiation codon (Miesfeld et al, 1986). All oligodeoxynucleotides were phosphorothioated in all positions, except the 3' and 5' base positions.…”

Section: Methodsmentioning

confidence: 99%

Antisense to the glucocorticoid receptor in hippocampal dentate gyrus reduces immobility in forced swim test

Korte

Kloet

Buwalda

et al. 1996

European Journal of Pharmacology

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Section: Methodsmentioning

confidence: 99%

Antisense to the glucocorticoid receptor in hippocampal dentate gyrus reduces immobility in forced swim test

Korte

Kloet

Buwalda

et al. 1996

European Journal of Pharmacology

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“…pTL2-GR consists of a 2.9-kb BamHI restriction fragment encompassing the full-length open reading frame of the rat GR (20) inserted into pTL2 (a derivative of pSG5, Ref. 21, containing an expanded multiple cloning site) digested with BglII and BamHI.…”

Section: Methodsmentioning

confidence: 99%

Acute Phase Mediators Modulate Thrombin-activable Fibrinolysis Inhibitor (TAFI) Gene Expression in HepG2 Cells

Boffa¹,

Hamill²,

Maret³

et al. 2003

Journal of Biological Chemistry

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Thrombin-activable fibrinolysis inhibitor (TAFI) has recently been identified as a positive acute phase protein in mice, an observation that may have important implications for the interaction of the coagulation, fibrinolytic, and inflammatory systems. Activated TAFI (TAFIa) inhibits fibrinolysis by removing the carboxylterminal lysines from partially degraded fibrin that are important for maximally efficient plasminogen activation. In addition, TAFIa has been shown to be capable of removing the carboxyl-terminal arginine residues from the anaphylatoxins and bradykinin, thus implying a role for the TAFI pathway in the vascular responses to inflammation. In the current study, we investigated the ability of acute phase mediators to modulate human TAFI gene expression in cultured human hepatoma (HepG2) cells. Surprisingly, we found that treatment of HepG2 cells with a combination of interleukin (IL)-1␤ and IL-6 suppressed endogenous TAFI mRNA abundance in HepG2 cells (ϳ60% decrease), while treatment with IL-1␤ or IL-6 alone had no effect. Treatment with IL-1␤ and/or IL-6 had no effect on TAFI promoter activity as measured using a luciferase reporter plasmid containing the human TAFI 5 -flanking region, whereas treatment with IL-1␤ and IL-6 in combination, but not alone, decreased the stability of the endogenous TAFI mRNA. Treatment with the synthetic glucocorticoid dexamethasone resulted in a 2-fold increase of both TAFI mRNA levels and promoter activity. We identified a functional glucocorticoid response element (GRE) in the human TAFI promoter between nucleotides ؊92 and ؊78. The GRE was capable of binding the glucocorticoid receptor, as assessed by gel mobility shift assays, and mutation of this element markedly decreased the ability of the TAFI promoter to be activated by dexamethasone.Thrombin activable fibrinolysis inhibitor (TAFI) 1 was first identified in 1989 by two independent groups as a basic carboxypeptidase present in fresh serum that was distinct from the constitutive basic carboxypeptidase N (1, 2). By virtue of the intrinsic instability of this enzyme, whose activity disappeared within 2 h upon incubation at 37°C, Hendriks et al.(1) designated the novel activity "unstable" carboxypeptidase or carboxypeptidase U (1). Campbell and Okada (2) determined that the enzyme removed arginine residues from substrates more efficiently than lysines and therefore designated it carboxypeptidase R (2). In 1991, Eaton et al. (3) isolated a cDNA encoding the zymogen form of the enzyme and found that it was highly homologous to pancreatic procarboxypeptidase B. Bajzar et al. (4) independently isolated a protein on the basis of its ability to inhibit fibrinolysis in the setting of sustained activation of the coagulation cascade; on the basis of this property, they named the protein TAFI. Amino acid sequence analysis of TAFI revealed it to be identical to plasma procarboxypeptidase B and procarboxypeptidases U and R. TAFI can be activated by thrombin (4), plasmin (5), and thrombin in complex with thrombomodulin (6), wi...

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“…For the overexpression vectors, full-length ERF189, ERF199, ERF115, ERF168, and ERF179 cDNAs were cloned into pGWB2 using Gateway cloning technology (Clontech). To generate the 35S-ERF189-GR vector, the full-length ERF189 cDNA and a rat glucocorticoid receptor (GR) sequence (Miesfeld et al, 1986) were inserted at BamHI and XbaI sites, and XbaI and SacI sites of pBluescriptII, respectively, and then the fusion constructs were placed into pBI121 at the BamHI and SacI sites. To generate the PMT2pro236-GUS binary vector for stable transformation, a promoter region of PMT2 (2236 to 21, numbered from the first ATG) was amplified from Nicotiana sylvestris genomic DNA by PCR and cloned upstream of the GUS sequence in pBI101 at SalI and BamHI sites.…”

Section: Plant Transformationmentioning

confidence: 99%

Clustered Transcription Factor Genes Regulate Nicotine Biosynthesis in Tobacco

2010

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Tobacco (Nicotiana tabacum) synthesizes nicotine and related pyridine alkaloids in the root, and their synthesis increases upon herbivory on the leaf via a jasmonate-mediated signaling cascade. Regulatory NIC loci that positively regulate nicotine biosynthesis have been genetically identified, and their mutant alleles have been used to breed low-nicotine tobacco varieties. Here, we report that the NIC2 locus, originally called locus B, comprises clustered transcription factor genes of an ethylene response factor (ERF) subfamily; in the nic2 mutant, at least seven ERF genes are deleted altogether. Overexpression, suppression, and dominant repression experiments using transgenic tobacco roots showed both functional redundancy and divergence among the NIC2-locus ERF genes. These transcription factors recognized a GCC-box element in the promoter of a nicotine pathway gene and specifically activated all known structural genes in the pathway. The NIC2-locus ERF genes are expressed in the root and upregulated by jasmonate with kinetics that are distinct among the members. Thus, gene duplication events generated a cluster of highly homologous transcription factor genes with transcriptional and functional diversity. The NIC2-locus ERFs are close homologs of ORCA3, a jasmonate-responsive transcriptional activator of indole alkaloid biosynthesis in Catharanthus roseus, indicating that the NIC2/ORCA3 ERF subfamily was recruited independently to regulate jasmonate-inducible secondary metabolism in distinct plant lineages.

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Genetic complementation of a glucocorticoid receptor deficiency by expression of cloned receptor cDNA

Cited by 679 publications

References 34 publications

Antisense to the glucocorticoid receptor in hippocampal dentate gyrus reduces immobility in forced swim test

Antisense to the glucocorticoid receptor in hippocampal dentate gyrus reduces immobility in forced swim test

Acute Phase Mediators Modulate Thrombin-activable Fibrinolysis Inhibitor (TAFI) Gene Expression in HepG2 Cells

Clustered Transcription Factor Genes Regulate Nicotine Biosynthesis in Tobacco

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