Publications
1032 results found
Finney PA, Belvisi MG, Adcock IM, et al., 1998, Chronic treatment with salbutamol causes <i>in vivo </i>heterologous desensitisation of β<sub>2</sub>-adrenoceptors and down-regulation of G<sub>sα</sub> in Sprague-Dawley rats, Publisher: SPRINGER VERLAG, Pages: R648-R648, ISSN: 0028-1298
Adcock IM, Barnes PJ, 1998, Transcription factors in asthma, 5th International Conference on Asthma, Publisher: ELSEVIER ACADEMIC PRESS INC, Pages: 25-45
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- Citations: 2
Seybold J, Newton R, Wright L, et al., 1997, Transcriptional up-regulation of cAMP phosphodiesterases 4A5, 4D1, 4D2 and 4D3 in jurkat T-cells:: Role in β<sub>2</sub>-adrenoceptor desensitisation, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 122, Pages: U34-U34, ISSN: 0007-1188
Newton R, Stevens DA, Hart LA, et al., 1997, Superinduction of COX-2 mRNA by cycloheximide and interleukin-1 beta involves increased transcription and correlates with increased NF-kappa B and JNK activation, FEBS LETTERS, Vol: 418, Pages: 135-138, ISSN: 1873-3468
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- Citations: 104
Newton R, Kuitert LME, Bergmann M, et al., 1997, Evidence for involvement of NF-kappa B in the transcriptional control of COX-2 gene expression by IL-1 beta, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 237, Pages: 28-32, ISSN: 0006-291X
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- Citations: 349
Liu SF, Haddad E, Adcock I, et al., 1997, Inducible nitric oxide synthase after sensitization and allergen challenge of Brown Norway rat lung, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 121, Pages: 1241-1246, ISSN: 0007-1188
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- Citations: 40
Webb BLJ, Lindsay MA, Seybold J, et al., 1997, Identification of the protein kinase C isoenzymes in human lung and airways smooth muscle at the protein and mRNA level, BIOCHEMICAL PHARMACOLOGY, Vol: 54, Pages: 199-205, ISSN: 0006-2952
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- Citations: 38
Adcock IM, Newton R, Barnes PJ, 1997, NF-kappa B involvement in IL-1 beta-induction of GM-CSF and COX-2: Inhibition by glucocorticoids does not require I-kappa B., BIOCHEMICAL SOCIETY TRANSACTIONS, Vol: 25, Pages: S154-S154, ISSN: 0300-5127
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- Citations: 16
Adcock IM, 1997, Transcription factors as activators of gene transcription: AP-1 and NF-kappa B., Monaldi Arch Chest Dis, Vol: 52, Pages: 178-186, ISSN: 1122-0643
Cells respond to a range of cytokines and other inflammatory stimuli by selectively expressing a wide range of genes. These proinflammatory signals bind to receptors and initiate intracellular signalling cascades. This results in the activation of proinflammatory deoxyribonucleic acid (DNA)-binding proteins or transcription factors such as activator protein-1 (AP-1) or nuclear factor-kappa B (NF-kappa B). Following activation, these factors bind to specific recognition sequences in the control regions (promoters) of target genes causing modulation of gene transcription. Furthermore, numerous sites for regulation of cytokine and cytokine receptor genes by these transcription factors are found in their promoter regions. Many factors affect the formation and activity of AP-1 dimers (Fos and Jun heterodimers) through protein specific interactions or by the modulation of pre-existing complexes by phosphorylation. These complexes can vary markedly in their ability to stimulate gene transcription. Thus, induction of AP-1 activity is regulated by stimuli that either induce the de novo synthesis of AP-1 subunits or increase the activity of previously formed AP-1 dimers. NF-kappa B is activated by a number of agents including tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), lipopolysaccharide (LPS) and viruses. NF-kappa B plays a central role in a range of immunological responses due to its ability to switch on inflammatory genes which lead to further activation of NF-kappa B is a heterodimer of proteins which vary in their ability to bind to DNA and/or to activate gene transcription. NF-kappa B activation is primarily regulated by sequestration of heterodimers within the cytoplasm as inactive complexes with inhibitory molecules (inhibitory-kappa B (I-kappa B)). Treatment of cells with inducing agents results in the phosphorylation of the I-kappa B molecule which is targeted for rapid degradation. This causes a rapid dissociation of the cytoplasmic NF
Blease K, Seybold J, Adcock I, et al., 1997, Synergism between interleukin-4 and lipopolysaccharide in the induction of VCAM-1 on human lung microvascular endothelial cells, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 120, Pages: P57-P57, ISSN: 0007-1188
Barnes PJ, Adcock IM, 1997, NF-kappa B: A pivotal role in asthma and a new target for therapy, TRENDS IN PHARMACOLOGICAL SCIENCES, Vol: 18, Pages: 46-50, ISSN: 0165-6147
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- Citations: 178
Adcock IM, Newton R, Barnes PJ, 1997, NF-KB involvement in IL-1β-induction of GM-CSF and COX-2: Inhibition by glucocorticoids does not require l-κB, ISSN: 0300-5127
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- Citations: 14
Kuitert LM, Newton R, Barnes NC, et al., 1996, Eicosanoid mediator expression in mononuclear and polymorphonuclear cells in normal subjects and patients with atopic asthma and cystic fibrosis, THORAX, Vol: 51, Pages: 1223-1228, ISSN: 0040-6376
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- Citations: 21
Newton R, Kuitert LM, Slater DM, et al., 1996, Cytokine induction of cytosolic phospholipase A(2) and cyclooxygenase-2 mRNA is suppressed by glucocorticoids in human epithelial cells, LIFE SCIENCES, Vol: 60, Pages: 67-78, ISSN: 0024-3205
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- Citations: 135
Adcock IM, Newton R, Barnes PJ, 1996, NF-kappa B involvement in IL-1 beta-induction of GM-CSF and COX-2: Inhibition by glucocorticoids does not require I-kappa B., IMMUNOLOGY, Vol: 89, Pages: A2-A2, ISSN: 0019-2805
Adcock IM, Gilbey T, Gelder CM, et al., 1996, Glucocorticoid receptor localization in normal and asthmatic lung, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 154, Pages: 771-782, ISSN: 1073-449X
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- Citations: 136
Adcock IM, Brown CR, Barnes PJ, 1996, Tumour necrosis factor alpha causes retention of activated glucocorticoid receptor within the cytoplasm of A549 cells, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 225, Pages: 545-550, ISSN: 0006-291X
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- Citations: 19
Adcock IM, 1996, Steroid resistance in asthma - Molecular mechanisms, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 154, Pages: S58-S61, ISSN: 1073-449X
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- Citations: 29
Liu SF, Adcock IM, Old RW, et al., 1996, Differential regulation of the constitutive and inducible nitric oxide synthase mRNA by lipopolysacchride treatment in vivo in the rat, CRITICAL CARE MEDICINE, Vol: 24, Pages: 1219-1225, ISSN: 0090-3493
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- Citations: 115
Adcock IM, Barnes PJ, 1996, Ligand-induced differentiation of glucocorticoid receptor (GR) trans-repression and transactivation., Biochem Soc Trans, Vol: 24, ISSN: 0300-5127
Gelder CM, Barnes PJ, O'Connor BJ, et al., 1996, Cytokine mRNA profiles of normal and asthmatic peripheral blood cells and endobronchial biopsies., Biochem Soc Trans, Vol: 24, ISSN: 0300-5127
Gelder CM, Morrison JF, Chung KF, et al., 1996, T cell receptor repertoire in peripheral blood and bronchial biopsies from normal and asthmatic subjects., Biochem Soc Trans, Vol: 24, ISSN: 0300-5127
Haddad EB, Salmon M, Koto H, et al., 1996, Ozone induction of cytokine-induced neutrophil chemoattractant (CINC) and nuclear factor-kappa b in rat lung: Inhibition by corticosteroids, FEBS LETTERS, Vol: 379, Pages: 265-268, ISSN: 0014-5793
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- Citations: 89
Newton R, Adcock IM, Barnes PJ, 1996, Superinduction of NF-kappa B by actinomycin D and cycloheximide in epithelial cells, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 218, Pages: 518-523, ISSN: 0006-291X
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- Citations: 77
Adcock IM, Gilbey T, Gelder CM, et al., 1996, Glucocorticoid receptor localization in normal and asthmatic lung, American Journal of Respiratory and Critical Care Medicine, Vol: 154, Pages: 771-782, ISSN: 1073-449X
The localization and distribution of the human glucocorticoid receptor (GR) mRNA and protein was investigated in human lung obtained from transplant donors and recipients by in situ hybridization, RNA blot analysis, immunolocalization, and Western analysis. Subjects were either nonasthmatic or had mild asthma requiring only β2-agonists. No difference in amount of GR mRNA was found in total RNA isolated from nonasthmatic or asthmatic donor lung. In situ hybridization showed the highest concentration of GR mRNA in the alveolar walls and vascular endothelium and smooth muscle, with lesser amounts in the airway epithelium and smooth muscle. There was no change in the level or sites of expression of GR mRNA between normal and asthmatic subjects. Immunolocalization of GR confirmed the in situ hybridization data. There was no change in the level or sites of expression of GR, in either the lung or airway, between normal and asthmatic subjects. Immunolocalization of GR in bronchial biopsies from two normal and asthmatic subjects confirmed the localization and distribution of GR. Western analysis and mobility shift assays confirmed no differences in GR levels between the two subject groups. The localization of GR mRNA and protein to specific cell types within lung and airway will make it possible to study the cellular targets of glucocorticoid therapy in inflammatory lung diseases such as asthma.
Adcock IM, 1996, Steroid resistance in asthma: Molecular mechanisms, American Journal of Respiratory and Critical Care Medicine, Vol: 154, ISSN: 1073-449X
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- Citations: 36
Adcock IM, Stevens DA, Barnes PJ, 1996, Interactions of glucocorticoids and beta(2)-agonists, EUROPEAN RESPIRATORY JOURNAL, Vol: 9, Pages: 160-168, ISSN: 0903-1936
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- Citations: 61
Adcock IM, Lane SJ, Brown CR, et al., 1995, Abnormal glucocorticoid receptor-activator protein 1 interaction in steroid-resistant asthma, Journal of Experimental Medicine, Vol: 182, Pages: 1951-1958, ISSN: 1540-9538
BARNES PJ, ADCOCK IM, 1995, TRANSCRIPTION FACTORS, CLINICAL AND EXPERIMENTAL ALLERGY, Vol: 25, Pages: 46-49, ISSN: 0954-7894
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- Citations: 9
XU WB, HADDAD EB, TSUKAGOSHI H, et al., 1995, INDUCTION OF MACROPHAGE INFLAMMATORY PROTEIN-2 GENE-EXPRESSION BY INTERLEUKIN-1-BETA IN RAT LUNG, THORAX, Vol: 50, Pages: 1136-1140, ISSN: 0040-6376
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- Citations: 24
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