AP-1-glucocorticoid receptor crosstalk taken to a higher level

Journal of Endocrinology

Volumn 169, Issue 3, 2001, Pages 447-451

  Karin, M ^a   Chang, L ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

COLLAGENASE; COLLAGENASE TYPE 1; CYTOKINE; GENE PRODUCT; GLUCOCORTICOID; GLUCOCORTICOID RECEPTOR; GROWTH FACTOR; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; JUN PROTEIN; PHOSPHOTRANSFERASE; STEROID HORMONE; TRANSCRIPTION FACTOR; TRANSCRIPTION FACTOR AP 1; UNCLASSIFIED DRUG;

AMINO TERMINAL SEQUENCE; ANIMAL EXPERIMENT; ANTIINFLAMMATORY ACTIVITY; ARTICLE; CHRONIC INFLAMMATION; CONTROLLED STUDY; GENE CONTROL; GENE REPRESSION; HOMEOSTASIS; HORMONE ACTION; HORMONE BLOOD LEVEL; IMMUNOSUPPRESSIVE ACTIVITY; INFLAMMATION; MODULATION; MOLECULAR BIOLOGY; MOUSE; NEGATIVE FEEDBACK; NONHUMAN; PRIORITY JOURNAL; PROTEIN INTERACTION; REGULATORY MECHANISM; SIGNAL TRANSDUCTION; STRESS; TRANSCRIPTION REGULATION;

GENE EXPRESSION REGULATION; HUMANS; HYPOTHALAMO-HYPOPHYSEAL SYSTEM; PITUITARY-ADRENAL SYSTEM; RECEPTORS, GLUCOCORTICOID; STRESS, PSYCHOLOGICAL; TRANSCRIPTION FACTOR AP-1;

EID: 0034965832     PISSN: 00220795     EISSN: None     Source Type: Journal    
DOI: 10.1677/joe.0.1690447     Document Type: Article

References (31)

1. Activation of SRF-regulated chromosomal templates by Rho-family GTPases requires a signal that also induces H4 hyperacetylation
2. The role of Jun, Fos and the AP-1 complex in cell-proliferation and transformation
3. Immunosuppression by glucocorticoids: Inhibition of NF-kB activity through induction of IkB synthesis
4. Nuclear factor-κB - A pivotal transcription factor in chronic inflammatory diseases
5. Gene regulation by steroid hormones
6. Immunoregulatory feedback between interleukin-1 and glucocorticoid hormones
7. Transcriptional silencing in yeast is associated with reduced nucleosome acetylation
8. Nuclear hormone receptor antagonism with AP-1 by inhibition of the JNK pathway
9. Induction of c-fos expression through JNK-mediated TCF/Elk-1 phosphorylation
10. The hypothalamic-pituitary-adrenal axis and immune-mediated inflammation
11. Targeted disruption of the glucocorticoid receptor gene blocks adrenergic chromaffin cell development and severely retards lung maturation
12. Transcription factor interactions: Selectors of positive or negative regulation from a single DNA element
13. Glucocorticoids antagonize AP-1 by inhibiting the activation/phosphorylation of JNK without affecting its subcellular distribution
14. Signal transduction by the c-Jun NH-2-terminal kinase (JNK) - From inflammation to development
15. Antitumor promotion and anti-inflammation: Down-modulation of AP-1 (Fos/Jun) activity by glucocorticoid hormone
16. c-Jun can recruit JNK to phosphorylate dimerization partners via specific docking interactions
17. A CBP integrator complex mediates transcriptional activation and AP-1 inhibition by nuclear receptors
18. The regulation of AP-1 activity by mitogen-activated protein kinases
19. New twists in gene regulation by glucocorticoid receptor: Is DNA binding dispensable?
20. The beginning of the end: IκB kinase (IKK) and NF-κB Activation
21. Characterization of DNA sequences through which cadmium and glucocorticoid hormones induce human metallothionein-IIA gene
22. Major upper airways obstruction associated with Sjogren's syndrome: A case report and literature review
23. Interference between pathway-specific transcription factors: Glucocorticoids antagonize phorbol ester-induced AP-1 activity without altering AP-1 site occupation in vivo
24. Allosteric effects of DNA on transcriptional regulators
25. DNA binding of the glucocorticoid receptor is not essential for survival
26. Antagonism of glucocorticoid receptor transcriptional activation by the c-Jun N-terminal kinase
27. Negative transcriptional regulation by nuclear receptors
28. Functional antagonism between oncoprotein c-Jun and the glucocorticoid receptor
29. Phosphorylation of cJun on serines 63 and 73 is required for oncogenic and transcriptional cooperation with Ha-Ras
30. Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) is required for lipopolysaccharide stimulation of tumor necrosis factor α (TNF-α) translation: Glucocorticoids inhibit TNF-α translation by blocking JNK/SAPK
31. Transcriptional interference between cJun and the glucocorticoid receptor: Mutual inhibition of DNA-binding due to direct protein-protein interaction