New insights into the molecular mechanisms of alcoholic hepatitis: A potential role for NF-κB activation?

Journal of Laboratory and Clinical Medicine

Volumn 135, Issue 5, 2000, Pages 367-369

  Szabo, Gyongyi ^a  

^a UNIVERSITY OF MASSACHUSETTS MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 0033806801     PISSN: 00222143     EISSN: None     Source Type: Journal    
DOI: 10.1067/mlc.2000.106452     Document Type: Article

References (22)

1. Inducibility of kappa immunoglobulin enhancer-binding protein NF-κB by a posttranslational mechanism
2. Signal transduction through NF-κB
3. NF-κ3 and Rel proteins: Evolutionarily conserved mediators of immune responses
4. Pro-inflammatory signaling: Last pieces in the NF-κ3 puzzle?
5. The IκB proteins: Multifunctional regulators of Rel/NFκB transcription factors
6. Rheumatoid arthritis
7. NF-κB: A pivotal role in the systemic inflammatory response syndrome and new target for therapy
8. Increased tumor necrosis factor production by monocytes in alcoholic patients
9. Circulating and tissue levels of the neutrophil chemotaxin IL-8 are elevated in severe acute alcoholic hepatitis, and tissue levels correlate with neutrophil infiltration
10. Circulating tumor necrosis factor, interleukin-1 and interleukin-6 concentrations in chronic alcoholic patients
11. Cytokines in alcoholic liver disease
12. IκB: A specific inhibitor of the NF-κB transcription factor
13. Increased monocyte nuclear factor-κB activation and tumor necrosis factor production in alcoholic hepatitis
14. Inhibition of LPS-mediated NF-κB activation by ethanol in human monocytes
15. Alcohol suppresses lipopolysaccharide-induced tumor necrosis factor activity in serum and lung
16. High DNA-binding activity of transcription factor NF-κB in synovial membranes of patients with rheumatoid arthritis
17. NF-κB in Crohn's disease
18. A randomized trial of prednisolone in patients with severe alcoholic hepatitis
19. Role of transcriptional activation of I kappa B alpha in mediation of immunosuppression by glucocorticoids
20. Negative cross-talk between RelA and the glucocorticoid receptor: A possible mechanism for the antiinflammatory action of glucocorticoids
21. Distinct domains of the RelA NF-κB subunit are required for negative cross-talking and direct interaction with the glucocorticoid receptor
22. Glucocorticoid and mineralocorticoid receptors: Biology and clinical relevance