Glucocorticoid Receptor Recruitment of Histone Deacetylase 2 Inhibits Interleukin-1β-Induced Histone H4 Acetylation on Lysines 8 and 12

By Kazuhiro Ito, P. Barnes, Ian M. Adcock. Molecular and Cellular Biology, 2000

763 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/d43475cd5d00992eabe8cfdac3b37b3d01482cfb

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. A. Baldwin
2. S. Westerheide
3. B. P. Ashburner
4. P. Barnes
5. W. Vanden Berghe
6. G. Haegeman
7. K. De Bosscher

In Oncology

1. A. Baldwin
2. S. Westerheide
3. B. P. Ashburner
4. P. Barnes
5. G. Haegeman
6. N. Perkins

Citations in the corpus

• Mediators of Chronic Obstructive Pulmonary Disease (2004, background): “, 2001a), which is recruited to activated inflammatory genes by glucocorticoid receptors to switch off inflammatory genes (Ito et al., 2000).”
• How corticosteroids control inflammation: Quintiles Prize Lecture 2005 (2006, methodology): “Activated GR may bind to CBP or other coactivators directly to inhibit their HAT activity (Ito et al., 2000), thus reversing the unwinding of DNA around core histones and thereby repressing inflammatory genes.”
• Corticosteroid resistance in patients with asthma and chronic obstructive pulmonary disease. (2013, background): “Activated GRs interact with corepressor molecules to attenuate NF-kB–associated coactivator activity, thus reversing histone acetylation and chromatin remodeling actions.(6) Reduction of histone acetylation more importantly occurs through the recruitment of histone deacetylase (HDAC) 2 to the activa”
• The p65 (RelA) Subunit of NF-κB Interacts with the Histone Deacetylase (HDAC) Corepressors HDAC1 and HDAC2 To Negatively Regulate Gene Expression (2001, methodology): “When the in vitro transcribed and translated p65 was incubated with GST-HDAC1, interactions were seen with full-length p65 as well as with all three C-terminal deletions [p65 wt, p65(1-521), p65(1-313), and p65(1-276)] (Fig.”
• Pharmacokinetics and Pharmacodynamics of Systemically Administered Glucocorticoids (2005, background): “DNA transcription, ing of proinflammatory genes.[150,151] Induction of once started, is independent of the further presence IκB or HDAC might play an additional role as a”
• The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. (2003, background): “Interestingly, HAT and HDAC activities coexist within the same complex in the presence of p65 and GR, and they can each act independently without competing with each other, as revealed by in vivo chromatin immunoprecipitations (77, 427).”