PMID- 12637584
OWN - NLM
STAT- MEDLINE
DCOM- 20031218
LR  - 20161124
IS  - 0888-8809 (Print)
IS  - 0888-8809 (Linking)
VI  - 17
IP  - 6
DP  - 2003 Jun
TI  - CBP recruitment and histone acetylation in differential gene induction by 
      glucocorticoids and progestins.
PG  - 1085-94
AB  - We have analyzed histone acetylation at the steroid-responsive mouse mammary 
      tumor virus (MMTV) promoter in five separate cell lines that express functional 
      glucocorticoid and/or progesterone receptors. Chromatin immunoprecipitation 
      assays reveal that glucocorticoid and progesterone receptors bind the MMTV 
      promoter after hormone addition but that receptor binding is not associated with 
      an increase in acetylation of histone H3 or H4. We have, however, found one 
      exception to this rule. Previously we described a cell line [T47D(C&L)] that 
      displayed a remarkable differential induction of MMTV by glucocorticoids and 
      progestins. At one chromosomal locus (MMTV-luciferase), MMTV is preferentially 
      induced by glucocorticoids, whereas at another locus within the same cell 
      (MMTV-CAT), MMTV is activated by both glucocorticoids and progestins. Here we 
      show that the glucocorticoid-mediated induction of MMTV-luciferase is accompanied 
      by increased recruitment of CBP to the promoter and increased histone H3 and H4 
      acetylation, whereas the hormonal induction of MMTV-CAT in the same cell exhibits 
      a more modest CBP recruitment without any increase in histone acetylation. These 
      studies suggest that increased histone acetylation may serve a potentiating 
      function for MMTV promoter activation at certain loci. However, increased histone 
      acetylation is not requisite for steroid-mediated induction of transcription at 
      all genes.
FAU - Lambert, James R
AU  - Lambert JR
AD  - Department of Pathology and Program in Molecular Biology, University of Colorado 
      Health Sciences Center, Denver, Colorado 80262, USA.
FAU - Nordeen, Steven K
AU  - Nordeen SK
LA  - eng
GR  - DK-09554/DK/NIDDK NIH HHS/United States
GR  - DK-37061/DK/NIDDK NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20030313
PL  - United States
TA  - Mol Endocrinol
JT  - Molecular endocrinology (Baltimore, Md.)
JID - 8801431
RN  - 0 (Chromatin)
RN  - 0 (Histones)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Receptors, Glucocorticoid)
RN  - 0 (Receptors, Progesterone)
RN  - 0 (Trans-Activators)
RN  - EC 2.3.1.48 (CREB-Binding Protein)
RN  - EC 2.3.1.48 (Crebbp protein, mouse)
SB  - IM
MH  - Acetylation
MH  - Animals
MH  - CREB-Binding Protein
MH  - Chromatin
MH  - Gene Expression Regulation
MH  - Histones/*metabolism
MH  - Mammary Tumor Virus, Mouse/genetics/*metabolism
MH  - Mice
MH  - Nuclear Proteins/*metabolism
MH  - Promoter Regions, Genetic/genetics/*physiology
MH  - Protein Binding/physiology
MH  - Receptors, Glucocorticoid/*metabolism
MH  - Receptors, Progesterone/*metabolism
MH  - Trans-Activators/*metabolism
MH  - Transcription, Genetic/physiology
MH  - Transcriptional Activation
EDAT- 2003/03/15 04:00
MHDA- 2003/12/19 05:00
CRDT- 2003/03/15 04:00
PHST- 2003/03/15 04:00 [pubmed]
PHST- 2003/12/19 05:00 [medline]
PHST- 2003/03/15 04:00 [entrez]
AID - me.2001-0183 [pii]
AID - 10.1210/me.2001-0183 [doi]
PST - ppublish
SO  - Mol Endocrinol. 2003 Jun;17(6):1085-94. doi: 10.1210/me.2001-0183. Epub 2003 Mar 
      13.