PMID- 29241532
OWN - NLM
STAT- MEDLINE
DCOM- 20180723
LR  - 20220129
IS  - 2211-1247 (Electronic)
VI  - 21
IP  - 11
DP  - 2017 Dec 12
TI  - Glucocorticoid Receptor Binding Induces Rapid and Prolonged Large-Scale Chromatin 
      Decompaction at Multiple Target Loci.
PG  - 3022-3031
LID - S2211-1247(17)31705-9 [pii]
LID - 10.1016/j.celrep.2017.11.053 [doi]
AB  - Glucocorticoids act by binding to the glucocorticoid receptor (GR), which binds 
      to specific motifs within enhancers of target genes to activate transcription. 
      Previous studies have suggested that GRs can promote interactions between gene 
      promoters and distal elements within target loci. In contrast, we demonstrate 
      here that glucocorticoid addition to mouse bone-marrow-derived macrophages 
      produces very rapid chromatin unfolding detectable by fluorescence in situ 
      hybridization (FISH) at loci associated with GR binding. Rapid chromatin 
      decompaction was generally not dependent on transcription at those loci that are 
      known to be inducible in both mouse and human macrophages and was sustained for 
      up to 5 days following ligand removal. Chromatin decompaction was not dependent 
      upon persistent GR binding, which decayed fully after 24 hr. We suggest that 
      sustained large-scale chromatin reorganization forms an important part of the 
      response to glucocorticoid and might contribute to glucocorticoid sensitivity and 
      resistance.
CI  - Copyright (c) 2017 The Author(s). Published by Elsevier Inc. All rights reserved.
FAU - Jubb, Alasdair W
AU  - Jubb AW
AD  - MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, The 
      University of Edinburgh, Crewe Road, Edinburgh EH4 2XU, UK; The Roslin Institute 
      and Royal (Dick) School of Veterinary Studies, The University of Edinburgh, 
      Easter Bush, Midlothian EH25 9RG, UK; Department of Medicine, University of 
      Cambridge, Box 93, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK.
FAU - Boyle, Shelagh
AU  - Boyle S
AD  - MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, The 
      University of Edinburgh, Crewe Road, Edinburgh EH4 2XU, UK.
FAU - Hume, David A
AU  - Hume DA
AD  - The Roslin Institute and Royal (Dick) School of Veterinary Studies, The 
      University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK; Mater 
      Research-University of Queensland, Translational Research Institute, 37 Kent 
      Street, Woolloongabba, QLD 4102, Australia. Electronic address: 
      david.hume@roslin.ed.ac.uk.
FAU - Bickmore, Wendy A
AU  - Bickmore WA
AD  - MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, The 
      University of Edinburgh, Crewe Road, Edinburgh EH4 2XU, UK. Electronic address: 
      wendy.bickmore@igmm.ed.ac.uk.
LA  - eng
GR  - Wellcome Trust/United Kingdom
GR  - MC_PC_U127527202/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PL  - United States
TA  - Cell Rep
JT  - Cell reports
JID - 101573691
RN  - 0 (Chromatin)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Kruppel-Like Factor 4)
RN  - 0 (Kruppel-Like Transcription Factors)
RN  - 0 (NCOA5 protein, human)
RN  - 0 (Nuclear Receptor Coactivators)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (Receptors, Glucocorticoid)
RN  - 0 (Transcription Factors)
RN  - 148770-78-9 (HIVEP2 protein, human)
RN  - 7S5I7G3JQL (Dexamethasone)
SB  - IM
CIN - Trends Endocrinol Metab. 2018 Apr;29(4):204-207. PMID: 29477282
MH  - Animals
MH  - Binding Sites
MH  - Chromatin/*chemistry/metabolism
MH  - Chromatin Assembly and Disassembly/*drug effects
MH  - DNA-Binding Proteins/genetics/metabolism
MH  - Dexamethasone/*pharmacology
MH  - Gene Expression Regulation
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Kinetics
MH  - Kruppel-Like Factor 4
MH  - Kruppel-Like Transcription Factors/genetics/metabolism
MH  - Macrophages/cytology/*drug effects/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nuclear Receptor Coactivators/genetics/metabolism
MH  - Primary Cell Culture
MH  - Promoter Regions, Genetic
MH  - Protein Binding
MH  - Proto-Oncogene Proteins c-fos/genetics/metabolism
MH  - Receptors, Glucocorticoid/*genetics/metabolism
MH  - Signal Transduction
MH  - Transcription Factors/genetics/metabolism
PMC - PMC5745231
OTO - NOTNLM
OT  - chromatin remodeling
OT  - enhancer
OT  - fluorescence in situ hybridization
OT  - glucocorticoid receptor
OT  - macrophage
EDAT- 2017/12/16 06:00
MHDA- 2018/07/24 06:00
PMCR- 2017/12/12
CRDT- 2017/12/16 06:00
PHST- 2015/12/15 00:00 [received]
PHST- 2017/10/01 00:00 [revised]
PHST- 2017/11/15 00:00 [accepted]
PHST- 2017/12/16 06:00 [entrez]
PHST- 2017/12/16 06:00 [pubmed]
PHST- 2018/07/24 06:00 [medline]
PHST- 2017/12/12 00:00 [pmc-release]
AID - S2211-1247(17)31705-9 [pii]
AID - 10.1016/j.celrep.2017.11.053 [doi]
PST - ppublish
SO  - Cell Rep. 2017 Dec 12;21(11):3022-3031. doi: 10.1016/j.celrep.2017.11.053.