PMID- 17261755
OWN - NLM
STAT- MEDLINE
DCOM- 20070313
LR  - 20091119
IS  - 0077-8923 (Print)
IS  - 0077-8923 (Linking)
VI  - 1089
DP  - 2006 Nov
TI  - Chromatin remodeling and control of cell proliferation by progestins via cross 
      talk of progesterone receptor with the estrogen receptors and kinase signaling 
      pathways.
PG  - 59-72
AB  - Transcription from the mouse mammary tumor virus (MMTV) promoter can be induced 
      by glucocorticoids or progestins. Progesterone treatment of cultured cells 
      carrying an integrated single copy of an MMTV transgene leads to recruitment of 
      progesterone receptor (PR), SWI/SNF, and SNF2h-related complexes to MMTV 
      promoter. Recruitment is accompanied by selective displacement of histones H2A 
      and H2B from the nucleosome B. In nucleosomes assembled on promoter sequences, 
      SWI/SNF displaces histones H2A and H2B from MMTV nucleosome B, but not from other 
      MMTV nucleosomes or from an rDNA promoter nucleosome. Thus, the outcome of 
      nucleosome remodeling by purified SWI/SNF depends on the DNA sequence. On the 
      other hand, 5 min after hormone treatment, the cytoplasmic signaling cascade 
      Src/Ras/Erk is activated via an interaction of PR with the estrogen receptor, 
      which activates Src. As a consequence of Erk activation PR is phosphorylated, 
      Msk1 is activated, and a ternary complex PR-Erk-Msk1 is recruited to MMTV 
      nucleosome B. Msk1 phosphorylates H3 at serine 10, which is followed by 
      acetylation at lysine 14, displacement of HP1gamma, and recruitment of Brg1, 
      PCAF, and RNA polymerase II. Blocking Erk activation or Msk1 activity prevents 
      induction of the MMTV transgene. Thus, the rapid nongenomic effects of progestins 
      are essential for their transcriptional effects on certain progestin target 
      genes. In rat endometrial stromal cells, picomolar concentrations of progestins 
      trigger the cross talk of PR with ERbeta that activates the Erk and Akt kinase 
      pathways leading to cell proliferation in the absence of direct transcriptional 
      effects of the ligand-activated PR. Thus, depending on the cellular context rapid 
      kinase activation and transcriptional effect play different roles in the 
      physiological response to progestins.
FAU - Vicent, Guillermo P
AU  - Vicent GP
AD  - Centre de Regulacio Genomica (CRG), Universitat Pompeu Fabra (UPF), PRBB, Dr 
      Aiguader 88, 08003 Barcelona, Spain.
FAU - Ballare, Cecilia
AU  - Ballare C
FAU - Zaurin, Roser
AU  - Zaurin R
FAU - Saragueta, Patricia
AU  - Saragueta P
FAU - Beato, Miguel
AU  - Beato M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (Progestins)
RN  - 0 (Receptors, Estrogen)
RN  - 0 (Receptors, Progesterone)
RN  - EC 2.7.- (Protein Kinases)
SB  - IM
MH  - Animals
MH  - Cell Proliferation/*drug effects
MH  - *Chromatin Assembly and Disassembly
MH  - *Gene Expression Regulation
MH  - Mammary Tumor Virus, Mouse/*drug effects/genetics
MH  - Mice
MH  - Progestins/*pharmacology
MH  - Promoter Regions, Genetic/drug effects/genetics
MH  - Protein Kinases/metabolism
MH  - Rats
MH  - Receptors, Estrogen/*metabolism
MH  - Receptors, Progesterone/*metabolism
MH  - Signal Transduction
RF  - 39
EDAT- 2007/01/31 09:00
MHDA- 2007/03/14 09:00
CRDT- 2007/01/31 09:00
PHST- 2007/01/31 09:00 [pubmed]
PHST- 2007/03/14 09:00 [medline]
PHST- 2007/01/31 09:00 [entrez]
AID - 1089/1/59 [pii]
AID - 10.1196/annals.1386.025 [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2006 Nov;1089:59-72. doi: 10.1196/annals.1386.025.