Cyclin E associates with BAF155 and BRG1, components of the mammalian SWI-SNF complex, and alters the ability of BRG1 to induce growth arrest

Typeset version

 

TY  - JOUR
  - Shanahan, F.,Seghezzi, W.,Parry, D.,Mahony, D.,Lees, E.
  - 1999
  - February
  - Cyclin E associates with BAF155 and BRG1, components of the mammalian SWI-SNF complex, and alters the ability of BRG1 to induce growth arrest
  - Validated
  - ()
  - 19
  - 22
  - 1460
  - 14691460
  - SWI-SNF complexes have been implicated in transcriptional regulation by chromatin remodeling We have identified an interaction between two components of the mammalian SWI-SNF complex and cyclin E, an essential cell cycle regulatory protein required for G(1)/S transition. BRG1 and BAF155, mammalian homologs of yeast SWI2 and SWI3, respectively, are found in cyclin E complexes and are phosphorylated by cyclin E-associated kinase activity. In this report, we show that overexpression of BRG1 causes growth arrest and induction of senescence-associated beta-galactosidase activity, which can be overcome by cyclin E. Our results suggest that cyclin E may modulate the activity of the SWI-SNF apparatus to maintain the chromatin in a transcriptionally permissive state.SWI-SNF complexes have been implicated in transcriptional regulation by chromatin remodeling We have identified an interaction between two components of the mammalian SWI-SNF complex and cyclin E, an essential cell cycle regulatory protein required for G(1)/S transition. BRG1 and BAF155, mammalian homologs of yeast SWI2 and SWI3, respectively, are found in cyclin E complexes and are phosphorylated by cyclin E-associated kinase activity. In this report, we show that overexpression of BRG1 causes growth arrest and induction of senescence-associated beta-galactosidase activity, which can be overcome by cyclin E. Our results suggest that cyclin E may modulate the activity of the SWI-SNF apparatus to maintain the chromatin in a transcriptionally permissive state.
  - 0270-73060270-7306
  - ://WOS:000078140900048://WOS:000078140900048
DA  - 1999/02
ER  - 
@article{V235379802,
   = {Shanahan,  F. and Seghezzi,  W. and Parry,  D. and Mahony,  D. and Lees,  E. },
   = {1999},
   = {February},
   = {Cyclin E associates with BAF155 and BRG1, components of the mammalian SWI-SNF complex, and alters the ability of BRG1 to induce growth arrest},
   = {Validated},
   = {()},
   = {19},
   = {22},
  pages = {1460--14691460},
   = {{SWI-SNF complexes have been implicated in transcriptional regulation by chromatin remodeling We have identified an interaction between two components of the mammalian SWI-SNF complex and cyclin E, an essential cell cycle regulatory protein required for G(1)/S transition. BRG1 and BAF155, mammalian homologs of yeast SWI2 and SWI3, respectively, are found in cyclin E complexes and are phosphorylated by cyclin E-associated kinase activity. In this report, we show that overexpression of BRG1 causes growth arrest and induction of senescence-associated beta-galactosidase activity, which can be overcome by cyclin E. Our results suggest that cyclin E may modulate the activity of the SWI-SNF apparatus to maintain the chromatin in a transcriptionally permissive state.SWI-SNF complexes have been implicated in transcriptional regulation by chromatin remodeling We have identified an interaction between two components of the mammalian SWI-SNF complex and cyclin E, an essential cell cycle regulatory protein required for G(1)/S transition. BRG1 and BAF155, mammalian homologs of yeast SWI2 and SWI3, respectively, are found in cyclin E complexes and are phosphorylated by cyclin E-associated kinase activity. In this report, we show that overexpression of BRG1 causes growth arrest and induction of senescence-associated beta-galactosidase activity, which can be overcome by cyclin E. Our results suggest that cyclin E may modulate the activity of the SWI-SNF apparatus to maintain the chromatin in a transcriptionally permissive state.}},
  issn = {0270-73060270-7306},
   = {://WOS:000078140900048://WOS:000078140900048},
  source = {IRIS}
}
AUTHORSShanahan, F.,Seghezzi, W.,Parry, D.,Mahony, D.,Lees, E.
YEAR1999
MONTHFebruary
JOURNAL_CODE
TITLECyclin E associates with BAF155 and BRG1, components of the mammalian SWI-SNF complex, and alters the ability of BRG1 to induce growth arrest
STATUSValidated
TIMES_CITED()
SEARCH_KEYWORD
VOLUME19
ISSUE22
START_PAGE1460
END_PAGE14691460
ABSTRACTSWI-SNF complexes have been implicated in transcriptional regulation by chromatin remodeling We have identified an interaction between two components of the mammalian SWI-SNF complex and cyclin E, an essential cell cycle regulatory protein required for G(1)/S transition. BRG1 and BAF155, mammalian homologs of yeast SWI2 and SWI3, respectively, are found in cyclin E complexes and are phosphorylated by cyclin E-associated kinase activity. In this report, we show that overexpression of BRG1 causes growth arrest and induction of senescence-associated beta-galactosidase activity, which can be overcome by cyclin E. Our results suggest that cyclin E may modulate the activity of the SWI-SNF apparatus to maintain the chromatin in a transcriptionally permissive state.SWI-SNF complexes have been implicated in transcriptional regulation by chromatin remodeling We have identified an interaction between two components of the mammalian SWI-SNF complex and cyclin E, an essential cell cycle regulatory protein required for G(1)/S transition. BRG1 and BAF155, mammalian homologs of yeast SWI2 and SWI3, respectively, are found in cyclin E complexes and are phosphorylated by cyclin E-associated kinase activity. In this report, we show that overexpression of BRG1 causes growth arrest and induction of senescence-associated beta-galactosidase activity, which can be overcome by cyclin E. Our results suggest that cyclin E may modulate the activity of the SWI-SNF apparatus to maintain the chromatin in a transcriptionally permissive state.
PUBLISHER_LOCATION
ISBN_ISSN0270-73060270-7306
EDITION
URL://WOS:000078140900048://WOS:000078140900048
DOI_LINK
FUNDING_BODY
GRANT_DETAILS