Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-11-15
pubmed:abstractText
The identification of protein components in complex networks of co-regulators responsible for the modulation of proliferation versus differentiation modes of cell growth is a major problem. We use a combination of surface enhanced laser desorption/ionization mass spectrometry, surface plasmon resonance coupled to electrospray mass spectrometry, and immunoelectromobility shift assays to identify members of the MAX/MAD family binding to a specific DNA silencer fragment involved in the regulation of transcription for the human T-cell receptor Vbeta2.2 segment. We also identify the cofactors mSin3 and N-CoR known to interact with histone deacetylases. Inhibition of deacetylase activity in Jurkat cells prevented transcription inhibitor complex formation at the Vbeta2.2 segment, suggesting that this is either directly or indirectly dependent on the presence of HDACs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
325
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1021-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Repression of transcription at the human T-cell receptor Vbeta2.2 segment is mediated by a MAX/MAD/mSin3 complex acting as a scaffold for HDAC activity.
pubmed:affiliation
Unité INSERM 462, Hôpital Saint-Louis, 1 Avenue Claude Vellefaux, 75010 Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't