Linked Life Data

20308430

Source:http://linkedlifedata.com/resource/pubmed/id/20308430

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-3-23
pubmed:abstractText
Oncogenic stress induces expression of the alternate reading frame (Arf) tumor suppressor protein. Arf then stabilizes p53, which leads to cell cycle arrest or apoptosis. The mechanisms that distinguish both outcomes are incompletely understood. In this study, we show that Arf interacts with the Myc-associated zinc finger protein Miz1. Binding of Arf disrupts the interaction of Miz1 with its coactivator, nucleophosmin, induces the sumoylation of Miz1, and facilitates the assembly of a heterochromatic complex that contains Myc and trimethylated H3K9 in addition to Miz1. Arf-dependent assembly of this complex leads to the repression of multiple genes involved in cell adhesion and signal transduction and induces apoptosis. Our data point to a tumor-suppressive pathway that weakens cell-cell and cell-matrix interactions in response to expression of Arf and that may thereby facilitate the elimination of cells harboring an oncogenic mutation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1540-8140
pubmed:author
pubmed:issnType
Electronic
pubmed:day
22
pubmed:volume
188
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
905-18
pubmed:dateRevised
2010-9-24
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
The Arf tumor suppressor protein inhibits Miz1 to suppress cell adhesion and induce apoptosis.
pubmed:affiliation
Theodor-Boveri-Institute and 2 Rudolf-Virchow-Center, University of Würzburg, D-97070 Würzburg, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't