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  • 1
    Publication Date: 2002-04-06
    Description: Sur2 is a metazoan Mediator subunit that interacts with the adenovirus E1A protein and functions in a mitogen-activated protein kinase pathway required for vulva development in Caenorhabditis elegans. We generated sur2-/- embryonic stem cells to analyze its function as a mammalian Mediator component. Our results show that Sur2 forms a subcomplex of the Mediator with two other subunits, TRAP/Med100 and 95. Knock-out of Sur2 prevents activation by E1A-CR3 and the mitogen-activated protein kinase-regulated ETS transcription factor Elk-1, but not by multiple other transcription factors. These results imply that specific activation domains stimulate transcription by binding to distinct Mediator subunits. Activation by E1A and Elk-1 requires recruitment of Mediator to a promoter by binding to its Sur2 subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, Jennitte L -- Cantin, Greg T -- Wang, Gang -- Shevchenko, Andrej -- Shevchenko, Anna -- Berk, Arnold J -- CA25235/CA/NCI NIH HHS/ -- GM07185/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):755-8. Epub 2002 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles, 611 Charles Young Drive East, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11934987" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1A Proteins/*metabolism ; Adenoviruses, Human/physiology ; Animals ; Carrier Proteins/genetics/*metabolism ; Cells, Cultured ; *DNA-Binding Proteins ; Genes, Immediate-Early ; HeLa Cells ; Humans ; *MAP Kinase Signaling System ; Mediator Complex ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/metabolism ; Stem Cells/*metabolism ; *Trans-Activators ; Transcription Factors/metabolism ; *Transcription, Genetic ; *Transcriptional Activation ; Transfection ; ets-Domain Protein Elk-1
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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