Investigation Title	"Transcription profiling of mouse embryonic day 13.5 and 15.5 fetal livers lacking p38alpha, a mitogen-activated kinase that controls inflammatory responses and cell proliferation"		
Comment[Submitted Name]	Expression data from p38 knock out versus wild type fetal liver		
Experimental Design	development_or_differentiation_design	individual_genetic_characteristics_design	co-expression_design
Experimental Design Term Source REF	The MGED Ontology	The MGED Ontology	The MGED Ontology
Comment[ArrayExpressReleaseDate]	2007-12-13		
Comment[SecondaryAccession]	GSE7342		
Comment[AEMIAMESCORE]	5		
Comment[SecondaryAccession]	GDS2693		
Comment[ArrayExpressAccession]	E-GEOD-7342		
Comment[MAGETAB TimeStamp_Version]	2010-08-07 18:29:27 Last Changed Rev: 13058		
Comment[AEExperimentType]	transcription profiling by array		
Experimental Factor Name	genotype	developmental stage	
Experimental Factor Type	genotype	developmental stage	
Experimental Factor Term Source REF			
Person Last Name	Schweifer		
Person First Name	Norbert		
Person Mid Initials			
Person Email	norbert.schweifer@vie.boehringer-ingelheim.com		
Person Address	"Boehringer Ingelheim Austria, Dr. Boehringer Gasse 5-11, Vienna, 1120, Austria"		
Person Affiliation	Boehringer Ingelheim Austria		
Person Roles	submitter		
Public Release Date	2007-12-13		
PubMed ID	17468757		
Publication DOI	10.1038/ng2033		
Publication Author List	"Lijian Hui, Latifa Bakiri, Andreas Mairhorfer, Norbert Schweifer, Christian Haslinger, Lukas Kenner, Vukoslav Komnenovic, Harald Scheuch, Hartmut Beug, Erwin F Wagner"		
Publication Title	p38alpha suppresses normal and cancer cell proliferation by antagonizing the JNK-c-Jun pathway.		
Publication Status	journal_article		
Publication Status Term Source REF	The MGED Ontology		
Experiment Description	"The mitogen-activated protein kinase (MAPK) p38alpha controls inflammatory responses and cell proliferation. Using mice carrying conditional p38alpha alleles, we investigated its function in postnatal development and tumorigenesis. When p38alpha is specifically deleted in the mouse embryo, fetuses develop to term but die shortly after birth, likely due to lung dysfunction. Fetal hematopoietic cells and embryonic fibroblasts deficient in p38alpha display increased proliferation, resulting from sustained activation of the c-Jun N-terminal kinase (JNK)/c-Jun pathway. Importantly, in chemical-induced liver cancer development, mice with liver-specific deletion of p38alpha show enhanced hepatocyte proliferation and tumor development that also correlates with JNK/c-Jun upregulation. Furthermore, increased proliferation of p38alpha-deficient hepatocytes and tumor cells is suppressed by inactivation of JNK or c-Jun.  These results reveal a novel mechanism whereby p38alpha negatively regulates cell proliferation through antagonizing the JNK/c-Jun pathway in multiple cell types and in liver cancer development. We used microarrays to identifiy differental regulated genes by p38alpha in fetal liver cells Experiment Overall Design: Wild type and p38 deficient fetal liver cell were used for RNA extraction and hybridization on Affymetrix microarrays."		
Protocol Name	P-G7342-2	P-G7342-3	P-G7342-4
Protocol Type	nucleic acid extraction protocol	nucleic acid labeling protocol	nucleic acid hybridization to array protocol
Protocol Description	Trizol extraction of total RNA was performed according to the manufacturer's instructions.	"Biotinylated cRNA were prepared according to the standard Affymetrix protocol from 5 microg total RNA (Expression Analysis Technical Manual, 2001, Affymetrix)."	"Following fragmentation, 10 microg of cRNA were hybridized for 16 hr at 45C on Murine Genome U74 Version 2 Set MG-U74A. GeneChips were washed and stained in the Affymetrix Fluidics Station 400."
Protocol Term Source REF	EFO	EFO	EFO
SDRF File	E-GEOD-7342.sdrf.txt		
Term Source Name	The MGED Ontology	ArrayExpress	EFO
Term Source File	http://mged.sourceforge.net/ontologies/MGEDontology.php	http://www.ebi.ac.uk/arrayexpress	http://www.ebi.ac.uk/efo/
Term Source Version