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<biogps><data><item key="platform">6</item><item key="owner">ArrayExpress Uploader</item><item key="pop_total">0</item><item key="species">mouse</item><item key="factors"><item><item key="GSE10422GSM263652"/></item><item><item key="GSE10422GSM263653"/></item><item><item key="GSE10422GSM263654"/></item><item><item key="GSE10422GSM263643"/></item><item><item key="GSE10422GSM263645"/></item><item><item key="GSE10422GSM263646"/></item><item><item key="GSE10422GSM263642"/></item><item><item key="GSE10422GSM263640"/></item><item><item key="GSE10422GSM263641"/></item><item><item key="GSE10422GSM263647"/></item><item><item key="GSE10422GSM263648"/></item><item><item key="GSE10422GSM263644"/></item><item><item key="GSE10422GSM263649"/></item><item><item key="GSE10422GSM263650"/></item><item><item key="GSE10422GSM263651"/></item></item><item key="id">5300</item><item key="ownerprofile_id">arrayexpress_sid</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-10422</item><item key="summary_wrapped">Tumor necrosis factor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a co-operative and non-redundant manner to...</item><item key="pubmed_id">18313334</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">0</item><item key="sample_count">15</item><item key="tags"><item>cell</item><item>genome</item><item>lymph</item><item>lymph node</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_gds_id"/><item key="slug">transcription-profiling-of-mouse-lymph-node-derive</item><item key="geo_id_plat">E-GEOD-10422_A-AFFY-45</item><item key="name">Transcription profiling of mouse lymph node derived B cells from Traf2 and Traf3 B cell knockout mice and Baff tg mice</item><item key="created">Nov.10, 2014</item><item key="summary">Tumor necrosis factor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a co-operative and non-redundant manner to suppress nuclear factor-&#954;B2 (NF-&#954;B2) activation, gene expression and survival in mature B cells. In the absence of this suppressive activity, B cells developed independently of the obligatory B cell survival factor, BAFF (B cell activating factor of the tumor necrosis factor family).  This constitutive, lineage-specific suppression of B cell survival by TRAF2 and TRAF3 determines the requirement for BAFF to sustain B cell development in vivo.  We wished to investigate the effect on gene expression in B cells which lacked the negative regulators TRAF2 and TRAF3, and hence had hyperactive NF-kB2 signalling.  As Baff-tg mice display a similar phenotype, and have a genetic modification which acts in the same pathway, yet further up, than TRAF2 and TRAF3, we wished to compare and contrast Baff-tg B cells with TRAF2 and TRAF3 deficient B cells.  This analysis should identify genes that are important in B cell survival. Experiment Overall Design: Lymph node B cells were purified from Traf2 B cell knockout mice, Traf3 B cell knockout mice, Baff-tg mice and respective controls.  RNA was extracted and hybridised to Affymetrix 430 2.0 Mouse Genome Arrays.  Samples were processed and hence analysed on three spearate days.  Day 1 two control mice: Traf2lox/lox pool and CD19-cretg were compared to two knockout mice: Traf2DB 80 and Traf3DB 94.  On Day 2 three control mice: Traf2lox/lox 77, Traf2lox/lox 79 and Traf3lox/lox 97 were compared to two knockout mice: Traf2DB 76 and Traf3DB 01.  On Day 3 three control mice: WT33, WT34, WT35 were compared to three Baff-tg mice: Baff-tg 99, Baff-tg 100, Baff-tg 101.</item><item key="geo_gse_id">E-GEOD-10422</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-10422/samples/</item></data></biogps>
