{"owner": "ArrayExpress Uploader", "pop_total": 0, "species": "human", "factors": [{"GSM1088405": {"SHRNA": "shSTAT1"}}, {"GSM1088405": {"SHRNA": "shSTAT1"}}, {"GSM1088405": {"SHRNA": "shSTAT1"}}, {"GSM1088405": {"SHRNA": "shSTAT1"}}, {"GSM108840": {"SHRNA": "shTYK2"}}, {"GSM108840": {"SHRNA": "shTYK2"}}, {"GSM108840": {"SHRNA": "shTYK2"}}, {"GSM108840": {"SHRNA": "shTYK2"}}, {"GSM1088397": {"SHRNA": "shLuc"}}, {"GSM1088397": {"SHRNA": "shLuc"}}, {"GSM1088395": {"SHRNA": "shGFP"}}, {"GSM1088395": {"SHRNA": "shGFP"}}], "id": 2504, "ownerprofile_id": "arrayexpress_sid", "platform": 4, "summary_wrapped": "Targeted molecular therapy has yielded remarkable outcomes in certain cancers, but specific therapeutic targets remain elusive for many...", "geo_gse_id": "E-GEOD-44652", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 1, "sample_count": 12, "tags": ["acute lymphoblastic leukemia", "cell", "leukemia", "line", "lymphoblastic leukemia", "protein", "tyrosine"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_gds_id": "", "slug": "gene-expression-profile-of-the-human-t-all-cell-li", "geo_id_plat": "E-GEOD-44652_A-AFFY-44", "name": "Gene expression profile of the human T-ALL cell line JURKAT after TYK2 and STAT1 knockdown", "created": "Jul.12, 2014", "summary": "Targeted molecular therapy has yielded remarkable outcomes in certain cancers, but specific therapeutic targets remain elusive for many others. As a result of two independent RNA interference (RNAi) screens, we identified pathway dependence on a member of the JAK tyrosine kinase family, TYK2, and its downstream effector STAT1 in T-cell acute lymphoblastic leukemia (T-ALL). Gene knockdown experiments consistently demonstrated TYK2 dependence in both T-ALL primary specimens and cell lines, and a small-molecule inhibitor of JAK kinase activity induced T-ALL cell death. Activation of this TYK2-STAT1 pathway in T-ALL cell lines occurs by gain-of-function TYK2 mutations or activation of IL-10 receptor signaling, and this pathway mediates T-ALL cell survival through upregulation of the anti-apoptotic protein BCL2. These findings indicate that in many T-ALL cases, the leukemic cells are dependent upon the TYK2-STAT1-BCL2 pathway for continued survival, supporting the development of molecular therapies targeting TYK2 and other components of this pathway. Human T-ALL cell line JURKAT cells were transduced with TYK2 (TYK2#2 or #3), STAT1 (STAT1#2 or #3) or control shRNAs (GFP and Luc). Experiment was done in biological duplicate (\"dup1\" and \"dup2\") . A total of 12 RNA samples (4 control, 4 TYK2 knockdown and 4 STAT1 knockdown) were used for microarray gene expression analysis.", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-44652", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-44652/samples/"}