Gene expression profile of the human T-ALL cell line JURKAT after TYK2 and STAT1 knockdown

ABSTRACT: 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-apopt

ORGANISM(S): Homo sapiens

SUBMITTER: Takaomi Sanda 

PROVIDER: E-GEOD-44652 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress