(Q24303657)

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Annique Wilson-Weekes

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Gem S Burgess

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Carissa A Phillips

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Katie J Hincher

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Larry D Cripe

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H Scott Boswell

The jun proto-oncogene is positively autoregulated by its product, Jun/AP-1

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language of work or name

English

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publication date

October 2006

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published in

Experimental Hematology

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volume

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issue

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page(s)

1360-76

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cites work

1 reference

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Regulation of human glutathione S-transferase pi gene transcription: influence of 5'-flanking sequences and trans-activating factors which recognize AP-1-binding sites

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Single cell profiling of potentiated phospho-protein networks in cancer cells.

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Src family tyrosine kinases are activated by Flt3 and are involved in the proliferative effects of leukemia-associated Flt3 mutations

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Catalytic domains of tyrosine kinases determine the phosphorylation sites within c-Cbl

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Criteria for analyzing interactions between biologically active agents

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The mammalian UV response: c-Jun induction is required for exit from p53-imposed growth arrest

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Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53

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Oncogenic and transcriptional cooperation with Ha-Ras requires phosphorylation of c-Jun on serines 63 and 73

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Inactivation of the Wip1 phosphatase inhibits mammary tumorigenesis through p38 MAPK-mediated activation of the p16(Ink4a)-p19(Arf) pathway

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Probing tumor phenotypes using stable and regulated synthetic microRNA precursors

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MLL translocations specify a distinct gene expression profile that distinguishes a unique leukemia

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Survival signaling mediated by c-Jun NH(2)-terminal kinase in transformed B lymphoblasts.

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Targeting JNK for therapeutic benefit: from junk to gold?

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FLT3 signaling in hematopoietic cells involves CBL, SHC and an unknown P115 as prominent tyrosine-phosphorylated substrates

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Role of the adapter protein CRKL in signal transduction of normal hematopoietic and BCR/ABL-transformed cells

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Role for c-jun N-terminal kinase in treatment-refractory acute myeloid leukemia (AML): signaling to multidrug-efflux and hyperproliferation

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FLT3 receptors with internal tandem duplications promote cell viability and proliferation by signaling through Foxo proteins

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Identification of novel FLT-3 Asp835 mutations in adult acute myeloid leukaemia

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The Bcr-Abl leukemia oncogene activates Jun kinase and requires Jun for transformation

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SYK is upstream of phosphoinositide 3-kinase in B cell receptor signaling

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T cell activation induces direct binding of the Crk adapter protein to the regulatory subunit of phosphatidylinositol 3-kinase (p85) via a complex mechanism involving the Cbl protein

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Role of p38alpha Map kinase in Type I interferon signaling

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Role of the p38 mitogen-activated protein kinase pathway in the generation of the effects of imatinib mesylate (STI571) in BCR-ABL-expressing cells

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Transforming growth factor-beta1 (TGF-beta)-induced apoptosis of prostate cancer cells involves Smad7-dependent activation of p38 by TGF-beta-activated kinase 1 and mitogen-activated protein kinase kinase 3

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Regulation of JNK signaling by GSTp

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A direct interaction between JNK1 and CrkII is critical for Rac1-induced JNK activation

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Control of cell cycle progression by c-Jun is p53 dependent

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Mitogenic Signalling and Substrate Specificity of the Flk2/Flt3 Receptor Tyrosine Kinase in Fibroblasts and Interleukin 3-Dependent Hematopoietic Cells

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Loss of oncogenic H-ras-induced cell cycle arrest and p38 mitogen-activated protein kinase activation by disruption of Gadd45a

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Regulation of MAP Kinase Signaling Modules by Scaffold Proteins in Mammals

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Acute myeloid leukemia

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SU5416 and SU5614 inhibit kinase activity of wild-type and mutant FLT3 receptor tyrosine kinase

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FLT3 and MLL intragenic abnormalities in AML reflect a common category of genotoxic stress

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Biologic and clinical significance of the FLT3 transcript level in acute myeloid leukemia

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FLT3 ligand causes autocrine signaling in acute myeloid leukemia cells

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Pim-1 is up-regulated by constitutively activated FLT3 and plays a role in FLT3-mediated cell survival

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RNAi-induced down-regulation of FLT3 expression in AML cell lines increases sensitivity to MLN518.

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AML-associated Flt3 kinase domain mutations show signal transduction differences compared with Flt3 ITD mutations.

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Direct recruitment of CRK and GRB2 to VEGFR-3 induces proliferation, migration, and survival of endothelial cells through the activation of ERK, AKT, and JNK pathways

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The presence of a FLT3 internal tandem duplication in patients with acute myeloid leukemia (AML) adds important prognostic information to cytogenetic risk group and response to the first cycle of chemotherapy: analysis of 854 patients from the Unite

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A FLT3-targeted tyrosine kinase inhibitor is cytotoxic to leukemia cells in vitro and in vivo

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