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Publikationer (hämtat ur Lunds universitets publikationsdatabas)
- Deregulation of protein phosphatase expression in acute myeloid leukemia
- FLT3 mutations in patients with childhood acute lymphoblastic leukemia (ALL)
- FLT3 signals via the adapter protein Grb10 and overexpression of Grb10 leads to aberrant cell proliferation in acute myeloid leukemia.
- Phosphorylation of the activation loop tyrosine 823 in c-Kit is crucial for cell survival and proliferation.
- Protein kinase C (PKC) as a drug target in chronic lymphocytic leukemia.
- Selective mutation in ATP-binding site reduces affinity of drug to the kinase: a possible mechanism of chemo-resistance
- Suppressor of cytokine signaling 2 (SOCS2) associates with FLT3 and negatively regulates downstream signaling.
- The PI3-kinase isoform p110δ is essential for cell transformation induced by the D816V mutant of c-Kit in a lipid-kinase-independent manner.
- The presence or absence of IL-3 during long-term culture of Flt3-ITD and c-Kit-D816V expressing Ba/F3 cells influences signaling outcome.
- The tyrosine kinase CSK associates with FLT3 and c-Kit receptors and regulates downstream signaling.
- Adaptor protein Lnk binds to and inhibits normal and leukemic FLT3
- Src-Like Adaptor Protein (SLAP) Binds to the Receptor Tyrosine Kinase Flt3 and Modulates Receptor Stability and Downstream Signaling.
- Suppressor Of cytokine signaling 6 (SOCS6) negatively regulates Flt3 signal transduction through direct binding to phosphorylated Tyr 591 and Tyr 919 of Flt3.
- Bioinformatic prediction and analysis of eukaryotic protein kinases in the rat genome.
- Celecoxib-induced growth inhibition in SW480 colon cancer cells is associated with activation of protein kinase G
- Induction of the nuclear proto-oncogene c-fos by the phorbol ester TPA and v-H-Ras.
- Role of Regulatory Domain Mutants of PKC Isoforms in c-fos Induction