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- Aberrant activation of the PI3K/mTOR pathway promotes resistance to sorafenib in AML
- Expression of GADS enhances FLT3-induced mitogenic signaling.
- FYN expression potentiates FLT3-ITD induced STAT5 signaling in acute myeloid leukemia.
- HIF2α contributes to antiestrogen resistance via positive bilateral crosstalk with EGFR in breast cancer cells.
- Src-like adaptor protein 2 (SLAP2) binds to and inhibits FLT3 signaling
- BEX1 acts as a tumor suppressor in acute myeloid leukemia.
- Brain-Expressed X-linked (BEX) proteins in human cancers.
- PI3 kinase is indispensable for oncogenic transformation by the V560D mutant of c-Kit in a kinase-independent manner.
- Role of SRC-like adaptor protein (SLAP) in immune and malignant cell signaling.
- The Phosphatases STS1 and STS2 Regulate Hematopoietic Stem and Progenitor Cell Fitness.
- The activation loop tyrosine 823 is essential for the transforming capacity of the c-Kit oncogenic mutant D816V.
- The role of HOXB2 and HOXB3 in acute myeloid leukemia.
- Grb10 is a dual regulator of receptor tyrosine kinase signaling
- Keratin 19 expression correlates with poor prognosis in breast cancer
- SOCS proteins in regulation of receptor tyrosine kinase signaling.
- SOCS6 (suppressor of cytokine signaling 6)
- SOCS6 is a selective suppressor of receptor tyrosine kinase signaling
- SYK Is a Critical Regulator of FLT3 in Acute Myeloid Leukemia.
- Src-Like Adaptor Protein (SLAP) differentially regulates normal and oncogenic c-Kit 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.
- 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.
- Protein kinase C expression is deregulated 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 basic helix-loop-helix (bHLH) proteins in breast cancer progression
- 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.
- Comparative Studies on Human and Rat Basic Helix-loop-helix Proteins
- Comparative analysis of human and bovine protein kinases reveals unique relationship and functional diversity
- Maximum likelihood analysis of mammalian p53 indicates the presence of positively selected sites and higher tumorigenic mutations in purifying sites
- The mechanism of protein kinase C regulation
- 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