Harald Polzer
YOU?
Author Swipe
Supplementary Methods and Figure Legend from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 69K.
Data from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
Activating mutations of the class III receptor tyrosine kinase FLT3 are the most frequent molecular aberration in acute myeloid leukemia (AML). Mutant FLT3 accelerates proliferation, suppresses apoptosis, and correlates with poor prognosis…
Supplementary Figure 6 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 46K, IL-3-independent Ba/F3 cells expressing FLT3-ITD are more strongly affected by LBH589/AC220 combinations than IL-3-dependent control cells.
Supplementary Figure 2 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 43K, FLT3-ITD knockdown sensitizes AML cells for HDACi-induced apoptosis.
Supplementary Figure 3 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 38K, Caspase 3 contributes to the degradation of FLT3.
Supplementary Figure 5 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 54K, LBH589 and AC220 specifically induce degradation of STAT5 in leukemic cells expressing FLT3-ITD.
Supplementary Figure 6 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 46K, IL-3-independent Ba/F3 cells expressing FLT3-ITD are more strongly affected by LBH589/AC220 combinations than IL-3-dependent control cells.
Supplementary Figure 3 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 38K, Caspase 3 contributes to the degradation of FLT3.
Supplementary Figure 4 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 48K, LBH589 and AC220 synergistically induce Apoptosis in MV4-11 cells.
Supplementary Figure 5 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 54K, LBH589 and AC220 specifically induce degradation of STAT5 in leukemic cells expressing FLT3-ITD.
Supplementary Figure 1 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 31K, LBH589 induces histone acetylation in MV4-11 cells.
Supplementary Figure 1 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 31K, LBH589 induces histone acetylation in MV4-11 cells.
Data from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
Activating mutations of the class III receptor tyrosine kinase FLT3 are the most frequent molecular aberration in acute myeloid leukemia (AML). Mutant FLT3 accelerates proliferation, suppresses apoptosis, and correlates with poor prognosis…
Supplementary Figure 4 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 48K, LBH589 and AC220 synergistically induce Apoptosis in MV4-11 cells.
Supplementary Methods and Figure Legend from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 69K.
Supplementary Figure 2 from Breakdown of the FLT3-ITD/STAT5 Axis and Synergistic Apoptosis Induction by the Histone Deacetylase Inhibitor Panobinostat and FLT3-Specific Inhibitors Open
PDF file, 43K, FLT3-ITD knockdown sensitizes AML cells for HDACi-induced apoptosis.
Targeting FLT3 with a new-generation antibody-drug conjugate in combination with kinase inhibitors for treatment of AML Open
Fms-like tyrosine kinase 3 (FLT3) is often overexpressed or constitutively activated by internal tandem duplication (ITD) and tyrosine kinase domain (TKD) mutations in acute myeloid leukemia (AML). Despite the use of receptor tyrosine kina…
The target landscape of clinical kinase drugs Open
An atlas for drug interactions Kinase inhibitors are an important class of drugs that block certain enzymes involved in diseases such as cancer and inflammatory disorders. There are hundreds of kinases within the human body, so knowing the…
The new and recurrent FLT3 juxtamembrane deletion mutation shows a dominant negative effect on the wild-type FLT3 receptor Open
In acute myeloid leukemia (AML), the Fms-like tyrosine kinase 3 ( FLT3) is one of the most frequently mutated genes. Recently, a new and recurrent juxtamembrane deletion mutation (p.Q569Vfs*2) resulting in a truncated receptor was identifi…