Hochschulschrift
Identification of Protein Tyrosine Phosphatases regulating FLT3 activity and of PTPs regulated by FLT3 ITD
- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- Extent
-
Online-Ressource
- Language
-
Deutsch
- Notes
-
Jena, Friedrich-Schiller-Universität Jena, Dissertation, 2010
- Keyword
-
Phosphatases
Identification
Tyrosine
- Event
-
Veröffentlichung
- (where)
-
Jena
- (who)
-
Friedrich-Schiller-Universität Jena
- (when)
-
2011
- Creator
- Contributor
-
Böhmer, Frank-Dietmar
Huijsduijnen, Rob Hooft van
Scholl, Sebastian
- URN
-
urn:nbn:de:gbv:27-20110201-112909-6
- Rights
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
25.03.2025, 1:42 PM CET
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Object type
- Hochschulschrift
Associated
- Arora, Deepika
- Böhmer, Frank-Dietmar
- Huijsduijnen, Rob Hooft van
- Scholl, Sebastian
- Friedrich-Schiller-Universität Jena
Time of origin
- 2011
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The RET receptor tyrosine kinase promotes AML through protection of mutant FLT3 from autophagic degradation
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BCL-2 inhibition synergizes with dual targeting of FLT3 and AXL in FLT3 wildtype AML via downregulation of MCL-1
Combined targeting of the Menin-MLL chromatin regulatory complex and the FLT3 tyrosine kinase as a novel therapeutic approach against NPM1mut and MLL-r leukemia with concurrent FLT3 mutation
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Remarkable leukemogenic potency of the novel FLT3-N676K mutant
FLT3-ITD regulated miRs in AML
Receptor protein-tyrosine phosphatases controlling activity of the oncoprotein FLT3 ITD
Abnormal Localization and Accumulation of FLT3-ITD, a Mutant Receptor Tyrosine Kinase Involved in Leukemogenesis
The RET receptor tyrosine kinase promotes AML through protection of mutant FLT3 from autophagic degradation
FLT3-Mutationen und ihre Signaltransduktion
Oxidation of protein tyrosine phosphatases as an oncogenic event in FLT3-ITD positive acute myeloid leukemia
CCL5 mediates target-kinase independent resistance to FLT3 inhibitors in FLT3-ITD-positive AML
Modulation of FLT3-ITD Localization and Targeting of Distinct Downstream Signaling Pathways as Potential Strategies to Overcome FLT3-Inhibitor Resistance
BCL-2 inhibition synergizes with dual targeting of FLT3 and AXL in FLT3 wildtype AML via downregulation of MCL-1
Combined targeting of the Menin-MLL chromatin regulatory complex and the FLT3 tyrosine kinase as a novel therapeutic approach against NPM1mut and MLL-r leukemia with concurrent FLT3 mutation
Impact of FLT3 internal tandem duplications (FLT3-ITD) on functional biology and sensitivity to therapy depending on their location
Remarkable leukemogenic potency of the novel FLT3-N676K mutant
FLT3-ITD regulated miRs in AML
Receptor protein-tyrosine phosphatases controlling activity of the oncoprotein FLT3 ITD
Abnormal Localization and Accumulation of FLT3-ITD, a Mutant Receptor Tyrosine Kinase Involved in Leukemogenesis
The RET receptor tyrosine kinase promotes AML through protection of mutant FLT3 from autophagic degradation
FLT3-Mutationen und ihre Signaltransduktion
Oxidation of protein tyrosine phosphatases as an oncogenic event in FLT3-ITD positive acute myeloid leukemia
CCL5 mediates target-kinase independent resistance to FLT3 inhibitors in FLT3-ITD-positive AML
Modulation of FLT3-ITD Localization and Targeting of Distinct Downstream Signaling Pathways as Potential Strategies to Overcome FLT3-Inhibitor Resistance
BCL-2 inhibition synergizes with dual targeting of FLT3 and AXL in FLT3 wildtype AML via downregulation of MCL-1
Combined targeting of the Menin-MLL chromatin regulatory complex and the FLT3 tyrosine kinase as a novel therapeutic approach against NPM1mut and MLL-r leukemia with concurrent FLT3 mutation
Impact of FLT3 internal tandem duplications (FLT3-ITD) on functional biology and sensitivity to therapy depending on their location