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Oliver Hantschel

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Publications associées (44)

Structural and functional dissection of the DH and PH domains of oncogenic Bcr-Abl tyrosine kinase

Florence Pojer, Oliver Hantschel, Sandrine Madeleine Suzanne Georgeon, Delphine Maude Tardivon, Sina Maren Reckel, Barbara Gerig, Tim Kükenshöner, Sara Raquel Pereira Pinho, Charlotte Julie Caroline Gehin

The two isoforms of the Bcr-Abl tyrosine kinase, p210 and p190, are associated with different leukemias and have a dramatically different signaling network, despite similar kinase activity. To provide a molecular rationale for these observations, we study ...

Springer Nature2017

NDEL1-PDGFRB fusion gene in a myeloid malignancy with eosinophilia associated with resistance to tyrosine kinase inhibitors

Oliver Hantschel

Nature Publishing Group2016

Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases

Oliver Hantschel

Leukemias expressing constitutively activated mutants of ABL1 tyrosine kinase (BCR-ABL1, TEL-ABL1, NUP214-ABL1) usually contain at least 1 normal ABL1 allele. Because oncogenic and normal ABL1 kinases may exert opposite effects on cell behavior, we examine ...

American Society of Hematology2016

Identification and Characterization of Tyrosine Kinase Nonreceptor 2 Mutations in Leukemia through Integration of Kinase Inhibitor Screening and Genomic Analysis

Oliver Hantschel, Sina Maren Reckel

The amount of genomic information about leukemia cells currently far exceeds our overall understanding of the precise genetic events that ultimately drive disease development and progression. Effective implementation of personalized medicine will require t ...

American Association for Cancer Research2016

Allosteric Inhibition of Bcr-Abl Kinase by High Affinity Monobody Inhibitors Directed to the Src Homology 2 (SH2)-Kinase Interface

Oliver Hantschel, Allan Joaquim Lamontanara, Barbara Gerig

Bcr-Abl is a constitutively active kinase that causes chronic myelogenous leukemia. We have shown that a tandem fusion of two designed binding proteins, termed monobodies, directed to the interaction interface between the Src homology 2 (SH2) and kinase do ...

American Society for Biochemistry and Molecular Biology2016

Alkaline phosphatase-fused repebody as a new format of immuno-reagent for an immunoassay

Oliver Hantschel

Enzyme-linked immunoassays based on an antibody-antigen interaction are widely used in biological and medical sciences. However, the conjugation of an enzyme to antibodies needs an additional chemical process, usually resulting in randomly cross-linked mol ...

Elsevier2016

2016 International Symposium on Chemical Biology of the NCCR Chemical Biology Campus Biotech, Geneva 13-15.1.2016

Oliver Hantschel, Beat Fierz

Schweizerische Chemische Gesellschaft2016

Modulating protein-protein interaction with a molecular tether

Kai Johnsson, Oliver Hantschel, Helen Rebecca Ostlund Farrants

Wiley-Blackwell2015

Unexpected Off-Targets and Paradoxical Pathway Activation by Kinase Inhibitors

Oliver Hantschel

Protein kinase inhibitors are an increasingly important class of targeted anticancer therapeutics. More than two dozen new drugs of this class have entered routine clinical use over the past decade. This review article focuses on how the development of met ...

2015

Kinase Regulation in Mycobacterium tuberculosis: Variations on a Theme

Oliver Hantschel, Sina Maren Reckel

In this issue of Structure, Lisa et al. (2015) examine how the PknG protein kinase of M. tuberculosis efficiently binds and phosphorylates substrates. The work highlights interesting parallels between PknG and eukaryotic protein kinases. ...

Elsevier2015

Crystal structure of an SH2-kinase construct of c-Abl and effect of the SH2 domain on kinase activity

Oliver Hantschel

Constitutive activation of the non-receptor tyrosine kinase c-Abl (cellular Abelson tyrosine protein kinase 1, Abl1) in the Bcr (breakpoint cluster region)-Abl1 fusion oncoprotein is the molecular cause of chronic myeloid leukaemia (CML). Recent studies ha ...

Portland Press2015

Targeting BCR-ABL and JAK2 in Ph+ ALL

Oliver Hantschel

In this issue of Blood, Appelmann et al provide evidence for prolonged survival and prevention of resistance in a mouse model of Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) by combined targeting of the BCR-ABL kinase and Janus ...

2015

The SH2 Domain of BCR-ABL1 Regulates Kinase Autophosphorylation By Controlling Activation Loop Accessibility

Oliver Hantschel, Sandrine Madeleine Suzanne Georgeon, Allan Joaquim Lamontanara

Amer Soc Hematology2014

NUP214-ABL1 mediated cell proliferation in T-cell acute lymphoblastic leukemia is dependent on the LCK kinase and various interacting proteins

Oliver Hantschel

The NUP214-ABL1 fusion protein is a constitutively active protein tyrosine kinase that is found in 6% of patients with T-cell acute lymphoblastic leukemia and that promotes proliferation and survival of T-lymphoblasts. Although NUP214-ABL1 is sensitive to ...

Pensiero Scientifico / Ferrata Storti Foundation2014

Specificity and mechanism-of-action of the JAK2 tyrosine kinase inhibitors ruxolitinib and SAR302503 (TG101348)

Roland Moser, Oliver Hantschel, Sandrine Madeleine Suzanne Georgeon

Nature Publishing Group2014

The SH2 domain of Abl kinases regulates kinase autophosphorylation by controlling activation loop accessibility

Oliver Hantschel, Sandrine Madeleine Suzanne Georgeon, Allan Joaquim Lamontanara

The activity of protein kinases is regulated by multiple molecular mechanisms, and their disruption is a common driver of oncogenesis. A central and almost universal control element of protein kinase activity is the activation loop that utilizes both confo ...

Nature Research2014

Mechanisms of resistance to BCR-ABL and other kinase inhibitors

Emel Basak Gencer Akçok, Oliver Hantschel, Orest Kuzyk, Allan Joaquim Lamontanara

In this article, we are reviewing the molecular mechanisms that lead to kinase inhibitor resistance. As the oncogenic BCR-ABL kinase is the target of the first approved small-molecule kinase inhibitor imatinib, we will first focus on the structural and mec ...

Elsevier Science Bv2013

Dissection of the BCR-ABL signaling network using highly specific monobody inhibitors to the SHP2 SH2 domains

Emel Basak Gencer Akçok, Oliver Hantschel, Sandrine Madeleine Suzanne Georgeon

The dysregulated tyrosine kinase BCR-ABL causes chronic myelogenous leukemia in humans and forms a large multiprotein complex that includes the Src-homology 2 (SH2) domain-containing phosphatase 2 (SHP2). The expression of SHP2 is necessary for BCR-ABL-dep ...

National Academy of Sciences2013

Mig6 is a sensor of EGF receptor inactivation that directly activates c-Abl to induce apoptosis during epithelial homeostasis

Oliver Hantschel

A fundamental aspect of epithelial homeostasis is the dependence on specific growth factors for cell survival, yet the underlying mechanisms remain obscure. We found an "inverse" mode of receptor tyrosine kinase signaling that directly links ErbB receptor ...

Cell Press - Elsevier2012

Structure, regulation, signaling, and targeting of abl kinases in cancer

Oliver Hantschel

Abl kinases are prototypic cytoplasmic tyrosine kinases and are involved in a variety of chromosomal aberrations in different cancers. This causes the expression of Abl fusion proteins, such as Bcr-Abl, that are constitutively activated and drivers of tumo ...

2012

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