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

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Location: Deutsche Nationalbibliothek Frankfurt am Main

Extent: Online-Ressource

Language: Englisch

Bibliographic citation: In: Nature Communications, 8.2017, Nr. 1, Art. 2101, doi:10.1038/s41467-017-02313-6

Classification: Biowissenschaften, Biologie

Event: Veröffentlichung

(where): Frankfurt am Main

(who): Universitätsbibliothek Johann Christian Senckenberg

(when): 2017

Creator: Reckel, Sina
Gehin, Charlotte
Tardivon, Delphine
Georgeon, Sandrine
Kükenshöner, Tim
Löhr, Frank
Koide, Akiko
Buchner, Lena
Panjkovich, Alejandro
Reynaud, Aline
Pinho, Sara
Gerig, Barbara
Svergun, Dmitri
Pojer, Florence
Güntert, Peter
Dötsch, Volker
Koide, Shohei
Gavin, Anne-Claude
Hantschel, Oliver

URN: urn:nbn:de:hebis:30:3-456101

Rights: Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 14.08.2025, 10:46 AM CEST

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Associated

Reckel, Sina
Gehin, Charlotte
Tardivon, Delphine
Georgeon, Sandrine
Kükenshöner, Tim
Löhr, Frank
Koide, Akiko
Buchner, Lena
Panjkovich, Alejandro
Reynaud, Aline
Pinho, Sara
Gerig, Barbara
Svergun, Dmitri
Pojer, Florence
Güntert, Peter
Dötsch, Volker
Koide, Shohei
Gavin, Anne-Claude
Hantschel, Oliver
Universitätsbibliothek Johann Christian Senckenberg

Time of origin

2017

Other Objects (12)

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

Bcr-Abl tyrosine kinase inhibitors- current status

Combined targeting of GPX4 and BCR-ABL tyrosine kinase selectively compromises BCR-ABL+ leukemia stem cells

Pharmacological difference between degrader and inhibitor against oncogenic BCR-ABL kinase

Hochschulschrift

Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen

BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?

Targeted degradation of oncogenic BCR-ABL by silencing the gene of NEDD8 E3 ligase RAPSYN

The pro-metastasis tyrosine phosphatase, PRL-3 (PTP4A3), is a novel mediator of oncogenic function of BCR-ABL in human chronic myeloid leukemia

BCR/ABL positive thrombocythemia: a diagnostic dilemma

Vergleich der Dynamik von BCR-ABL Transkripten und BCR-ABL DNA-Kopienzahlen unter Imatinibtherapie bei der Chronisch Myeloischen Leukämie

Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis

The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification

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

Bcr-Abl tyrosine kinase inhibitors- current status

Combined targeting of GPX4 and BCR-ABL tyrosine kinase selectively compromises BCR-ABL+ leukemia stem cells

Pharmacological difference between degrader and inhibitor against oncogenic BCR-ABL kinase

Hochschulschrift

Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen

BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?

Targeted degradation of oncogenic BCR-ABL by silencing the gene of NEDD8 E3 ligase RAPSYN

The pro-metastasis tyrosine phosphatase, PRL-3 (PTP4A3), is a novel mediator of oncogenic function of BCR-ABL in human chronic myeloid leukemia

BCR/ABL positive thrombocythemia: a diagnostic dilemma

Vergleich der Dynamik von BCR-ABL Transkripten und BCR-ABL DNA-Kopienzahlen unter Imatinibtherapie bei der Chronisch Myeloischen Leukämie

Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis

The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification

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

Bcr-Abl tyrosine kinase inhibitors- current status

Combined targeting of GPX4 and BCR-ABL tyrosine kinase selectively compromises BCR-ABL+ leukemia stem cells

Pharmacological difference between degrader and inhibitor against oncogenic BCR-ABL kinase

Hochschulschrift

Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen

BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?

Targeted degradation of oncogenic BCR-ABL by silencing the gene of NEDD8 E3 ligase RAPSYN

The pro-metastasis tyrosine phosphatase, PRL-3 (PTP4A3), is a novel mediator of oncogenic function of BCR-ABL in human chronic myeloid leukemia

BCR/ABL positive thrombocythemia: a diagnostic dilemma

Vergleich der Dynamik von BCR-ABL Transkripten und BCR-ABL DNA-Kopienzahlen unter Imatinibtherapie bei der Chronisch Myeloischen Leukämie

Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis

The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification

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

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Other Objects (12)

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

Bcr-Abl tyrosine kinase inhibitors- current status

Combined targeting of GPX4 and BCR-ABL tyrosine kinase selectively compromises BCR-ABL+ leukemia stem cells

Pharmacological difference between degrader and inhibitor against oncogenic BCR-ABL kinase

Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen

BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?

Targeted degradation of oncogenic BCR-ABL by silencing the gene of NEDD8 E3 ligase RAPSYN

The pro-metastasis tyrosine phosphatase, PRL-3 (PTP4A3), is a novel mediator of oncogenic function of BCR-ABL in human chronic myeloid leukemia

BCR/ABL positive thrombocythemia: a diagnostic dilemma

Vergleich der Dynamik von BCR-ABL Transkripten und BCR-ABL DNA-Kopienzahlen unter Imatinibtherapie bei der Chronisch Myeloischen Leukämie

Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis

The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification

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

Bcr-Abl tyrosine kinase inhibitors- current status

Combined targeting of GPX4 and BCR-ABL tyrosine kinase selectively compromises BCR-ABL+ leukemia stem cells

Pharmacological difference between degrader and inhibitor against oncogenic BCR-ABL kinase

Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen

BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?

Targeted degradation of oncogenic BCR-ABL by silencing the gene of NEDD8 E3 ligase RAPSYN

The pro-metastasis tyrosine phosphatase, PRL-3 (PTP4A3), is a novel mediator of oncogenic function of BCR-ABL in human chronic myeloid leukemia

BCR/ABL positive thrombocythemia: a diagnostic dilemma

Vergleich der Dynamik von BCR-ABL Transkripten und BCR-ABL DNA-Kopienzahlen unter Imatinibtherapie bei der Chronisch Myeloischen Leukämie

Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis

The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification

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

Bcr-Abl tyrosine kinase inhibitors- current status

Combined targeting of GPX4 and BCR-ABL tyrosine kinase selectively compromises BCR-ABL+ leukemia stem cells

Pharmacological difference between degrader and inhibitor against oncogenic BCR-ABL kinase

Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen

BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?

Targeted degradation of oncogenic BCR-ABL by silencing the gene of NEDD8 E3 ligase RAPSYN

The pro-metastasis tyrosine phosphatase, PRL-3 (PTP4A3), is a novel mediator of oncogenic function of BCR-ABL in human chronic myeloid leukemia

BCR/ABL positive thrombocythemia: a diagnostic dilemma

Vergleich der Dynamik von BCR-ABL Transkripten und BCR-ABL DNA-Kopienzahlen unter Imatinibtherapie bei der Chronisch Myeloischen Leukämie

Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis

The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification

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