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

to related objects

Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 2041-1723

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Structural and functional dissection of the DH and PH domains of oncogenic Bcr-Abl tyrosine kinase ; volume:8 ; number:1 ; day:13 ; month:12 ; year:2017 ; pages:1-14 ; date:12.2017
Nature Communications ; 8, Heft 1 (13.12.2017), 1-14, 12.2017

Classification: Biowissenschaften, Biologie

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

Contributor: SpringerLink (Online service)

DOI: 10.1038/s41467-017-02313-6

URN: urn:nbn:de:101:1-2019070801325469362869

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:35 AM CEST

Data provider

This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.

Show original at data provider

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
SpringerLink (Online service)

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

Cultural heritage institutions wishing to register will find more information here.

Fields marked * need to be filled in.

Username*

Please enter your username

Email*

Please enter your email address

Please do not fill this field

First name

Last name

Password*

Please enter your password

Confirm password*

Please enter the same password

I have read the terms of use and the privacy policy for the collection of personal data and accept them. *

This field is required.

I would like to subscribe to the newsletter of the Deutsche Digitale Bibliothek. See newsletter subscription info.

Account created

Your "My DDB" account has been successfully created. Before you can log in to your account, you must click the confirmation link in the message we just sent to the email address you provided.

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

Object Details

References and Relationships

Classification and Topics

Contributors, Places and Time

Further information

Data provider

Associated

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

Related objects

Reset password