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ABL Tyrosine Kinase Phosphorylates DGCR8 to Stimulate MicroRNA Processing in DNA Damage Response

ABSTRACT: miR-seq to find miRs that are induced by DNA damage and whose induction requires ABL kinase activity

ORGANISM(S): Homo sapiens

PROVIDER: GSE59028 | GEO | 2015/07/01

SECONDARY ACCESSION(S): PRJNA254155

REPOSITORIES: GEO

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ABL Tyrosine Kinase Phosphorylates DGCR8 to Stimulate MicroRNA Processing in DNA Damage Response

Project description:miR-seq to find miRs that are induced by DNA damage and whose induction requires ABL kinase activity Use p53-inactive HEK293T cells. Use doxorubicin to induce DNA damage. Use imatinib co-treatment to inhibit ABL kinase activity

2015-07-01 | E-GEOD-59028 | biostudies-arrayexpress

The kinase ABL phosphorylates the microprocessor subunit DGCR8 to stimulate primary microRNA processing in response to DNA damage.

Project description: Not available

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Project description:Tyrosine kinase activity is the crucial enzymatic activity driving all known functions of the BCR-ABL protein and is required for protection from apoptosis by BCR-ABL, therefore, targeting this enzyme is an effective approach for therapeutic strategies. Recently, a novel structural entity, imatinib (STI571; Novartis, Basel, Switzerland), a potent and selective inhibitor of the tyrosine kinase activity of BCR-ABL, has shown promise against Ph-positive leukemia in human clinical trials. However, the emergence of imatinib resistance in patients with acute forms of Ph-positive leukemia has highlighted the need for overriding chemotherapy to eradicate this disease. AMN107 and BMS-354825 are clinically active “next-generation” BCR-ABL inhibitors. One potentially powerful approach is to use these compounds in combination with imatinib. The rationale for such approaches is that an inhibitor cocktail may target the widest range of resistant clones and thereby delay the onset of acquired drug resistance. More potent BCR-ABL inhibitors would be to target residual leukemia that persists in patients in whom imatinib induces durable remission but failed to eradicate the disease. From these points, our studies are performed to determine (1) the differences of molecular signaling pathways between BMS-354825 and imatinib (2) the mechanisms by which drug resistance of BMS-354825 and imatinib occur except for point mutation of BCR-ABL kinase domain. Keywords: drug sensitivity

2006-03-31 | GSE2810 | GEO

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Project description:Gene expression profile variation between 4 BCR-Abl transduced cell lines: 1-Mouse DA1-3b cell line as reference, 2-DR1 imatinib resistant clone with E255K BCR-abl mutation 3-DRBMSR 2 dasatinib resistant clone with E255K and T315I BCR-Abl mutation. 4-DRBMSR 7 dasatinib resistant clone with E255K and T315I and V299L BCR-Abl mutation BCR-ABL is an oncogenic tyrosine kinase involved in the development of chronic myelogenous leukaemia (CML).

2007-08-01 | E-MEXP-772 | biostudies-arrayexpress

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Project description: Not available

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Abl subtrates using tyrosine phosphoproteomics

Project description:In this study, we have prepared a mouse embryonic fibrobalst (MEF) cell line stably expressing R367A mutant human Abl in which the native mouse Abl1 and Abl2 were genetically deleted. We have used these R367A mutant Abl cells in combination with mass spectrometry to identify phosphorylation targets of Abl. Below, we describe these findings and their potential biological significance.

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The Hippo pathway kinase Lats2 prevents DNA damage-induced apoptosis through inhibition of the tyrosine kinase c-Abl.

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An East-Asian polymorphism underlies BCR-ABL mutation-independent resistance to tyrosine kinase inhibitors in chronic myelogenous leukemia

Project description:We used massively parallel DNA sequencing of paired-end ditags (DNA-PET) to identify structural genetic factors associated with disease progression and drug-resistance in representative samples from four CML patients and one CML cell line. The functional consequences of our genetic findings were evaluated in primary CML cells and cell lines, and validated in a larger CML cohort. We discovered a novel intronic deletion that correlated with imatinib-resistance, and was subsequently confirmed to be a polymorphism in normal East-Asian, but not African or Caucasian, populations. We found that the polymorphism favored expression of transcripts lacking a pro-apoptotic domain, which is critical for imatinib-induced cell death. A CML cell line containing the polymorphism also exhibited BCR-ABL-independent imatinib-resistance.

2012-02-27 | GSE28303 | GEO

An East-Asian polymorphism underlies BCR-ABL mutation-independent resistance to tyrosine kinase inhibitors in chronic myelogenous leukemia

2012-02-27 | E-GEOD-28303 | biostudies-arrayexpress

CEA_SGF:E00010#bcr-abl

Project description:Chronic myelogenous leukemia (CML) is a malignant disease of the hematopoietic stem cell, characterized by the expression of the Bcr-Abl oncogene by leukemic cells. In order to analyze the molecular pathways modulated by Bcr-Abl, we have previously generated an inducible model of Bcr-Abl expression in the murine Ba/F3 cell line based on the Tet-OFF system. In the present study, through a microarray approach applied to cells grown with (Bcr-Abl-expression OFF) or without (Bcr-Abl-expression ON) doxycycline, a tetracycline analogue, we analyzed the gene expression variations upon Bcr-Abl expression. Keywords: repeat sample

2005-05-01 | GSE1429 | GEO

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