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Mus musculus

ABSTRACT: BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein

PROVIDER: PRJNA254523 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1508470.fastq.gz	Fastqsanger.gz
	SRR1508471.fastq.gz	Fastqsanger.gz
	SRR1508472.fastq.gz	Fastqsanger.gz
	SRR1508473.fastq.gz	Fastqsanger.gz
	SRR1508474.fastq.gz	Fastqsanger.gz

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BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein

Project description:Coordinated BCR-ABL1 kinase-dependent and -independent mechanisms convert p27 from a nuclear tumor suppressor to a cytoplasmic oncogene. Persistence of oncogenic p27 functions despite effective inhibition of BCR-ABL1 may contribute to resistance to tyrosine kinase inhibitors. BCR-ABL1 induced p27 versus knockout, controlling with Empty vector p27 versus knock out

2014-10-08 | E-GEOD-59168 | biostudies-arrayexpress

BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein

2014-10-08 | GSE59168 | GEO

Effect of Imatinib (1microM, 24 hours) on the microRNA repertoire of chronic myeloid leukemia cell line K562

Project description:Using a microarray-based miRNA profiling, we found in a model of chronic myeloid leukemia (CML) that the activity of the oncoprotein BCR-ABL1 regulates the expression of miR-21, a "onco-microRNA" known to be overexpressed in numerous cancers. This relies on the phosphorylation status of STAT5, a transcription factor known to be activated by the kinase activity of BCR-ABL1. Mir-21 regulates the expression of PDCD4 (programmed cell death protein 4), a tumor suppressor identified here through a proteomics approach

2017-09-01 | GSE78037 | GEO

Effect of Imatinib (1microM, 24 hours) on the microRNA repertoire of chronic myeloid leukemia cell line K562

2016-09-01 | E-GEOD-78037 | biostudies-arrayexpress

Mus musculus

Project description:Efficacy of retinoids in IKZF1-mutated BCR-ABL1 acute lymphoblastic leukemia

| PRJNA282594 | ENA

SHP2 Is Required for BCR-ABL1-Induced Hematologic Neoplasms

Project description:BCR-ABL1-targeting tyrosine kinase inhibitors (TKIs) have revolutionized treatment of Philadelphia chromosome-positive (Ph+) hematologic neoplasms. Nevertheless, acquired TKI resistance remains a major problem in chronic myeloid leukemia (CML), and TKIs are less effective against Ph+ B-cell acute lymphoblastic leukemia (B-ALL). GAB2, a scaffolding adaptor that binds and activates SHP2, is essential for leukemogenesis by BCR-ABL1, and a GAB2 mutant lacking SHP2 binding cannot mediate leukemogenesis. Using a genetic loss-of-function approach and bone marrow transplantation (BMT) models for CML and BCR-ABL1+ B-ALL, we show that SHP2 is required for BCR-ABL1-evoked myeloid and lymphoid neoplasia. Ptpn11 deletion impairs initiation and maintenance of CML-like myeloproliferative neoplasm, and compromises induction of BCR-ABL1+ B-ALL. SHP2, and specifically, its SH2 domains, PTP activity and C-terminal tyrosines, is essential for BCR-ABL1+, but not WT, pre-B cell proliferation. The MEK/ERK pathway is regulated by SHP2 in WT and BCR-ABL1+ pre-B cells, but is only required for the proliferation of BCR-ABL1+ cells. SHP2 is required for SRC family kinase (SFK) activation only in BCR-ABL1+ pre-B cells. RNAseq reveals distinct SHP2-dependent transcriptional programs in BCR-ABL1+ and WT pre-B cells. Our results suggest that SHP2, via SFKs and ERK, represses MXD3/4 to facilitate a MYC-dependent proliferation program in BCR-ABL1-transformed pre-B cells.

2017-06-06 | GSE99656 | GEO

De novo BCR-ABL linear kinase motifs revealed by phosphoproteomics in yeast

Project description:Protein tyrosine phosphorylation (pY) is central to many cellular signaling pathways. Deregulation of pY can lead to malignancies such as leukemia. Thus, assigning kinase-substrate relations is imperative to understand disease alterations. However, such efforts are complicated by kinase redundancy, overlapping specificity and magnitude differences in enzymatic activity. BCR/ABL, the predominant oncogene in leukemia, drives malignant transformation by deregulated tyrosine kinase activity. In this study, phosphorylation activity and specificity of human ABL1 and BCR/ABL have been examined in yeast by state-of-the-art phosphoproteomics. Linear sequence motif scores were generated and used for cross-kingdom (fungi to metazoa) phosphorylation analysis. Phosphoproteomic analysis of ABL1 and BCR/ABL yielded a high-confidence pY-dataset of 1186 peptides covering 1127 sites on 821 proteins. Motif scores generated from this dataset allow for examination of ABL1 and BCR/ABL kinase activity in human cell lines, and clearly identified BCR/ABL p210 in the chronic myeloid leukemia cell line K562. This cross-kingdom approach offers valuable insights into the human phosphoproteome.

2023-07-20 | PXD038551 | Pride

Mus musculus

Project description:Ikaros-regulated genes in a mouse model of BCR-ABL1+ acute lymphoblastic leukemia

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Mus musculus

Project description:CGH data from AID WT vs AID KO BCR-ABL1 mouse leukemia cells

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Comparison of copy number variations between wildtype and BCL6 knockout BCR-ABL1-driven acute lymphoblastic leukemia

Project description:This comparative genomic hybridization (CGH) study investigated the effect of BCL6 on clonal evolution in BCR-ABL1-driven acute lymphoblastic leukemia (ALL). The frequencies of copy number alterations in BCR-ABL1-transformed BCL6+/+ and BCL6-/- leukemias were determined.

2010-09-29 | GSE24400 | GEO

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