Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Beta-catenin interacting proteins in BCR-ABL1+ B-ALL cells [exp2]

ABSTRACT: Identification of beta-catenin interacting proteins via affinity purification with anti-beta-catenin antibody or IgG control in BCR-ABL1 transformed murine pre-B cells with induced beta-catenin activation via CTNNB1 exon3 fl/fl + Cre.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): B Cell, Bone Marrow

DISEASE(S): Acute Leukemia

SUBMITTER: Mark Robinson

LAB HEAD: Markus Muschen

PROVIDER: PXD067314 | Pride | 2025-08-13

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20-2022.mzid.gz	Mzid
	20-2022.mzid.gz_20200117_nst9054_20-2022_Muschen_Cosgun_B-Catenin_2__F025964_.MGF	Mzid
	20-2022.mzid.gz_20200117_nst9054_20-2022_Muschen_Cosgun_B-catenin_1__F025963_.MGF	Mzid
	20-2022.mzid.gz_20200117_nst9054_20-2022_Muschen_Cosgun_B-catenin_3__F025965_.MGF	Mzid
	20-2022.mzid.gz_20200117_nst9054_20-2022_Muschen_Cosgun_Flag1__F025966_.MGF	Mzid

Items per page:

1 - 5 of 20

Similar Datasets

Beta-catenin interacting proteins in BCR-ABL1+ B-ALL cells [exp1]

Project description:Identification of beta-catenin interacting proteins via affinity purification with anti-beta-catenin antibody or IgG control in BCR-ABL1 transformed murine pre-B cells with induced beta-catenin activation via CTNNB1 exon3 fl/fl + Cre.

2025-08-13 | PXD067271 | Pride

Beta-catenin interacting proteins in WT and Ikzf1/3-KO BCR-ABL1 transformed B-ALL

Project description:Identification of beta-catenin interacting proteins via affinity purification with anti-beta-catenin antibody or IgG control in WT (NTC control) or Ikzf1/Ikzf3-KO (dual CRISPR KO) BCR-ABL1 transformed murine pre-B cells with CTNNB1 activation via a Ctnnb1 Ex3 fl/fl + Ert2Cre model.

2025-08-13 | PXD067318 | Pride

Identifying beta-catenin interacting proteins in a panel of cell lines

Project description:Affinity purification of beta-catenin interacting proteins with anti-beta-catenin antibody and IgG control in a panel of cell lines: MXP2 (B-ALL), Jeko (Mantle cell lymphoma), Molm13 (AML), Koptk (T-ALL), SW480 (Colorectal) and H446 (Lung).

2025-08-13 | PXD067306 | Pride

Role and function of STAT5 in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of STAT5 in ALL, we isolated bone marrow cells from STAT5 fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-GFP or empty vector control (GFP) and subjected to gene expression analysis.

2011-08-24 | GSE24814 | GEO

Role and function of Sox4 in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of Sox4 in ALL, we isolated bone marrow cells from Sox4 fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-ERT2 or empty vector control (ERT2) and subjected to gene expression analysis.

2014-07-04 | GSE36543 | GEO

Role and function of Inpp5d in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of Inpp5d in ALL, we isolated bone marrow cells from Inpp5d fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-ERT2 or ERT2 (PMIP) and after 2 days of treatment with 4OH-Tamoxifen (0.5 micromolar) subjected to gene expression analysis.

2013-06-03 | GSE34830 | GEO

Role and function of Pten in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of Pten in ALL, we isolated bone marrow cells from Pten fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-ERT2 or ERT2 (PMIP) and after 2 days of treatment with 4OH-Tamoxifen (0.5 micromolar) subjected to gene expression analysis.

2013-06-03 | GSE34829 | GEO

Role and function of SPRY1/2 in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of SPRY1 and SPRY2 in ALL, we isolated bone marrow cells from Spry1 and 2 fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-ERT2 or ERT2 (PMIP) and after 2 days of treatment with 4OH-Tamoxifen (0.5 micromolar) subjected to gene expression analysis.

2013-06-03 | GSE34834 | GEO

gamma-catenin (junction plakoglobin, Jup) dependent signals mediate the progression of BCR-ABL1+ B-ALL

Project description:The BCR-ABL1 translocation product is the cause of Chronic Myeloid Leukemia (CML) and of a significant fraction of adult-onset B-Acute Lymphoblastic Leukemia (B-ALL) cases. Here we identify an essential role for gamma-catenin (junction plakoglobin) in B lineage restricted cells for the progression of B-ALL in a mouse model. The array analysis of preleukemic B cells aimed at identifying genes that explain the deficient B-ALL progression in the absence gamma-catenin. Total bone marrow cells from chimeric mice expressing or lacking gamma-catenin in the hematopoietic compartment were transduced with BCR-ABL1+ IRES GFP retrovirus before transplantation into lethally irradiated wild type recipients. Three weeks later, GFP+ (BCR-ABL1+) B220+ BP-1+ B cells were flow sorted from the bone marrow of preleukemic recipient mice. The analysis includes 3 replicates for gamma-catenin WT and 3 replicates for gamma-catenin KO BCR-ABL1+ BP1+ B cells.

2014-02-08 | E-GEOD-54793 | biostudies-arrayexpress

SFPQ-ABL1 and BCR-ABL1 utilise different signalling networks to drive B-cell acute lymphoblastic leukaemia

Project description:Philadelphia-like (Ph-like) acute lymphoblastic leukaemia (ALL) is a high-risk subtype of B-cell ALL characterised by a gene expression profile resembling Philadelphia Chromosome positive ALL (Ph+ ALL) in the absence of BCR-ABL1. Tyrosine kinase activating fusions, some involving ABL1, are recurrent drivers of Ph-like ALL and are targetable with tyrosine kinase inhibitors (TKIs). We identified a rare instance of SFPQ-ABL1 in a child with Ph-like ALL. SFPQ-ABL1 expressed in cytokine-dependent cell lines was sufficient to transform cells which were sensitive to ABL1-targeting TKIs. In contrast to BCR-ABL1, SFPQ-ABL1 localised to the nuclear compartment and was a weaker driver of cellular proliferation. Phosphoproteomics analysis showed upregulation of cell cycle, DNA replication and spliceosome pathways, and downregulation of signal transduction pathways, including ErbB, NF-kappa B, VEGF, and MAPK signalling in SFPQ-ABL1-, compared to BCR-ABL1-expressing cells. SFPQ-ABL1 expression did not activate PI3K/AKT signalling and was associated with phosphorylation of G2/M cell cycle proteins. SFPQ-ABL1 was sensitive to navitoclax and S-63845 and promotes cell survival through upregulation of Mcl-1 and Bcl-xL. SFPQ-ABL1 has functionally distinct mechanisms by which it drives ALL, including subcellular localisation, proliferative capacity, and activation of cellular pathways, highlighting the role that fusion partners have in mediating the function of ABL1 fusions.

2022-05-20 | PXD028925 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data