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Next generation sequencing transcriptomic analysis of bone marrow derived macrophages within control, Cbl-/-, Cbl-b -/- and DKO genotypes

ABSTRACT: Next generation sequencing transcriptomic analysis of bone marrow derived macrophages within control, Cbl-/-, Cbl-b -/- and DKO genotypes

PROVIDER: PRJNA540522 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8992790.fastq.gz	Fastqsanger.gz
	SRR8992800.fastq.gz	Fastqsanger.gz
	SRR8992810.fastq.gz	Fastqsanger.gz
	SRR8992820.fastq.gz	Fastqsanger.gz
	SRR8992830.fastq.gz	Fastqsanger.gz

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Next generation sequencing transcriptomic analysis of bone marrow derived macrophages within control, Cbl-/-, Cbl-b -/- and DKO genotypes

Project description:The goal of the transcriptomic profiling is to understand what genes or pathway Cbl and Cbl-b regulate for CSF-1R dependent growth signaling

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Quantitative Analysis of Wild Type CBL, CBL 70Z and Y371S 3T3 Stable Cell Transcriptomes

Project description:Cbl (Casitas B-lineage lymphoma) is a prominent post-translational regulator of protein tyrosine kinases (PTKs) that targets activated receptors for ubiquitination-mediated degradation. However, mutations within its E3 ubiquitin ligase activity rendering RING domain are often not sufficient to induce transformation. Rather, a conserved residue (Y371) within the linker helix region (LHR) of Cbl has been a mutational hotspot in myeloproliferative diseases. Interestingly, phosphorylation of Y371 is a prerequisite for Cbl’s ability to ubiquitinate PTKs. We have previously shown that Y371 mutations affect the conformation of Cbl that can be related to its transformation potential. We wanted to investigate for any additional advantage that the Cbl-Y371 mutants could gain over their wild-type counterpart so as to explain their oncogenicity. In our current study, we wanted to investigate the transcriptome profiles of cells overexpressing WT CBL or CBL-70Z, a well-characterized oncogenic CBL mutant lacking residues 366-382 and Y371S a prevalent MDS/MPN CBL mutant. We found an interesting inverse correlationship between the transcriptome of cells expressing WT CBL and the mutant CBLs. The results from this study can be linked to the oncogenic abilities of the mutant CBLs.

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Comparative analysis of WT CBL and CBL 70Z interactomes.

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2021-02-26 | PXD011369 | Pride

Genome wide transcriptional profiling of c-Cbl deficient hematopoietic stem and progenitor cells

Project description:Expression of genes that are differentially expressed between c-Cbl control and c-Cbl mutant hematopoietic stem and progenitor cells were identified through this approach. Interestingly, several leukemia associated genes, particularly transcription factors, were differentially expressed between c-Cbl WT and c-Cbl mutant hematopoietic stem and progenitor cells. Hematopoietic stem and progenitor cells of c-Cbl control and c-Cbl mutant mice were sorted based on their defined immunophenotype. Gene expression studies were performed using Illumina microarray chips.

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Genome wide transcriptional profiling of c-Cbl deficient hematopoietic stem and progenitor cells

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Cbl family proteins are required to maintain the proteome homeostasis in mammary epithelial cells

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Quantitative Analysis of Wild Type CBL, CBL 70Z and Y371S 3T3 Stable Cell Transcriptomes

Project description:Quantitative Analysis of Wild Type CBL, CBL 70Z and Y371S 3T3 Stable Cell Transcriptomes

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Project description:We applied quantitative mass spectrometry (MS)-based proteomics to study the roles of Cbl and Cbl-b in long-term signaling responses related to neurite outgrowth and differentiation of SH-SY5Y neuroblastoma cells. Using stable isotope labeling by amino acids in cell culture (SILAC) and tandem mass tag (TMT)-labeling in combination with off-line high-pH reversed-phase fractionation and LC-MS/MS we analyzed how Cbl and Cbl-b depletion by siRNA affected the proteome, phosphoproteome and ubiquitylome of the neuroblastoma cells. SILAC proteome SILAC (Light Arg0/Lys0, medium Arg6/Lys4, heavy Arg10/Lys8) SH-SY5Y cells were treated with Cbl and Cbl-b or control (GFP) siRNA for 72 hours. For combined stimulation with ligand cocktail (FGF-2, IGF-1 PDGF-BB, TGFα) cells were treated with ligands for 48 h. Samples were analyzed in triplicates with set-up as described below: Set-up 1, 3 replicates (R1-3): Light: siGFP, Heavy: siCbl/siCbl-b Set-up 2, 3 replicates (E1-3): Light: siGFP + ligand cocktail, Medium: siCbl/siCbl-b, Heavy: siCbl/siCbl-b + ligand cocktail TMT phosphoproteome and proteome SH-SY5Y cells were treated with Cbl and Cbl-b siRNA, control (GFP) siRNA or Retinoic acid (RA) for 24 hours. Samples were prepared in triplicates and labelled with TMT10-plex reagents according to the set-up below: TMT10-126: siGFP E1 TMT10-127N: siCbl/siCbl-b E1 TMT10-127C: Retinoic acid E1 TMT10-128N: siGFP E2 TMT10-128C: siCbl/siCbl-b E2 TMT10-129N: Retinoic acid E2 TMT10-129C: siGFP E3 TMT10-130N: siCbl/siCbl-b E3 TMT10-130C: Retinoic acid E3 TMT10-131: Mix of the 9 samples SILAC Ubiquitin pulldown SILAC (Light Arg0/Lys0, heavy Arg10/Lys8) SH-SY5Y cells were treated with Cbl and Cbl-b or control (GFP) siRNA for 24 hours. Samples were analyzed in duplicates with set-up as described below: Light: siGFP, Heavy: siCbl/siCbl-b

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