Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effect of spleen tyrosine kinase on bone marrow monocytes in atherosclerosis

ABSTRACT: The effect of spleen tyrosine kinase on bone marrow monocytes in atherosclerosis

PROVIDER: PRJNA848678 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

The effect of spleen tyrosine kinase on bone marrow monocytes in atherosclerosis

Project description:Spleen tyrosine kinase (Syk)del/del mice suppressed atherosclerosis and Sykdeldel macrophages showed cell migration impairment. To investigate the Syk-associated genes in cell migration, we analyzed RNA-Seq of bone marrow monocytes.

2023-07-20 | GSE205972 | GEO

Tyrosine Kinase Inhibitor Cardiotoxicity

Project description:Tyrosine Kinase Inhibitor Cardiotoxicity

| PRJNA352077 | ENA

Therapeutic potential of spleen tyrosine kinase inhibition for treatment of high-risk precursor B-cell acute lymphoblastic leukemia

Project description:This study revealed pathogenic role of pre-BCR-independent SYK activation in high-risk B-ALL. Intensified and central nervous system (CNS)-directed chemotherapy has significantly improved outcomes for pediatric B-acute lymphoblastic leukemia (B-ALL), but confers significant late-effect morbidities. Moreover, many patients suffer relapses, underscoring the need to develop novel, molecularly targeted B-ALL therapies. Using a mouse model, we showed that leukemic B-cells require pre-B-cell receptor (pre-BCR)-independent spleen tyrosine kinase (SYK) signaling in vivo. In diagnostic samples from human B-ALL patients, SYK and downstream targets were phosphorylated regardless of pre-BCR expression or genetic subtype. Two small molecule SYK inhibitors, fostamatinib and BAY61-3606, attenuated growth of 69 B-ALL samples, including high-risk (HR) subtypes. Orally administered fostamatinib significantly reduced high disease burden after xenotransplantation of HR B-ALL samples into immune-deficient mice, and decreased leukemia dissemination into spleen, liver, kidneys and the CNS of recipients. Thus, SYK activation sustains growth of multiple HR B-ALL subtypes, suggesting that SYK inhibitors may improve outcomes for HR and relapsed B-ALL. B-cell leukemia samples (3) from a mutant mouse model were compared to sorted or cultured preB or proB cells from normal mice using Affymetrix GeneChip arrays.

2014-03-29 | E-GEOD-56345 | biostudies-arrayexpress

Therapeutic potential of spleen tyrosine kinase inhibition for treatment of high-risk precursor B-cell acute lymphoblastic leukemia

2014-03-29 | GSE56345 | GEO

Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

Project description:Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

| PRJNA706448 | ENA

Proteomic analysis of human monocytes in atherosclerosis related and non-related to chronic kidney disease

Project description:We performed quantitative and qualitative proteomic analysis by nano LC-MS/MS to investigate global changes in the proteome of monocytes isolated from patients' peripheral blood by immunomagnetic separation. Cells were isolated from patients at different stages of non-related and chronic kidney disease-related atherosclerosis compared to healthy controls.

2024-01-23 | PXD041367 | Pride

Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

Project description:Fms-like tyrosine kinase 3 (Flt3) is a regulator of hematopoietic progenitor cells. It is a target of tyrosine kinase inhibitors (TKIs) used for acute myeloid leukemia treatment. Flt3 and its ligand (Flt3L) are expressed in the heart and cardiac side effects occur under Flt3-targeting TKIs. Whether Flt3/Flt3L also regulate cardiac progenitor cells (CPCs), however, is not known. The cardiac side population (SP) is a pool of heterogenous CPCs that can give rise to all cardiac lineages, hence contributing to cardiovascular homeostasis. Here we show that SP-CPCs produce and are responsive to Flt3L. Compared to wild-type, SP-CPCs from flt3L-/- mice are less abundant, with less contribution of CD45-CD34+ cells, and lower expression of gene sets related to epithelial-to-mesenchymal transition, cardiovascular development and stem cell differentiation. Upon culturing and compared to wild-type, flt3L-/- Sca1+CD31- SP-CPCs show increased proliferation and less vasculogenic commitment, but differentiation can be induced in the presence of receptor tyrosine kinase-activating growth factors. The observed differences are associated with decreased microvascularisation and global systolic function of flt3L-/- hearts. Thus, Flt3 contributes to a receptor tyrosine kinase signature necessary for the maintenance and functionality of SP-CPCs. These findings have potential implications regarding cardiovascular side effects observed under TKI therapy.

2021-11-30 | GSE168207 | GEO

Histologic transformation induced by EGFR tyrosine kinase inhibitors

Project description:Histologic transformation induced by EGFR tyrosine kinase inhibitors

| PRJNA1145888 | ENA

Yes tyrosine kinase signaling promotes liver cancer development

Project description:Yes tyrosine kinase signaling promotes liver cancer development

| PRJNA744904 | ENA

Proteomic profiling by array of tyrosine kinase activity in metastatic malignant melanoma from human tissue specimens

Project description:Tyrosine kinase activity profiling of metatstatic malignant melanoma and normal skin tissue samples was performed using peptide kinase arrays. All samples were run in triplicates with and withouth inhbitor PLX4032 and Sutent Malate in order to identify how tyrosine kinases responds to kinase inhibitor treatment, ex vivo.

2013-01-17 | E-MTAB-1245 | biostudies-arrayexpress

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