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HDAC2 maintains receptor tyrosine kinase signaling of undifferentiated pancreatic cancer cells (ChIP-Seq)

ABSTRACT: HDAC2 maintains receptor tyrosine kinase signaling of undifferentiated pancreatic cancer cells (ChIP-Seq)

PROVIDER: PRJNA655482 | ENA |

REPOSITORIES: ENA

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HDAC2 maintains receptor tyrosine kinase signaling of undifferentiated pancreatic cancer cells

Project description:HDAC2 maintains receptor tyrosine kinase signaling of undifferentiated pancreatic cancer cells

| PRJNA655480 | ENA

HDAC2 maintains receptor tyrosine kinase signaling of undifferentiated pancreatic cancer cells (ATAC-Seq)

Project description:HDAC2 maintains receptor tyrosine kinase signaling of undifferentiated pancreatic cancer cells (ATAC-Seq)

| PRJNA655483 | ENA

HDAC2 maintains receptor tyrosine kinase signaling of undifferentiated pancreatic cancer cells (ChIP-Seq)

Project description:H3K27ac ChIP-se and ATAC-seq were used to determine epigenetic differences between Hdac2 knockout versus Hdac2 wildtype pancreatic cancer cells.

2021-11-12 | GSE155752 | GEO

HDAC2 maintains receptor tyrosine kinase signaling of undifferentiated pancreatic cancer cells (ATAC-Seq)

Project description:H3K27ac ChIP-se and ATAC-seq were used to determine epigenetic differences between Hdac2 knockout versus Hdac2 wildtype pancreatic cancer cells.

2021-11-12 | GSE155751 | GEO

Tyrosine Kinase Inhibitor Cardiotoxicity

Project description:Tyrosine Kinase Inhibitor Cardiotoxicity

| PRJNA352077 | ENA

HDAC2 maintains receptor tyrosine kinase signaling of undifferentiated pancreatic cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-11-12 | GSE155753 | 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

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

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

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