Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RIME of EVI-1 in HNT34 and UCSD/AML1 cell lines and one primary sample to identify interactors

ABSTRACT: Rapid Immunoprecipitation Mass spectrometry of Endogenous proteins (RIME) of two AML cell lines HNT34 and UCSD/AML1 and one primary sample. EVI-1 is immunoprecipitated and the nearby chromatin-bound proteins are identified.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Cell, Bone Marrow

DISEASE(S): Acute Leukemia

SUBMITTER: Andrea Gherli

LAB HEAD: Dr Giovanni Roti

PROVIDER: PXD042440 | Pride | 2023-05-23

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	HNT34.xlsx	Xlsx
	HNT34_IgG_Control_R1.zip	Other
	HNT34_IgG_Control_R2.zip	Other
	HNT34_R1.zip	Other
	HNT34_R2.zip	Other

Items per page:

1 - 5 of 13

Similar Datasets

RIME of EVI-1 in HNT34 and UCSD/AML1 cell lines and one primary sample to identify interactors

Project description:Rapid Immunoprecipitation Mass spectrometry of Endogenous proteins (RIME) of two AML cell lines HNT34 and UCSD/AML1 and one primary sample. EVI-1 is immunoprecipitated and the nearby chromatin-bound proteins are identified.

2023-03-23 | PXD038686 | Pride

Identification of CEBPA and RUNX1 interactors in 3q-rearranged AML

Project description:Chromatin immunoprecipitation with specific isolation of chromatin associated proteins (ChIP-SICAP) was used to identify chromatin-bound interactors of CEBPA and RUNX1 in the 3q-rearranged human myeloid leukemia cell line MUTZ-3.

2021-04-29 | PXD020045 | Pride

Identification of CEBPA and RUNX1 interactors in 3q-rearranged AML (MOLM-1)

2021-04-29 | PXD020050 | Pride

Identification of CEBPA and RUNX1 interactors in 3q-rearranged AML (HNT-34)

2021-04-29 | PXD020054 | Pride

Dissection of acetylomic profiles in T cell lymphoma following histone deacetylases inhibition

Project description:The aim was to dissect molecular changes in histone and non-histone protein acetylation dynamics following the genetic or pharmacological inhibition of HDAC activity in a model of Anaplastic Large Cell Lymphoma (ALCL), a T cell non-Hodgkin lymphoma, predominantly found in children and adolescents.

2022-10-14 | PXD030503 | Pride

PDHE1α, PARylation, Acetyl-CoA, Acetylation, Histones, DNA damage repair

Project description:Chromatin relaxation is a prerequisite step that allows the DNA repair machinery to access double-strand breaks (DSBs), and local histones around the DNA breaks suffer from prompt acetylation changes. However, an intriguing question remains as to where the large demands of acetyl-CoA is precisely produced promptly. Here, we report that pyruvate dehydrogenase 1α (PDHE1α) catalyzes pyruvate metabolism to provide acetyl-CoA promptly in response to DNA damage. PDHE1α was quickly recruited to chromatin in a PARylation-dependent manner, which further drove acetyl-CoA generation to support local chromatin acetylation around the DSB regions. In turn, this process increased the formation of relaxed chromatin to benefit repair factor loading, thus promoting DSB repair to ultimately maintain genome stability and contribute to the resistance of cancer cells to DNA-damaging treatments in vitro and in vivo. In accordance with this, blocking PARylation-based PDHE1α chromatin recruitment markedly attenuated chromatin relaxation and the DSB repair efficiency, resulting in genome instability and restoration of radiosensitivity. Collectively, these findings reveal an undescribed mechanism that underlies site-directed acetyl-CoA generation involving chromatin-associated PDHE1α and its instrumental function in DNA repair and regulating local chromatin acetylation around DSB sites.

2023-07-27 | PXD040676 | Pride

XX-650-23, an inhibitor of CREB-CBP interaction, effect on acute myeloid leukemia cell line

Project description:Analysis of acute myeloid leukemia KG1 cells treated with XX-650-23 (5 mM) for 12hrs. XX-650-23 inhibits proliferation of KG1 cells. Results provides insight into the molecular mechanisms underlying by the inhibitory activity of XX-650-23 on acute leukemia. mRNA profiles of KG1 cells treated with XX-650-23 were generated by deep sequencing. CREB genome binding profiles of KG1 cells treated with XX-650-23 were generated by deep sequencing.

2016-03-26 | E-GEOD-74928 | biostudies-arrayexpress

ChIP-seq O-GlcNac in mouse ES cells

Project description:Analysis of O-GlcNac occupancy on chromatin in mouse ES cells by ChIP-seq

2024-08-31 | E-MTAB-14310 | biostudies-arrayexpress

YAP regulates cell mechanics by controlling focal adhesion assembly

Project description:Hippo effectors YAP/TAZ act as on-off mechanosensing switches by sensing modifications in extracellular matrix (ECM) composition and mechanics. The regulation of their activity has been described so far through a hierarchical model in which elements of Hippo pathway are under the control of Focal Adhesions (FAs). Here we unveiled the molecular mechanism by which cell spreading and RhoA GTPase control FA formation through YAP to stabilize the anchorage of actin cytoskeleton to cell membrane. This mechanism required YAP co-transcriptional function and involved the activation of genes encoding for integrins and FA docking proteins. Tuning YAP transcriptional activity led to the modification of cell mechanics, force development, adhesion strength, determined cell shaping, migration and differentiation. These results provide new insights into the mechanism of YAP mechanosensing activity and qualify Hippo effector as the key determinant of cell mechanics in response to ECM cues.

2017-05-17 | E-MTAB-5217 | biostudies-arrayexpress

Canonical Wnt signaling negatively modulates T regulatory cell function

Project description:Foxp3 is crucial for both the development and function of regulatory T cells (Treg),however the post-translational mechanisms regulating Foxp3 transcriptional output remain poorly defined. Here, we demonstrate that TCF1 and Foxp3 interact in the nucleus of Treg, and that active Wnt-signaling disrupts Foxp3 transcriptional activity. Utilizing a global ChIP-seq comparison we demonstrate considerable overlap between Foxp3 and Wnt target genes in Treg. Activation of Wnt signaling significantly reduces Treg-mediated suppression both in vitro and in vivo, while disruption of Wnt signaling in Treg enhances their suppressive capacity. Activation of effector T cells increases Wnt3a production, and Wnt3a levels were found to be greatly increased in mononuclear cells isolated from synovial fluid versus peripheral blood of arthritis patients. We propose a model in which Wnt produced by activated mononuclear cells under inflammatory conditions represses Treg function allowing a productive immune response, but if uncontrolled could lead to the development of autoimmunity. Beta catenin ChIP-seq in Treg

2013-07-26 | E-GEOD-49199 | biostudies-arrayexpress