Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PIP3-dependent macropinocytosis is incompatible with chemotaxis

ABSTRACT:

SUBMITTER: Douwe M. Veltman

PROVIDER: S-JCBD-201309081 | bioimages |

REPOSITORIES: bioimages

ACCESS DATA

Json Xml

Similar Datasets

Video Education With Result Dependent dIsclosure

Project description:The overall study objective of this trial study is to identify and evaluate strategies to improve the accessibility of the video education with result dependent disclosure (VERDI) model, increasingly utilized as a pre-genetic testing (pretest) education alternative in clinical practice, to better serve a more diverse patient population at risk for hereditary cancers.

| 2403572 | ecrin-mdr-crc

A Study of LGK974 in Patients With Malignancies Dependent on Wnt Ligands

Project description:The primary purpose of this study is to find the recommended dose of LGK974 as a single agent and in combination with PDR001 that can be safely given to adult patients with selected solid malignancies that have progressed despite standard therapy or for which no effective standard therapy exists

| 2106471 | ecrin-mdr-crc

Chromatin landscape of medulloblastoma reveals context dependent driver

Project description:In this study, we defined subgroup specific chromatin landscape (H3K27ac, H3K27me3, RNA-Seq, 27ac hichip, WGS) of medulloblastoma to identify pathogenic epigenetic alterations that regulate expression of a context dependent driver gene.

| EGAS00001006741 | EGA

Construction of a binary intervention scheme for caregivers dependent relationship between patients with bowel cancer and their spouses with enterostomy

Project description:Interventions: Trail group:none Primary outcome(s): Perceived Stress Scale;Simplified Coping Style Questionnaire;Benefit Finding Scale;Mutuality Scale Study Design: Cross-sectional

| 105488 | ecrin-mdr-crc

Time-dependent characterization of CNS response in COVID-19

Project description:Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 primarily affects the respiratory system, but the observation of diverse neurological symptoms indicates that other organs, including the brain, may be involved. The pathophysiological mechanisms of COVID-19-associated effects on the central nervous system (CNS) have become clearer during the past two years. Nevertheless, the precise CNS-specific molecular mechanisms are still elusive and raise several questions. To further elucidate the host response at brain tissue level, we profiled single-nucleus transcriptomes and performed proteomics from olfactory mucosa, olfactory bulb, medulla oblongata and cerebellum at different timepoints of the disease in individuals who died of COVID-19 and underwent rapid autopsy.

| EGAS00001006442 | EGA

Metabolically-dependent Decomposers

Project description:Determining metabolic dependencies in Cellulose-degrading Consortia

| PRJEB33009 | ENA

Erk-dependent transcriptome

Project description:Erk-dependent transcriptome

| PRJNA434214 | ENA

GNPS - Colibactin pathway-dependent metabolites

Project description:Ethyl acetate extracts of clb+ and clbP mutant from E. coli IHE0334 clb genomic island. Files with WT = clb+ wild-type; Files labeled as "P" denotes clbP mutant. Both a peptide and unbiased isotope model was used for acquisition of MS/MS data.

2015-01-16 | MSV000078995 | GNPS

CTCF-dependent enhancer hijacking by the EVI1 oncogene in leukemia

Project description:Chromosomal rearrangements are a frequent cause of oncogene deregulation in human malignancies. Overexpression of EVI1 is found in a subgroup of acute myeloid leukemia (AML) with 3q26 chromosomal rearrangements which are often therapy resistant. In a cohort of primary t(3;8)(q26;q24) AML samples we observed the translocation of a MYC super-enhancer to EVI1. We generated a patient-based t(3;8)(q26;q24) model in vitro using CRISPR-Cas9 technology and demonstrated hyper-activation of EVI1 by the hijacked MYC super-enhancer. One MYC super-enhancer element in particular, which recruits early hematopoietic regulators, is critical for EVI1 expression and enhancer-promoter interaction. This interaction is facilitated by a CTCF-bound motif upstream of the EVI1 promoter that acts as an enhancer-docking site in t(3;8) AML. Genomic analyses of 3q26-rearranged AML samples point to a common mechanism by which EVI1 uses this CTCF-bound enhancer-docking site to hijack early hematopoietic enhancers.

| EGAS00001004808 | EGA

Human Autism Genetics and Activity Dependent Gene Activation

Project description:<p>The goal of this proposal is to bring together the power of 1) whole exome sequencing, 2) homozygosity mapping in consanguineous families, 3) genome-wide maps of neuronal transcription in response to neuronal activity, and 4) genome-wide maps of the binding sites of factors that regulate this transcription to generate and annotate a catalog of ASD-associated variants. The consanguineous families are already enrolled in research, and have been phenotyped. The neuronal transcription and binding site maps will be developed by the Greenberg Lab at Harvard Medical School. The whole exome sequencing will be done at the Broad Institute, and the Walsh lab at Children's Hospital will validate the results and analyze the variant data.</p>

| phs000639 | dbGaP

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