Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CD38 causes autophagic flux inhibition and cardiac dysfunction through a transcriptional inhibition pathway under hypoxia/ischemia conditions

ABSTRACT: To comprehensively identify CD38 binding sites on Plekhm1.

ORGANISM(S): Mus musculus

PROVIDER: GSE146275 | GEO | 2023/03/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

CD38 Causes Autophagic Flux Inhibition and Cardiac Dysfunction Through a Transcriptional Inhibition Pathway Under Hypoxia/Ischemia Conditions.

Project description: Not available

| S-EPMC7180518 | biostudies-literature

CLL: CD38+CD49d+ vs. CD38-CD49d-

Project description:CD38 and CD49d are associated negative prognosticators in chronic lymphocytic leukemia (CLL). Despite evidence that both molecules are involved in interactions occurring between CLL and normal cells in the context of CLL-involved tissues, a functional link is still missing. Using gene expression profiles comparing CD38+CD49d+ vs. CD38-CD49d- CLL cells, we demonstrated overexpression of the CCL3 and CCL4 chemokines in cells from the former group. These chemokines were also upregulated by CD38 signals in CLL; moreover, CCL3 was expressed by CLL cells from bone marrow biopsies (BMB) of CD38+CD49d+ but not CD38-CD49d- cases. High levels of CCR1 and, to a lesser extent, CCR5, the receptors for CCL3 and CCL4, were found in CLL-derived monocyte-macrophages. Consistently, CCL3 increased monocyte migration, and CD68+ macrophage infiltration was particularly high in BMB from CD38+CD49d+ CLL. Conditioned media from CCL3-stimulated macrophages induced endothelial cells to express VCAM-1, the CD49d ligand, likely through TNFα over-production. These effects were apparent in BMB from CD38+CD49d+CLL, where lymphoid infiltrates were characterized by a prominent meshwork of VCAM-1+ stromal/endothelial cells. Lastly, CD49d engagement by VCAM-1-transfectants increased viability of CD38+CD49d+ CLL cells. Altogether, CD38 and CD49d can be thought of as a part of a consecutive chain of events ultimately leading to improved survival of CLL cells.

2009-03-03 | GSE14560 | GEO

Enhancement of autophagic flux after neonatal cerebral hypoxia-ischemia and its region-specific relationship to apoptotic mechanisms.

Project description: Not available

| S-EPMC2774060 | biostudies-literature

Analysis of CD38+ and CD38- sub-clones derived from the same CLL patient

Project description:CD38 expression is an important prognostic marker in CLL with high levels of CD38 associated with shorter overall survival. In this study, we used gene expression profiling and protein analysis of highly purified cell-sorted CD38+ and CD38- chronic lymphocytic leukemia cells to elucidate a molecular basis for the association between CD38 expression and inferior clinical outcome. Paired CD38+ and CD38- CLL cells derived from the same patient were shown to be monoclonal by VH gene sequencing but despite this, CD38+ CLL cells possessed a distinct gene expression profile when compared with their CD38- sub-clones. Keywords: Sub-clonal analysis of CLL cells derived from the same leukemia sample

2006-11-23 | GSE6321 | GEO

Diosmin inhibits glioma growth through inhibition of autophagic flux

Project description:RNA microarray was performed from glioma cell LN229 and GBM8401 that were treated with Diosmin (160 nM) for 48hr in comparison to DMSO vehicle control.

2022-03-24 | GSE174363 | GEO

Defective autophagosome trafficking contributes to impaired autophagic flux in coronary arterial myocytes lacking CD38 gene.

Project description: Not available

| S-EPMC3958620 | biostudies-literature

Expression data from native ZAP-70+CD38+ vs. ZAP-70-CD38- CLL cells

Project description:B-cell chronic lymphocytic leukemia (B-CLL) is a heterogenous disease with a highly variable clinical course and analysis of ZAP-70 and CD38 expression on B-CLL cells allowed for identification of patients with good (ZAP-70-CD38-), intermediate (discordant expression of ZAP-70 and CD38) and poor (ZAP-70+CD38+) prognosis. In an attempt to identify a molecular basis that may underly this diverse clinical behaviour DNA microarray technology was employed to compare eight ZAP-70+CD38+ with eight ZAP-70-CD38- B-CLL cases. We used microarrays to detail the global programme of gene expression distinguising B-CLL from patient with good (samples 1 to 8) and poor prognosis (sample 9 to 16) and identified distinct classes of up- and down-regulated genes. Keywords: Disease progression

2006-09-22 | GSE4392 | GEO

Salinomycin inhibits cholangiocarcinoma growth by inhibition of autophagic flux.

Project description: Not available

| S-EPMC5790487 | biostudies-literature

MMP9 inhibition increases autophagic flux in chronic heart failure.

Project description: Not available

| S-EPMC7792705 | biostudies-literature

Activation of Autophagic Flux Maintains Mitochondrial Homeostasis during Cardiac Ischemia/Reperfusion Injury.

Project description: Not available

| S-EPMC9265292 | biostudies-literature