Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeting Myelin FFA Compostion in PAR1 and PAR2 Mice after SCI

ABSTRACT:

ORGANISM(S): Mus Musculus

TISSUE(S): Spinal Cord

DISEASE(S): Spinal Cord Injury

PROVIDER: ST000862 | MetabolomicsWorkbench |

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	mwtab	Other

Items per page:

1 - 1 of 1

Similar Datasets

Targeting microvasculature for neuroprotection after SCI.

Project description: Not available

| S-EPMC3101824 | biostudies-literature

Targeting Myelin NEFA in PAR1 and PAR2 Mice after SCI

Project description: Not available

| ST000861 | MetabolomicsWorkbench

Targeting Myelin Cholesterol in PAR1 and PAR2 Mice after SCI

Project description: Not available

| ST000863 | MetabolomicsWorkbench

Targeting Myelin Ceramides in PAR1 and PAR2 Mice after SCI

Project description: Not available

| ST000864 | MetabolomicsWorkbench

miRQC PGM data

Project description:MicroRNAs are important negative regulators of protein coding gene expression, and have been studied intensively over the last few years. To this purpose, different measurement platforms to determine their RNA abundance levels in biological samples have been developed. In this study, we have systematically compared 12 commercially available microRNA expression platforms by measuring an identical set of 20 standardized positive and negative control samples, including human universal reference RNA, human brain RNA and titrations thereof, human serum samples, and synthetic spikes from homologous microRNA family members. We developed novel quality metrics in order to objectively assess platform performance of very different technologies such as small RNA sequencing, RT-qPCR and (microarray) hybridization. We assessed reproducibility, sensitivity, quantitative performance, and specificity. The results indicate that each method has its strengths and weaknesses, which helps guiding informed selection of a quantitative microRNA gene expression platform in function of particular study goals.

2013-09-01 | E-MTAB-1815 | biostudies-arrayexpress

Myelin regeneration in multiple sclerosis: targeting endogenous stem cells.

Project description: Not available

| S-EPMC3250284 | biostudies-literature

RNA sequencing from planarian tissues

Project description:The aim of the experiment was to compare the transcriptome of intact control and prep knock down animals.

2026-02-01 | E-MTAB-14438 | biostudies-arrayexpress

Targeting Non-classical Myelin Epitopes to Treat Experimental Autoimmune Encephalomyelitis.

Project description: Not available

| S-EPMC5086895 | biostudies-literature

Targeting N-linked Glycosylation for the Therapy 1 of Aggressive Lymphomas

Project description:Diffuse large B-cell lymphoma (DLBCL) is an aggressive cancer with two major biological subtypes, activated B-cell like (ABC) and germinal center B-cell-like (GCB) DLCBL. Self-antigen engagement of B-cell receptors (BCRs) in ABC tumors promotes their clustering in the plasma membrane, thereby initiating chronic active signaling and downstream activation of the pro-survival NF-kB and PI3 kinase pathways. The potential of therapeutics targeting chronic active BCR signaling in ABC DLBCL is highlighted by the frequent response of these tumors to inhibitors of BTK, a kinase that links BCR signaling to NF-kB activation. Here we used genome-wide CRISPR-Cas9 screens to identify regulators of the IRF4, a direct NF-kB target and essential transcription factor in ABC cells. Unexpectedly, inactivation of the oligosaccharyltransferase (OST) complex, which mediates N-linked protein glycosylation, reduced IRF4 expression and NF-kB activity in ABC cells, resulting in cell death. Using functional glycoproteogenomics we linked this phenomenon to defective BCR glycosylation. Pharmacologic inhibition of OST reduced the size and abundance of BCR microclusters in the plasma membrane and blocked their internalization. These reorganized BCRs associated with the inhibitory coreceptor CD22, which attenuated proximal BCR signaling, thereby reducing NF-kB and PI3 kinase activation. OST inhibition also blocked the trafficking of TLR9 to the endolysosomal compartment, preventing its association with the BCR in the My-T-BCR signaling complex that activates NF-kB in ABC cells. In GCB DLBCL, OST inhibition also attenuated constitutive BCR signaling, reducing PI3 kinase signaling and triggering cell death. Our data highlight the therapeutic potential of OST inhibitors for the treatment of diverse B cell malignancies in which constitutive BCR signaling is essential.

2023-04-24 | PXD038951 | Pride

Myelin modifications after chronic sleep loss in adolescent mice.

Project description: Not available

| S-EPMC5946929 | biostudies-literature