Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CRISPR screen identified CLEC16A suppresses astrocyte inflammasome-involved pathology via mitophagy: EAE study

ABSTRACT: CRISPR screen identified CLEC16A suppresses astrocyte inflammasome-involved pathology via mitophagy: EAE study

PROVIDER: PRJNA781239 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16967315_1.fastq.gz	Fastqsanger.gz
	SRR16967315_2.fastq.gz	Fastqsanger.gz
	SRR16967316_1.fastq.gz	Fastqsanger.gz
	SRR16967316_2.fastq.gz	Fastqsanger.gz
	SRR16967317_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

CRIPSR screen identified CLEC16A suppresses astrocyte inflammasome-involved pathology via mitophagy

Project description:CRIPSR screen identified CLEC16A suppresses astrocyte inflammasome-involved pathology via mitophagy

| PRJNA781235 | ENA

CRIPSR screen identified CLEC16A suppresses astrocyte inflammasome-involved pathology via mitophagy (Single Cell Dataset)

Project description:CRIPSR screen identified CLEC16A suppresses astrocyte inflammasome-involved pathology via mitophagy (Single Cell Dataset)

| PRJNA1193576 | ENA

CRIPSR screen identified CLEC16A suppresses astrocyte inflammasome-involved pathology via mitophagy: human in vitro study

Project description:CRIPSR screen identified CLEC16A suppresses astrocyte inflammasome-involved pathology via mitophagy: human in vitro study

| PRJNA781238 | ENA

CRIPSR screen identified CLEC16A suppresses astrocyte inflammasome-involved pathology via mitophagy (Single Cell Dataset)

Project description:Astrocytes promote neuroinflammation and neurodegeneration in multiple sclerosis (MS) through cell-intrinsic activities, and also via their ability to recruit and activate other cell types. Here, we report the results of a genome-wide CRISPR-based forward genetic screen investigating regulators of astrocyte proinflammatory responses, which identified CLEC16A, a gene linked to MS susceptibility, as a suppressor of NF-B signaling. Gene and small molecule perturbation studies in mouse primary and human embryonic stem cell-derived astrocytes in combination with multi-omic analyses established that CLEC16A promotes mitophagy, limiting mitochondrial dysfunction and the accumulation of mitochondrial products that activate NF-κB, the NLRP3 inflammasome and gasdermin D. Astrocytespecific Clec16a inactivation increased NF-κB, NLRP3 and gasdermin D activation in vivo, worsening experimental autoimmune encephalomyelitis, a mouse model of MS. Moreover, we detected disrupted mitophagic capacity and gasdermin D activation in astrocytes in samples from individuals with MS. These findings identify CLEC16A as a suppressor of astrocyte pathologic responses and a candidate therapeutic target in MS.

2024-12-03 | GSE283395 | GEO

RABID transcriptome from peak EAE astrocyte networks

Project description:Tracing astrocyte networks in EAE in B6 mice

2021-04-22 | GSE156583 | GEO

RABID transcriptome from priming EAE astrocyte networks

Project description:Tracing astrocyte networks in EAE priming in B6 mice

2021-04-22 | GSE165313 | GEO

RABID barcodes from priming EAE astrocyte networks

Project description:Tracing astrocyte networks in EAE priming in B6 mice

2021-04-22 | GSE165311 | GEO

RABID barcodes from peak EAE astrocyte networks

Project description:Tracing astrocyte networks in experimental autoimmune encephalomyelitis (EAE) in B6 mice