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CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [Single Cell Dataset]

ABSTRACT: CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [Single Cell Dataset]

PROVIDER: PRJNA1193576 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31588421_1.fastq.gz	Fastqsanger.gz
	SRR31588421_2.fastq.gz	Fastqsanger.gz
	SRR31588422_1.fastq.gz	Fastqsanger.gz
	SRR31588422_2.fastq.gz	Fastqsanger.gz
	SRR31588427_1.fastq.gz	Fastqsanger.gz

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CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [bulk RNA-Seq]

Project description:Astrocytes promote neuroinflammation and neurodegeneration in multiple sclerosis (MS) through cell-intrinsic activities and their ability to recruit and activate other cell types. Here, in a genome-wide CRISPR-based forward genetic screen investigating regulators of astrocyte proinflammatory responses, we identified the C-type lectin domain-containing 16A gene (CLEC16A), linked to MS susceptibility, as a suppressor of nuclear factor-κB (NF-κB) signaling. Gene and small-molecule perturbation studies in mouse primary and human embryonic stem cell-derived astrocytes in combination with mitochodrial, metabolic and multiomic 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. Astrocyte-specific 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 pathological responses and a candidate therapeutic target in MS. Scheduled for publication in Nature Neuroscience DOI: 10.1038/s41593-025-01875-9

2023-11-09 | GSE189030 | GEO

CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [Single Cell Dataset]

2024-12-03 | GSE283395 | GEO

CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [bulk RNA-Seq]

Project description:CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [bulk RNA-Seq]

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

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

| PRJNA781239 | ENA

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

Project description:CLEC16A conditional knockout using GFAP-Cre

2023-11-09 | GSE189029 | GEO

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: human in vitro study

Project description:CLEC16A knocked down human embryonic stem cell (hESC) derived astrocytes

2023-11-09 | GSE189028 | GEO

Clec16a maintains the Definitive Hematopoietic Stem and Progenitor Cells via Mitophagy in Zebrafish

Project description:Since clec16a signaling is imperative for HSPCs production in zebrafish, to further determine the regulatory mechanism by which clec16a signaling regulates HSPCs. Bulk RNA sequencing analysis is performed to dissect the function and molecular mechanism between the control groups and the clec16a morphants groups.

2026-01-06 | GSE281435 | GEO

Clec16a maintains the Definitive Hematopoietic Stem and Progenitor Cells via Mitophagy in Zebrafish

Project description:Clec16a maintains the Definitive Hematopoietic Stem and Progenitor Cells via Mitophagy in Zebrafish

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Astrocyte-produced HB-EGF limits autoimmune CNS pathology

Project description:Astrocyte-produced HB-EGF limits autoimmune CNS pathology

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