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

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

PROVIDER: PRJNA781235 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16967300_1.fastq.gz	Fastqsanger.gz
	SRR16967300_2.fastq.gz	Fastqsanger.gz
	SRR16967301_1.fastq.gz	Fastqsanger.gz
	SRR16967301_2.fastq.gz	Fastqsanger.gz
	SRR16967302_1.fastq.gz	Fastqsanger.gz

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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)

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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

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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

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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

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-09 | GSE189030 | GEO

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

Project description:CLEC16A conditional knockout using GFAP-Cre

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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

Astrocyte-produced HB-EGF limits autoimmune CNS pathology

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

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Astrocyte-produced HB-EGF limits autoimmune CNS pathology [WGBS]

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

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Microarray analysis of the astrocyte transcriptome in the ageing brain: relationship to Alzheimer's pathology and ApoE genotype

Project description:Astrocyte dysfunction impacts their normal function, including neuronal support, thereby contributing to neurodegenerative pathologies including Alzheimer's disease (AD). Therefore to understand the role of astrocytes in the pathogenesis of age-related disorders we analysed the gene expression profile of astrocytes with respect to Alzheimer-type pathology. The aim of the present study was to combine immuno-LCM and microarray analysis to characterise the astrocyte transcriptome at different Braak stages, and with respect to ApoE genotype, in post-mortem human temporal cortex sampled dervied from the Medical Research Council Cognitive Function and Ageing Study (MRC-CFAS). GFAP-positive astrocytes were isolated from age, sex and brain pH-matched cases derived from the MRC-CFAS cohort, using immuno laser capture microdissection. The extracted RNA was amplified and applied to HGU133 Plus 2.0 Affymetrix gene arrays. Genes were considered differentially expressed if they showed a minimum 1.5 fold change at p<0.02 in all 6 individual cases in each stage of pathology [18 cases in total: 6 cases Braak stages I-II (3 cases carried at least one ApoE epsilon4 allele and 3 were ApoEe4 negative); 6 cases Braak stages III-IV (3 ApoEe4 positive and 3 ApoEe4 negative; 6 cases Braak stages V-VI (3 ApoEe4 positive and 3 ApoEe4 negative)]. keywords: human GFAP-positive astrocytes

2011-06-01 | E-GEOD-29652 | biostudies-arrayexpress

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