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ScRNAseq of femoral artery segments in the context of hind limb ischemia in mice with or without an endothelial cell-specific deletion of transcription factor Prdm16

ABSTRACT: scRNAseq of femoral artery segments in the context of hind limb ischemia in mice with or without an endothelial cell-specific deletion of transcription factor Prdm16

PROVIDER: PRJEB41000 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4769030.fastq.gz	Fastqsanger.gz
	ERR4769031.fastq.gz	Fastqsanger.gz
	ERR4769032.fastq.gz	Fastqsanger.gz
	ERR4769033.fastq.gz	Fastqsanger.gz
	ERR4769034.fastq.gz	Fastqsanger.gz

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scRNAseq of femoral artery segments in the context of hind limb ischemia in mice with or without an endothelial cell-specific deletion of transcription factor Prdm16

Project description:Femoral artery segments from the ligated ('L') right side (downstream of the ligation site) as well as the corresponding segments from the unligated ('UL') left side were dissected out 3 days after femoral artery ligation in adult mice with or without a long-term (from post-natal day 1 onwards) endothelial-specific deletion of transcription factor Prdm16. Fragments from 4 donor mice were pooled to obtain sufficient cell numbers for sequencing. The experiment existed of 4 samples to be sequenced at single-cell resolution (Prdm16 wild-type L or 'Right_WT'; Prdm16 wild-type UL or 'Left_WT'; Prdm16 endothelial-specific knockout L or 'Right_KO'; Prdm16 endothelial-specific knockout UL or 'Left-KO'). The experiment was intended to identify in situ Prdm16 genotype-dependent genes and corresponding functional pathways in arterial endothelial cells that could be responsible for the observed endothelial dysfunction caused by endothelial-specific Prdm16 deletion in mice upon induction of hind limb ischemia.

2022-10-28 | E-MTAB-9703 | biostudies-arrayexpress

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