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Genome-wide RNAseq of liver tissue derived from humanized mice fed by CDA-HFD and treated with CLDN1 mAb or vehicle Control

ABSTRACT: Genome-wide RNAseq of liver tissue derived from humanized mice fed by CDA-HFD and treated with CLDN1 mAb or vehicle Control

PROVIDER: PRJNA730507 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14567570.fastq.gz	Fastqsanger.gz
	SRR14567571.fastq.gz	Fastqsanger.gz
	SRR14567572.fastq.gz	Fastqsanger.gz
	SRR14567573.fastq.gz	Fastqsanger.gz
	SRR14567574.fastq.gz	Fastqsanger.gz

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Genome-wide RNAseq of liver tissue derived from humanized mice fed by CDA-HFD and treated with CLDN1 mAb or vehicle Control

Project description:Six-week old Fah−/−/Rag2−/−/Il2rg −/− (FRG) –NOD breeding mice were intravenously injected with 1.5 x 10^9 plaque forming units (pfu) of an adenoviral vector encoding the secreted form of the human urokinase-like plasminogen activator (Ad-uPA). Forty-eight hours later, 10^6 PHH were injected intrasplenically. Successfully transplanted mice were fed with CDA-HFD for 16 weeks and then treated with humanized CLDN1 specific mAb 500 µg or vehicle for additional 8 weeks. RNA was extracted from non-tumorous liver tissue of 4 NASH fibrosis mice treated with CLDN1 mAb, 3 vehicle Control treated NASH fibrosis mice as well as 3 humanized mice fed by regular diet. Libraries were sequenced on the Illumina HiSeq 4000 as Single-Read 50 base reads.

2024-03-12 | GSE174543 | GEO

Genome-wide RNAseq of liver tissue derived from DEN-CDA-HFD mice treated with CLDN1 mAb or vehicle Control

Project description:Seven-week old male C57BL/6J mice received a single i.p. injection of DEN (100 mg/kg) and were subsequently fed with CDA-HFD after 3 weeks. After 6 weeks of diet, the mice were randomized in 2 groups, receiving weekly i.p. injections of 500 µg of either CLDN1 specific mAb or vehicle control for 16 weeks. RNA was extracted from non-tumorous liver tissue of 6 DEN-CDA-HFD mice treated with CLDN1 mAb, 6 DEN-CDA-HFD mice treated with vehicle Control as well as 5 C57BL/6J Control mice fed by regular diet. Libraries were sequenced on the Illumina HiSeq 4000 as Single-Read 50 base reads.

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Genome-wide RNAseq of liver tissue derived from DEN-CDA-HFD mice treated with CLDN1 mAb or vehicle Control

Project description:Genome-wide RNAseq of liver tissue derived from DEN-CDA-HFD mice treated with CLDN1 mAb or vehicle Control

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Project description:To understand the fibrotic response in the CDA-HFD induced NASH fibrosis model, we performed RNA-seq on liver samples collected from mice fed with normal chow (week 0) or CDA-HFD chow (weeks 8 and 16).

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Project description:Organoids were established from non-tumorous cirrhotic liver tissue and treated with CLDN1 mAb or Control mAb for 4 days. Organoids were harvested and mRNA was extracted. RNAsequencing was performed for comparative gene expression profiling.

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Project description:Discoidin domain-containing receptor 1 (DDR1) plays an important role in cancer progression. However, the DDR1 function in tumors is still elusive. We recently reported that DDR1 promoted collagen fiber alignment and formation of a physical barrier, which causes immune exclusion from tumors. We also demonstrated that our DDR1 ECD-targeting mAbs can disrupt collagen fiber alignment and increase T Cell infiltration in tumors. In this study, we humanized a DDR1 ECD-targeting mAb and showed significant antitumor efficacy in an immunocompetent mouse model. We determined the binding epitope using gene mutagenesis, hydrogen-deuterium exchange mass spectrometry (HDX-MS), and X-ray crystallography. Mechanistically, we showed that the humanized mAb inhibited DDR1 phosphorylation and, more importantly, blocked DDR1 shedding and disrupted a physical barrier formed by collagen fiber alignment in tumors. This study not only paves a pathway for development of PRTH-101 as a cancer therapeutic, but also broaden our understanding of the roles of DDR1 in modulation of collagen alignments in tumor extracellular matrix and tumor immune microenvironment.

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Effect of CLDN1 mAb on primary patient derived liver organoids

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