RAD51 knockout in murine liver (11-week)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1019697 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26142456_1.fastq.gz | Fastqsanger.gz | |||
| SRR26142456_2.fastq.gz | Fastqsanger.gz | |||
| SRR26142457_1.fastq.gz | Fastqsanger.gz | |||
| SRR26142457_2.fastq.gz | Fastqsanger.gz | |||
| SRR26142458_1.fastq.gz | Fastqsanger.gz |
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Project description:RAD51 knockout in murine liver (4-week)
| PRJNA1019234 | ENA
Project description:RAD51 is a highly conserved DNA repair protein and is indispensable for the execution of homologous recombination, thereby participating in maintaining genomic stability. Since constitutive Rad51 knockout mice exhibit embryonic lethality, the physiological functions of RAD51, and the consequences of lacking it, are largely unknown. We herein demonstrated a critical role of RAD51 in postnatal liver development and regeneration. RAD51 is highly expressed during liver development and during regeneration following hepatectomy and hepatic injury, and is also elevated in liver-related diseases. We generated hepatocyte-specific Rad51 deletion mouse model (Rad51-CKO) to evaluate the function of RAD51 in liver development and regeneration.RAD51 deletion in postnatal hepatocytes results in aborted mitosis, global polyploidization, oxidative stress and cellular senescence. Remarkable liver fibrosis occurs as early as in 3-month-old Rad51fl/fl; Alb-Cre+/+ mice.The senescence-associated secretory phenotype in the livers of Rad51-CKO mice creates a niche that favors the activation and propagation of hepatic progenitor cells (HPCs) in which Rad51 is spared due to lack of Alb-Cre expression. The Rad51 functional HPCs and immature hepatocytes can thus proliferate vigorously, acquire increased malignancy, and eventually give rise to HCC. Our results thus demonstrate a novel function of RAD51 in liver development, homeostasis and tumorigenesis. The RAD51-CKO mice represent a unique genetic model for premature liver senescence, fibrosis, impaired regeneration and hepatocellular carcinogenesis.
2025-01-22 | GSE243719 | GEO
Project description:RAD51 is a highly conserved DNA repair protein and is indispensable for the execution of homologous recombination, thereby participating in maintaining genomic stability. Since constitutive Rad51 knockout mice exhibit embryonic lethality, the physiological functions of RAD51, and the consequences of lacking it, are largely unknown. We herein demonstrated a critical role of RAD51 in postnatal liver development and regeneration. RAD51 is highly expressed during liver development and during regeneration following hepatectomy and hepatic injury, and is also elevated in liver-related diseases. We generated hepatocyte-specific Rad51 deletion mouse model (Rad51-CKO) to evaluate the function of RAD51 in liver development and regeneration.RAD51 deletion in postnatal hepatocytes results in aborted mitosis, global polyploidization, oxidative stress and cellular senescence. Remarkable liver fibrosis occurs as early as in 3-month-old Rad51fl/fl; Alb-Cre+/+ mice.The senescence-associated secretory phenotype in the livers of Rad51-CKO mice creates a niche that favors the activation and propagation of hepatic progenitor cells (HPCs) in which Rad51 is spared due to lack of Alb-Cre expression. The Rad51 functional HPCs and immature hepatocytes can thus proliferate vigorously, acquire increased malignancy, and eventually give rise to HCC. Our results thus demonstrate a novel function of RAD51 in liver development, homeostasis and tumorigenesis. The RAD51-CKO mice represent a unique genetic model for premature liver senescence, fibrosis, impaired regeneration and hepatocellular carcinogenesis.
2025-01-22 | GSE243614 | GEO
Project description:Lable-free quantification of 11-week NPC1 null mice relative to control pools
2018-02-24 | MSV000082096 | MassIVE
Project description:Label-free quantification of cerebellum and cerebral cortex proteomics in 11 week wild type and NPC1 null mice
2018-02-08 | MSV000082040 | MassIVE
Project description:DNMT1 KNOCKOUT IN MURINE LIVER
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Project description:The formation of RAD51/DMC1 filaments on single-stranded (ss)DNAs, which is essential for homology search and strand exchange in DNA double-strand break (DSB) repair and for the protection of stalled DNA replication forks, is tightly regulated in time and space. FIGNL1 AAA+++ ATPase plays positive and negative roles in the RAD51-mediated recombination in human cells. However, the role of FIGNL1 in gametogenesis remains unsolved. Here, we characterized a germ-line-specific conditional knockout (cKO) mouse of FIGNL1. The Fignl1 cKO male mice showed defective chromosome synapsis and impaired meiotic DSB repair with the accumulation of RAD51/DMC1 on chromosomes in mid-meiotic prophase I, supporting a role of FIGNL1 in a post-assembly stage of RAD51/DMC1 filaments. Fignl1 cKO spermatocytes accumulate RAD51 and DMC1 ensembles on chromosomes not only in early meiotic prophase I but also in meiotic S-phase. These RAD51/DMC1 assemblies are independent of meiotic DSB formation. Finally, we showed that purified FIGNL1 dismantles RAD51 filament on double-stranded (ds)DNA as well as ssDNA. These results suggest a critical role of FIGNL1 to limit the uncontrolled assembly of RAD51 and DMC1 on native dsDNAs during the meiotic S-phase and meiotic prophase I.
2023-03-31 | GSE227944 | GEO
Project description:label-free quantification using 11 week mouse tissue lysates from cerebellum and cerebral cortex of wild type and NPC1 null mice.
2018-02-08 | MSV000082039 | MassIVE
Project description:Mammalian meiotic recombination proceeds via repair of hundreds of programmed DNA double-strand breaks (DSBs). This process requires choreographed binding of RPA, DMC1 and RAD51 to single-stranded DNA (ssDNA) substrates and in vivo binding maps of these proteins provide insights into the underlying molecular mechanisms. When assayed in F1-hybrid mice, these maps can distinguish the broken chromosome from the homologous chromosome used as template for repair, which reveals further mechanistic detail and enables the structure of the recombination intermediates to be inferred. By applying CRISPR/Cas9 mutagenesis directly on F1-hybrid embryos, we have extended this powerful analysis technique to explore the molecular detail of recombination when a key component is knocked-out. As a proof-of-concept, we have generated biallelic knockouts of Dmc1 and built maps of meiotic binding of RAD51 and RPA in these knockout hybrid mice. Dmc1 mutants undergo meiotic arrest and comparison of these maps with those from wild-type mice is informative about the structure and timing of recombination intermediates in both genotypes. We confirm a complete abrogation of strand exchange in Dmc1 mutants, and observe a redistribution of RAD51 binding across both the distal and proximal ends of the resected DNA. We observe unexpected RPA and DMC1 binding in the wild-type, which suggests multiple rounds of strand invasion with template-switching in mouse. The methodology used involves direct phenotyping of hybrid “founder” mice following CRISPR mutagenesis and provides a high-throughput approach for the analysis of gene function during meiotic recombination, at low animal cost.
2023-10-16 | GSE239997 | GEO
Project description:Long non-coding RNAs (lncRNA) have been shown to play crucial roles in tumorigenesis. Little is known about lncRNA RAD51-AS1 in diseases. Here, we investigated the role of RAD51-AS1 in Epithelial ovarian cancer. Silencing RAD51-AS1 inhibited proliferation through cell cycle arrest and promotion in apoptosis, both in vitro and in vivo. But the mechanism of RAD51-AS1 downstream regulation remains unclear. In order to identify the downstream regulation of RAD51-AS1 in epithelial ovarian cancer, we used antisene oligotides targeting RAD51-AS1 / negative control to transfect Skov3.ip cells. Then, we used microarrays to identified differential expression genes and to look for possible target genes by knockdown RAD51-AS1 expression.
2017-08-17 | GSE89374 | GEO