Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiles in human ES cells and human iPS cells

ABSTRACT: Genome editing research of human ES/iPS cells has been accelerated by clustered regularly interspaced short palindromic repeats/CRISPR-associated 9 (CRISPR/Cas9) and transcription activator-like effector nucleases (TALEN) technologies. However, the efficiency of biallelic genetic engineering in transcriptionally inactive genes is still low, unlike that in transcriptionally active genes. To enhance the biallelic homologous recombination efficiency in human ES/iPS cells, we performed screenings of accessorial genes and compounds. We found that RAD51 overexpression and valproic acid treatment enhanced biallelic-targeting efficiency in human ES/iPS cells regardless of the transcriptional activity of the targeted locus. Importantly, RAD51 overexpression and valproic acid treatment synergistically increased the biallelic homologous recombination efficiency. Our findings would facilitate genome editing study using human ES/iPS cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69653 | GEO | 2017/03/26

SECONDARY ACCESSION(S): PRJNA286113

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RAD51 Interconnects Between DNA Replication, DNA Repair and Immunity

Project description:RAD51, a multifunctional protein, plays a central role in DNA replication and homologous recombination repair, and is known to be involved in cancer development. We identified a novel role for RAD51 in innate immune response signaling. Defects in RAD51 lead to the accumulation of self-DNA in the cytoplasm, triggering a STING-mediated innate immune response after replication stress and DNA damage. Our data suggest that in addition to playing roles in homologous recombination-mediated DNA double-strand break repair and replication fork processing, RAD51 is also implicated in the suppression of innate immunity. Thus, our study reveals a previously uncharacterized role of RAD51 in initiating immune signaling, placing it at the hub of new interconnections between DNA replication, DNA repair, and immunity.

2017-02-18 | GSE95050 | GEO

Expression data from HeLa cells overexpressing AK125393

Project description:Expression of RAD51, a crucial player in homologous recombination (HR) and DNA double-strand break (DSB) repair, is dysregulated in human tumors, and can contribute to genomic instability and tumor progression. To further understand RAD51 regulation we functionally characterized a long non-coding (lnc) RNA, AK125393, dubbed TODRA (Transcribed in the Opposite Direction of RAD51), transcribed 69bp upstream to RAD51, in the opposite direction. TODRA overexpression in HeLa cells induced expression of TPIP, a member of the TPTE family which includes PTEN. Similar to PTEN, we found that TPIP co-activates E2F1 induction of RAD51.

2015-02-19 | GSE66062 | GEO

RPA and RAD51 ChIP-seq from genetically modified Dmc1-knockout B6xCAST PRDM9-Humanized/CAST mouse testes

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

Genome-wide maps of double-strand breaks

Project description:Mapping physiological double strand breaks (DSBs) in cancer cells uncovers transcription-coupled repair mechanism at oncogenic super-enhancers in which RAD51 of the homologous recombination pathway plays a key role supporting the hyper-transcription of related oncogenes.

2019-08-27 | GSE136365 | GEO

Monitoring Homology Search during DNA Double-Strand Break Repair in vivo

Project description:Homologous recombination (HR) is crucial for genetic exchange, accurate repair of DNA double-strand breaks and pivotal for genome integrity. HR uses homologous sequences for repair, but how homology search, the exploration of the genome for homologous DNA sequences, is conducted in the nucleus remains poorly understood. Here, we use time-resolved chromatin immunoprecipitations of repair proteins to monitor homology search in vivo. We found that homology search proceeds by a probing mechanism, which commences around the break and samples preferentially on the broken chromosome. However, elements thought to instruct chromosome loops mediate homology search shortcuts, and centromeres, which cluster within the nucleus, may facilitate homology search on other chromosomes. Our study thus revealed crucial parameters for homology search in vivo and emphasizes the importance of linear distance, chromosome architecture and proximity for recombination efficiency. 2 new custom ChIP-chip platforms used; both Nimblegen; differ in oligo density: (platform 1: 2006-07-18_Scerevisiae_ChIP_Stefan Jentsch MPI Biochemistry S.cerevisiae 385K Tiling Array Version 1) ( platform 2: 100304_Scer2_MS_Chip_Stefan Jentsch MPI Biochemistry S.cerevisiae 135K Tiling Array Version 2) ChIP-chip profiling of DSB repair factors (Rad51, Rad52, RPA, gamma-H2A) upon single inducible DSBs in S.cerevisiae

2013-03-21 | E-GEOD-44844 | biostudies-arrayexpress

The inability to disassemble Rad51 nucleoprotein filaments leads to aberrant mitosis and cell death

Project description:The proper maintenance of genetic material is essential for the survival of living organisms. One of the main safeguards of genome stability is homologous recombination involved in the faithful repair of DNA double-strand breaks, the restoration of collapsed replication forks, and the bypass of replication barriers. Homologous recombination relies on the formation of Rad51 nucleofilaments which are responsible for the homology-based interactions between DNA strands. Here we demonstrate that without the regulation of these filaments by Srs2 and Rad54, which are known to remove Rad51 from single-stranded and double-stranded DNA respectively, the filaments strongly inhibit damage-associated DNA synthesis during DNA repair. Furthermore, this regulation is essential for cell survival under normal growth conditions as in the srs2Δ rad54Δ mutants unregulated Rad51 nucleofilaments cause activation of the DNA damage checkpoint, formation of mitotic bridges and loss of genetic material. These genome instability features may stem from the problems at stalled replication forks as the lack of Srs2 and Rad54 in the presence of Rad51 nucleofilaments impedes cell recovery from replication stress. This study demonstrates that the timely and efficient disassembly of recombination machinery is essential for genome maintenance and cell survival.

2023-03-16 | GSE227383 | GEO

NFKB2 Knockdown Reduces Expression of HR-Related Genes

Project description:Homologous recombination (HR) serves multiple roles in DNA repair that are essential for maintaining genomic stability. The central HR protein, RAD51, is frequently overexpressed in human malignancies, thereby elevating HR proficiency and promoting resistance to DNA-damaging therapies. Here we find that non-canonical NF-κB factors control the expression of RAD51 andother HR-promoting proteins. Transcriptional silencing of p100/p52 reduces RAD51 protein levels in multiple human cancer subtypes. RNA-seq after p100/p52 silencing identifies RAD51 as the most differentially expressed gene among 40 genes with known relevance to HR. While p100/p52 depletion inhibits HR function in human tumor cells, it does not influence the function of other double-strand DNA repair pathways including single-strand annealing, microhomology mediated annealing, or non-homologous end joining.

2022-06-07 | GSE148511 | GEO

Expression data from HeLa cells overexpressing AK125393

2015-02-19 | E-GEOD-66062 | biostudies-arrayexpress

A Study of Hansoh (HS)-10502 in Patients With Advanced Solid Tumors

Project description:HS-10502 is a Poly(ADP-ribose) polymerase 1 (PARP1)-specific selective inhibitor. The purpose if this study is to assess the safety, tolerability, pharmacokinetics (PK), and efficacy of HS-10502 in subjects with homologous recombination repair (HRR) gene mutant or homologous recombination deficiency (HRD) positive advanced solid tumors.

| 9330 | ecrin-mdr-crc

ena-DATASET-EMC-29-01-2018-10:48:52:289-175 - samples

Project description:Exome sequencing data from homologous recombination deficient primary breast cancers as assessed by the functional RAD51 based HR test. There are 12 tumour samples, of which 10 also have matching normal.

| EGAD00001003929 | EGA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data