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Human RAD51 Protein expressed in Escherichia coli (E. coli) - ABIN2452204
Kurumizaka, Aihara, Kagawa, Shibata, Yokoyama: Human Rad51 amino acid residues required for Rad52 binding. in Journal of molecular biology 1999
Show all 2 Pubmed References
Human RAD51 Protein expressed in Wheat germ - ABIN1317281
De, Donahue, Tabah, Castro, Mraz, Cruise, Campbell: A novel interaction [corrected] of nucleolin with Rad51. in Biochemical and biophysical research communications 2006
The expression of RAD51 recombinase (RAD51), a key recombinase in the homologous recombination (HR) repair pathway, decreased sharply in long non-coding RNA lnc-RI-depressed cells.
RAD51D splice variants and cancer-associated mutations reveal XRCC2 interaction to be critical for homologous recombination
increased RECQ5 levels stimulated 'alternative' HDR by single-stranded DNA donors, which is normally suppressed by RAD51; this was accompanied by stimulation of mutagenic end-joining. These results suggest that in some tumors, RECQ5 gene amplification may have profound consequences for genomic instability
Results suggest that mutant KRAS promotes RAD51 expression to enhance DNA damage repair and lung cancer cell survival.
In the current study, we have demonstrated that the combination of miRNA-mediated targeting of RAD51, PRKDC, LIG1 genes and ionizing radiation is effective to enhance cytotoxic effect of therapeutic doses of gamma-radiation in NSCLC A549 cells
The direct relationship between bromodomain containing 4 (BRD4) and breast cancer 1, early onset protein (BRCA1)/Rad51 Recombinase (RAD51) expression was confirmed in triple negative breast cancer (TNBC) cells.
SWSAP1 protects RAD51 filaments by antagonizing the anti-recombinase, FIGNL1.
Rectal cancer patients with CC genotype of RAD51 gene survived significantly longer than those with GG and GC genotypes and did not develop any recurrences or distant metastases. Female patients with Ku70 expression or RAD51CC genotype had significantly longer overall survival than those with Ku70 or RAD51GG,GC and male patients in the log-rank test.
The results suggest that RAD51 and survivin are potent markers that determine the therapeutic efficacy of proton beam therapy in patients with pancreatic cancer
RAD51 regulates REV1 recruitment to DNA double-strand break sites via pulsed laser microirradiation.
RAD51 gene plays a critical role in healthy motor system development.
A direct role of RAD51 in maintaining mtDNA integrity under replication stress conditions.
This study contributes to the characterization of the radioresistance mechanisms of GSCs, thereby supporting the rationale of targeting RAD51-dependent repair pathways in view of radiosensitizing GSCs.
uncovered DNA-PKcs-dependent DNA damage-induced ASF1A phosphorylation, which enhances chromatin assembly, promoting MMS22L-TONSL recruitment and, hence, Rad51 loading.
Evidence has been provided that the majority of the Cas9-induced single nicks at the target DNA strand rely on RAD51 and BRCA2 for efficient and scar-less DNA repair.
RAD51 135G>C polymorphism is not associated with colorectal cancer.
Data show that short ssDNA traverses the nuclear membrane, but is drawn into the nucleus by binding to the DNA replication and repair factors replication protein A (RPA) and Rad51 recombinase (Rad51).
region in the N terminus of BRCA2 exhibits DNA binding activity and promotes RAD51-mediated homologous recombination
We have identified and characterised a novel DNA damage response mechanism in melanoma. Instead of increasing levels of RAD51 on encountering cisplatin-induced interstrand crosslinks during replication, melanoma cells shut down RAD51 synthesis and instead boost levels of translesion synthesis DNA polymerase zeta to allow replication to proceed
Twenty-one different deleterious variants were identified in the RAD51 paralogs in 30 patients with ovarian and/or beast cancer.
Meiosis progression and female age affect expression profile of DNA repair RAD51 gene in bovine oocytes.
RAD51 plays a crucial role in halting cell death program induced by ionizing radiation in bovine oocytes.
Describe and demonstrate a model showing loss of RAD51 leads to Fanconi anemia-like symptoms in zebrafish.
Results suggest that RAD51-dependent homologous recombination acts as an essential backup to the telomerase for compensation of replicative telomere loss to ensure genome stability
Both AtRAD51 and AtDMC1 possess ATP hydrolyzing activity, filament formation activity and homologous pairing activity in vitro.
Although the presence of RAD51 protein provides essential support for the action of DMC1, these results show no significant effect of the absence of RAD51 strand-exchange activity on meiotic crossing-over rates or patterns in different chromosomal regions or across the whole genome of Arabidopsis, strongly supporting the argument that DMC1 catalyses repair of all meiotic DNA breaks, not only non-sister cross-overs.
The authors find that RBR1 is also required for RAD51 localization to DNA lesions.
RAD51 forms a protein complex with AtRAD51C-AtXRCC3 to facilitate RAD51 localization on chromosomes for meiotic recombination.
Our data demonstrate that RAD51 plays a supporting role for DMC1 in meiotic recombination in the flowering plant, Arabidopsis.
The present study demonstrates for the first time the involvement of a host RAD51 protein in mungbean yellow mosaic India virus replication.
Results demonstrate that DMC1 functions independently and spatially separated from RAD51 during meiosis and that ATR is an integral part of the regular meiotic program.
Establishment and stabilisation of pairing of homologous centromeric and pericentromeric regions depends principally upon DMC1, while pairing and synapsis of euchromatic chromosome arms of homologues requires the presence of RAD51
AtRAD51 is required to ensure the fidelity of homologous recombination during interchromosomal exchanges. It may also be required to ensure the fidelity of homologous recombination in the interchromosomal exchanges initiated by AtDMC1.
AtBRCA2 is required for proper meiotic synapsis and mediates the recruitment of AtRAD51 and AtDMC1.
Study provides the molecular evidence showing that the BRCA2-RAD51 complex, known for its function in HR, also plays a direct and specific role in transcription regulation during plant immune responses.
results show that loss of RAD51 caused hypersensitivity to the double-strand break-inducing agent bleomycin in P. patens but not Arabidopsis; data show importance of RAD51 for viability is independent of taxonomic position or complexity of an organism
RAD51 plays a critical role in maintaining chromosome integrity and mitochondrial activity during porcine oocyte maturation.
The complete cDNA sequences of the pig RAD51, RAD52, and RAD54 genes, which are closely related to homologous recombination events, arae identified using molecular cloning technique in pigs.
we observed the occurrence of synaptonemal complex bridges between bivalents, most likely representing chromosome translocation events that may involve DMC1, RAD51 or 53BP1.
Study propose that Rad51 acts as an "early responder" at stalled forks, binding single stranded daughter strand gaps on the arrested lagging strand, and that Rad51-mediated fork remodeling generates homologous recombination intermediates that are incapable of Ku binding and therefore invisible to the classical non-homologous end joining machinery.
Swi5-Sfr1 (S5S1) stimulates Rad51-mediated homologous recombination.
Rad51 negatively regulates Netrin-1 signaling by modulating the expression of Unc5s in developing motor cortex.
RT-PCR and immunobloting data show that inhibitory effect of sodium butyrate takes place at the level of Rad51 and XRCC5 gene transcription and the content of Rad51 and Ku80 proteins.
Data show that the expression of miR-193b-3p and Rad51 was altered in in response to low-dose irradiation (LDIR) exposure.
The anti-recombinase activity of BLM is of general importance for normal retention of RAD51 at DNA double strand break sites and regulation of homologous recombination.
Our results thus help establish the functional relevance of the trimeric RAD51-SWI5-SFR1 complex and provide insights into the mechanistic underpinnings of homology-directed DNA repair in mammalian cells.
Unlike directly induced DSBs, secondary DSBs were not efficiently repaired, although Rad51 and 53BP1 were recruited to these sites. H2AX was dramatically stabilized in response to DSBs directly caused by gamma-rays, enabling gammaH2AX foci formation and DSB repair, whereas H2AX was barely stabilized in response to secondary DSBs, in which gammaH2AX foci were small and DSBs were not efficiently repaired
HOP2-MND1 enhances the interaction of RAD51 with nucleotide cofactors and modifies its DNA-binding specificity.
Rad51 repaired DNA damage.
An antimorphic mRad51 mutation, when present in heterozygous condition over wild-type, displays defects in non-replication-associated DNA repair and not in replication-associated repair.
BRCA2-mediated sequestration of nuclear RAD51 serves to prevent inappropriate DNA interactions.
increased Rad51 concentration and homology length interact synergistically to promote 3' extension, presumably as a result of enhanced Brca2-mediated Rad51 polymerization
Results suggest that cellular levels of Brca2 and Rad51 are mutually dependent on each other, and that low levels of these proteins provide selective pressure for reduction of p53, which permits cell growth
FBH1 restraining RAD51 DNA binding under unperturbed growth conditions to prevent unwanted or unscheduled DNA recombination.
HELQ interacts directly with the RAD51 paralogue complex BCDX2 and functions in parallel to the Fanconi anaemia pathway to promote efficient homologous recombination at damaged replication forks
RAD51 recombinase inhibitor overcomes imatinib-resistance in chronic myeloid leukaemia.
activated Akt1 in Brca1-deficient cells impairs Chk1 nuclear localization and subsequently disrupts interaction of Chk1 and Rad51 leading to homologous recombination defects.
The control of protein levels of Rad51 in mouse embryonic stem cells and mouse embryo fibroblasts, was investigated.
Brca2 and Rad51 prevent formation of abnormal DNA replication intermediates, whose processing by Smarcal1 and Mre11 predisposes to genome instability.
Data show that MRE11- and RAD51-dependent fork repair leading to reloading of the GINS onto the MCM-CDC45 complex still engaged with the DNA could be sufficient to restore a functional CDC45-MCM-GINS (CMG) helicase complex.
By promoting CtIP-dependent resection of double-strand break (DSB) ends while preventing Rad51 chromatin assembly, Cdk1 inhibits both the nonhomologous and homologous modes of DSB repair during mitosis.
Rad51 has a role at the replication fork protecting DNA from Mre11-dependent degradation.
The protein encoded by this gene is a member of the RAD51 protein family. RAD51 family members are highly similar to bacterial RecA and Saccharomyces cerevisiae Rad51, and are known to be involved in the homologous recombination and repair of DNA. This protein can interact with the ssDNA-binding protein RPA and RAD52, and it is thought to play roles in homologous pairing and strand transfer of DNA. This protein is also found to interact with BRCA1 and BRCA2, which may be important for the cellular response to DNA damage. BRCA2 is shown to regulate both the intracellular localization and DNA-binding ability of this protein. Loss of these controls following BRCA2 inactivation may be a key event leading to genomic instability and tumorigenesis. Multiple transcript variants encoding different isoforms have been found for this gene.
BRCA1/BRCA2-containing complex, subunit 5
, DNA repair protein RAD51 homolog 1
, RAD51 homolog A
, RecA, E. coli, homolog of
, RecA-like protein
, recombination protein A
, RAD51 homolog (RecA homolog, E. coli)
, homolog to S.cerevisiae
, RAD51 homolog
, DNA repair protein RAD51
, DNA repair protein RAD51 homolog A
, RAD51 homolog (RecA homolog)
, DNA repair protein RAD51-like 1