RAD51D KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control provided.
BROVCA4, DNA repair protein RAD51 homolog 4, HsTRAD, OTTHUMP00000163851, OTTHUMP00000163852, OTTHUMP00000163853, R51H3, RA51D_HUMAN, RAD51 homolog D, RAD51 homolog D (S. cerevisiae), RAD51 like 3 (S. cerevisiae), RAD51 paralog D, RAD51, S. cerevisiae, homolog of, D, RAD51-like protein 3, Rad51l3, Recombination repair protein, S. cerevisiae RAD51-like 3, TRAD
RAD51D KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control provided.
Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.
1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.
Recommended control: Human wild-type HCT116 cell line (ab288559). Please note a wild-type cell line is not automatically included with a knockout cell line order, if required please add recommended wild-type cell line at no additional cost using the code WILDTYPE-TMTK1.
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our limited use license and patent pages.
Rad51D also known as RAD51L3 is a protein involved in homologous recombination repair of DNA. It has a molecular weight of approximately 37 kDa. Rad51D is primarily expressed in tissues with high cell division rates such as the testis and thymus. This protein belongs to the RAD51 family which is responsible for repairing DNA double-strand breaks (DSBs) that can arise during replication or after exposure to genotoxic agents. Rad51D's role centers on promoting the exchange of DNA strands during repair processes which helps maintain genome stability.
Rad51D plays a significant role in maintaining genomic integrity by facilitating homologous recombination. It interacts with Rad51 paralogs like Rad51C as part of the BCDX2 complex which also includes Rad51B and XRCC2. This complex is essential in the early steps of homologous recombination especially in forming the synaptic complex that searches for homology. The interactions among these proteins enable efficient strand invasion and exchange essential for error-free DNA repair.
Rad51D is an important component in DNA repair and damage response pathways. It primarily functions within the homologous recombination repair pathway. In this pathway Rad51D works closely with the RAD52 epistasis group including proteins such as BRCA1 and BRCA2 which assist in the proper localization and functioning of RAD51 recombinase. Rad51D's involvement in these pathways ensures accurate and effective DNA repair preventing genomic instability that could lead to cellular dysfunction.
Rad51D mutations have been linked to a higher risk of breast and ovarian cancer. Its association with the BRCA1 and BRCA2 proteins suggests a shared pathway in hereditary breast and ovarian cancer syndromes where deficient DNA repair leads to genomic mutations and tumorigenesis. Further research continues to explore Rad51D's potential as a biomarker for cancer susceptibility and its utility in developing targeted therapies.
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79 bp deletion (allele 1) and 77 bp deletion (allele 2) in exon 6, CCDS11287.1
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