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RAD51, DNA repair protein RAD51 homolog 1, its 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. The complete and accurate replication of the genome is essential to maintain genome integrity. As the central homologous recombination (HR) protein, this protein can form helical nucleoprotein filaments on tracts of single strand DNA, and interact with the ssDNA-binding protein RPA and RAD52, and it is thought to play central roles in homologous pairing, recombinational repair and strand transfer of DNA in eukaryotes. One additional thing to note is that Rad51 plays an important part in homologous strand exchange, a key step in DNA repair through HR. Rad51 is also involved in interstrand cross-link repair. This encoded protein binds to single and double-stranded DNA and exhibits DNA-dependent ATPase activity. Rad51 catalyzes the recognition of homology and strand exchange between homologous DNA partners to form a joint molecule between a processed DNA break and the repair template. It also binds to single-stranded DNA in an ATP-dependent manner to form nucleoprotein filaments which are essential for the homology search and strand exchange. Replication forks face many obstacles that can result in replication fork stalling or replication fork collapse. Besides its role in DNA double strand breaks (DSBs) repairing, a non-enzymatic function of RAD51 promotes replication fork regression, a process that has also been referred to as replication fork reversal, which involves branch migration in the direction opposite to replication to form a Holliday junction-containing chicken foot structure. In the same study, Jennifer M. Mason, etc. shows that RAD51 promotes replication restart by both strand exchange-dependent and strand exchange-independent mechanisms, and protects newly synthesized DNA from degradation.
RAD51 interacts (directly or indirectly) with a large number of proteins involved in DNA repair and the cell cycle. This RAD51 protein is found to interact with p53, BRCA1 and BRCA2, which may be important for the cellular response to DNA damage. Cooperation between the DNA recombinase RAD51 and the breast cancer susceptibility protein BRCA2 is crucial for the repair of double-strand DNA breaks. BRCA2 is shown to regulate both the intracellular localization and DNA-binding ability of this protein. Part of a PALB2-scaffolded HR complex containing BRCA2 and RAD51C, is thought to play a role in DNA repair by HR and regulating the copy number of mitochondrial DNA under conditions of oxidative stress in the presence of RAD51C and XRCC3. 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.
Fig. 1 RAD51, BRCA2 and DNA repair: a partial resolution (Christopher J Lord & Alan Ashworth, 2007)
It is well known that deficiencies in DNA repair can lead to carcinogenesis. Loss of RAD51 function would lead to accumulation of DNA damage and, therefore, to increased cancer risk. There is evidence to support a key role for RAD51 in breast cancer and breast tumourigenesis. Researchers did not detect any variation in the coding region of RAD51, which may further imply the importance of maintaining the structural integrity of such a vital component of the DNA repair pathway.
|Cancer||Over or Under expression||Evaluation method|
|Breast cancer (invasive ductal)||Over-expression||Immunohistochemistry|
|Breast cancer (BRCA1 deficient)||Over-expression||messenger RNA|
|Breast cancer (progesteron receptor negative)||Over-expression||messenger RNA|
|Head and neck squamous cancers||Over-expression||Immunohistochemistry|
|Non-small-cell lung cancer||Over-expression||Immunohistochemistry|
|Soft tissue sarcoma||Over-expression||Immunohistochemistry|
|Esophageal squamous cell cancer||Over-expression||Immunohistochemistry|
|Renal cell carcinoma||Under-expression||Western (protein) blotting and mRNA|
Table 1. RAD51 expression in sporadic cancers
Genome Editing is revolutionizing biomedical research, due to its high efficiency, ease-of-use, and relatively low cost. CRISPR/Cas9 PlatformCB, a global biotechnological company specializing in gene editing, is dedicated to offering comprehensive CRISPR/Cas9 gene editing products and services for academic research, biotech research and pharmaceutical drug discovery. With products for CRISPR-Cas9 clones, validation and screening kits, pre-made transfected stable cell lines, and more for precision genome editing, our complete solutions for genome editing provide you with a wealth of tools to help you every step of the way in your genome editing workflow.
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|Knockout Cell Line Service||Single gene knockout cell line||Available for any transfection-suitable cell lines, including A549, CHO-K1, HEK293, HEK293T, HCT116, MCF7, MDCK, U937, RPMI 8866, HT-29, MDA-MB-231, 4T1, A20, etc.|
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* It is preferred that customers provide their own cell lines, despite available cell lines can be purchased by Creative Biogene for an additional fee.
Guide RNA Design:
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|CSC-RT1456||Human RAD52 Knockout Cell Line-HeLa||Knockout Cell Line||Inquiry|
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