RAD51C Antibodies

DNA repair protein RAD51 homolog 3 (RAD51C)

Essential for the homologous recombination (HR) pathway of DNA repair. Involved in the homologous recombination repair (HRR) pathway of double-stranded DNA breaks arising during DNA replication or triggered by DNA-damaging agents.

Part of this RAD21 paralog protein complexes BCDX2 and CX3 which act at different stages of this BRCA1-BRCA2-dependent HR pathway. Upon DNA damage, BCDX2 seems to act downstream of BRCA2 recruitment and upstream of RAD51 recruitment; CX3 seems to act downstream of RAD51 recruitment; both complexes bind predominantly to the intersection of the four duplex arms of the Holliday junction (HJ) and to junction of replication forks.

Gene Information

Human
Gene Name:	RAD51C
Uniprot:	O43502
Entrez:	5889

Family

Belongs to:
RecA family

Alternative Names

BROVCA3; DNA repair protein RAD51 homolog 3; FANCO; MGC104277; R51H3; RAD51 homolog C (S. cerevisiae); RAD51 homolog C; RAD51L2RAD51 (S. cerevisiae) homolog C; RAD51-like protein 2; yeast RAD51 homolog 3

Molecular Weight

Mass (kDA):
42.19 kDA

Genomic Context

Human
Location:	17q22
Sequence:	17; NC_000017.11 (58692140..58735611)

Tissue Specificity

Expressed in a variety of tissues, with highest expression in testis, heart muscle, spleen and prostate.

Subcellular Localizations

Nucleus. Cytoplasm. Cytoplasm, perinuclear region. Mitochondrion. DNA damage induces an increase in nuclear levels. Accumulates in DNA damage induced nuclear foci or RAD51C foci which is formed during the S or G2 phase of cell cycle. Accumulation at DNA lesions requires the presence of NBN/NBS1, ATM and RPA.

Diseases

• Malignant Neoplasms
• Malignant Neoplasm Of Breast
• Malignant Neoplasm Of Ovary
• Neoplasms
• Mammary Neoplasms
• Ovarian Neoplasm
• Genomic Instability
• Fanconi Anemia
• Anemia
• Hereditary Breast And Ovarian Cancer Syndrome
• Cytogenetic Abnormality
• Aneuploidy
• Cell Transformation, Neoplastic

• Leukemia
• Carcinoma
• Instabilities, Chromosomal
• Infertility
• Lymphoma
• Epithelial Ovarian Cancer
• Hyperplasia

Interacting Proteins

• HELQ
• PALB2
• RAD51
• RAD51B
• RAD51D

• SWSAP1
• XRCC2
• XRCC3

Pathways

• Dna Repair
• Recombinational Repair
• Cell Cycle
• Double-strand Break Repair
• Meiosis
• Localization
• Hypersensitivity
• Dna Replication
• Sister Chromatid Cohesion
• Prophase
• Mitosis
• Rna Interference
• Gene Conversion

• Dna Recombination
• Telomere Maintenance
• Nuclear Transport
• Cellular Localization
• Pachytene
• Transport
• Chromosome Segregation

PTMs

• Phosphorylation
• Methylation

• Sumoylation
• Cleavage

• Ribosylation

Research Areas

• Breast Cancer
• Cancer
• Chromatin Research
• DNA Double Strand Break Repair
• DNA Repair

• Homologous Recombination

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/RAD51C

Best Uses of the RAD51C Marker in Breast Cancer

You may have already heard about the RAD51C Marker. If not, you might be interested in learning about the RAD51 protein family and its role in the regulation of mitochondrial DNA copy number under oxidative stress. In this article, we'll review the biology of the RAD51C Marker and discuss its application in the treatment of breast cancer. Here are some examples of its best uses:

RAD51C Marker

The RAD51C marker is a promising therapeutic target for cancer chemotherapy. The protein induces the epithelial-mesenchymal transition, one of the main contributors to chemotherapy resistance. The marker was associated with a positive response to anthracycline-based chemotherapy. However, the protein is not effective in all cancer types, and the RAD51C polymorphism is associated with a lower survival rate in melanoma.

The RAD51C anti-antibody by Boster Bio is an excellent choice for this application. The boster bio antibody reacts with Rat BRCA1 and Mouse BRCA1 in both IF and IHC. This antibody is suitable for the detection of human BRCA1 gene-related mutations. The Boster Bio antibody has been validated against rat BRCA1 by using negative and positive samples.

RAD51 plays a role in oxidative stress and is a transcription factor that binds to four-junctions. As a result, it regulates the copy number of mitochondrial DNA under oxidative stress. Further research is needed to determine if the RAD51 gene has any role in regulating the number of mtDNA molecules under oxidative stress.

The RAD51C gene product provides a highly specific marker for detecting mutations in RAD51. It is a 339 amino acid protein that plays an important role in homologous recombination (HR) during double-stranded DNA breakages. It is an essential component of the BRCA1 mouse embryo, and deficiency of RAD51 is associated with increased risk of cancer.

RAD51 protein family

Researchers have discovered a genetic mutation in the RAD51 protein family, which is implicated in breast cancer. The mutation affects the protein's ability to repair DNA and regulate its expression. As a result, it increases the risk for the development of breast cancer. Currently, scientists are researching the gene's effect on breast cancer risk in humans and mice. Boster Bio has developed a DNA repair gene targeting antibody.

This gene is essential for the repairing of DNA damage. Its underexpression results in increased unrepaired DNA damages. In addition, replication errors beyond DNA damages lead to mutations and cancer. The RAD51 protein family is conserved across three groups of life. Its function is crucial for homologous recombination repair in human cells. In addition to repairing damaged DNA, RAD51 catalyzes strand transfer between an undamaged and damaged sequence.

DNA damage response pathways are necessary for normal cell growth and function. The two major pathways are homologous recombination and double strand break repair. The RAD51 protein family is part of the DNA damage response pathway. As a result, it is an essential part of the immune system. This gene can also be a target for a therapeutic drug. Using a RAD51-targeted gene therapy, researchers can identify genetic mutations in humans and their relatives.

Rad51 is a DNA repair protein related to the BRCA2 complex. Rad51 contains an acidic patch, which is evolutionarily conserved. Mutations in these residues completely ablate Rad51-dependent DNA repair. Human RAD52 has been shown to mediate the assembly of RAD51 on ssDNA, although its efficiency is lower than BRCA2.

The antibody used to detect RAD51C was created to recognize DNA lesions in the cell. Antibodies to RAD51C were produced from mouse and rabbit. They have been used in many biological assays. The antibodies are monoclonal and polyclonal. They react with many types of animal samples. Boster Bio develops its antibodies to RAD51C by using mouse and rabbit. The antigen accumulates in DNA lesions and induces DNA damage. The RAD51C protein requires the proteins NBN/NBS1, ATM, and RPA.

RAD51C Marker's role in mitochondrial DNA copy number regulation under oxidative stress

The RAD51C Marker is a key component of the mtDNA repair machinery. This protein interacts with DNA via its ATP-dependent binding properties and forms nucleoprotein filaments, which are important for homology search and strand exchange. The RAD51C Marker is a key player in mitochondrial DNA copy number regulation under oxidative stress, and its deficiency increases the likelihood of a number of genetic diseases, including aging and invasive ductal carcinoma.

Several genes have been identified as contributing to CMT, and mutations in four of these genes are associated with the disorder. However, the genetics of the CMT/HMSN group are complicated by the fact that many patients have mutations in the same gene. The association between different phenotypes and mutations within a single gene is a promising sign that the condition may be a spectrum of related phenotypes. In particular, a duplication in the PMP22 gene is responsible for 70 to 80 percent of CMT1 cases.

However, the RAD51C Marker has a more complex role in mitochondrial DNA copy number regulation under extreme oxidative stress. In the current study, a genetic variant of the RAD51C Marker is associated with an increased risk of heart failure and reduced survival. This finding may be helpful in the development of therapeutics for individuals with CHD.

MH is associated with other disorders, including the PHCN gene. While the incidence of MH is small - around one in every 3,000 people - it is still lethal. To ensure optimal patient care, perioperative genetic testing, preparation of the anesthetic workstation, and use of non-triggering anesthetics should be implemented. Dantrolene should be readily available for monitoring.

RAD51C Marker's application in breast cancer

The first step in the investigation of RAD51C Marker's application to breast cancer is determining whether the variant is pathogenic or not. The expression of RAD51C is related to poor clinical outcome in patients with ER-positive and HER2-negative breast tumors. Loss-of-heterozygosity (LOH) in tumors is an important risk factor for the development of BC.

Functional studies have shown that the RAD51C c.571 + 4A>G variant is pathogenic, as it changes mRNA splicing. In addition, analysis of ovary and breast tumor samples reveals that there are 15 pathogenic variants of the gene. Moreover, carriers of this variant may benefit from tailored prevention and therapy protocols. This mutation increases the risk of breast cancer and ovarian cancer.

In a study of a single mother and three daughters, the RAD51C c.571 + 4A+G variant was associated with two or more types of breast cancer. Three patients were diagnosed with BC, one with OC, and one with both at the same time. However, not all samples were available for genotyping. For this reason, the RAD51C Marker's application in breast cancer is not yet fully understood.

Interestingly, estrogen-induced DNA damage has been found to cause tumors to progress from G0 to S-phase. Fortunately, estrogen-induced DNA damage in breast cancer tumors is also protected by RAD51C-related genes, including RAD51A. Consequently, increased expression of RAD51C may indicate genomic instability, a risk factor for worse outcomes. The RAD51C Marker's application in breast cancer is now becoming apparent.

Although the association between RAD51C and HBOC is relatively new, the NL genetic isolate can be used to establish transmission patterns. In addition, the RAD51C variant c.571 + 4A>G should be classified as pathogenic according to ACMG guidelines. Further, the frequency of RAD51C variants in the NL population is 52 times greater than the average Caucasian population. These results are consistent with the presence of a recent common ancestor or a strong founder effect.