RAD51C blocking peptide

RAD51C Antibody (Center) Blocking Peptide

• Gene Names: RAD51C; FANCO; R51H3; BROVCA3; RAD51L2
• Synonyms: RAD51C; RAD51C Antibody (Center) Blocking Peptide; DNA repair protein RAD51 homolog 3; R51H3; RAD51 homolog C; RAD51-like protein 2; RAD51L2; RAD51C blocking peptide

• Form/Format: Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.
• Sequence Length: 376

• Cellular Location: Nucleus. Cytoplasm. Cytoplasm, perinuclear region. Mitochondrion. Note: 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
• Tissue Location: Expressed in a variety of tissues, with highest expression in testis, heart muscle, spleen and prostate
• Preparation and Storage: Maintain refrigerated at 2-8 degree C for up to 6 months. For long term storage store at -20 degree C.

Related Product Information for RAD51C blocking peptide

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 induced by DNA-damaging agents. Part of the RAD21 paralog protein complexes BCDX2 and CX3 which act at different stages of the 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. The BCDX2 complex was originally reported to bind single-stranded DNA, single-stranded gaps in duplex DNA and specifically to nicks in duplex DNA. The BCDX2 subcomplex RAD51B:RAD51C exhibits single-stranded DNA-dependent ATPase activity suggesting an involvement in early stages of the HR pathway. Involved in RAD51 foci formation in response to DNA damage suggesting an involvement in early stages of HR probably in the invasion step. Has an early function in DNA repair in facilitating phosphorylation of the checkpoint kinase CHEK2 and thereby transduction of the damage signal, leading to cell cycle arrest and HR activation. Participates in branch migration and HJ resolution and thus is important for processing HR intermediates late in the DNA repair process; the function may be linked to the CX3 complex. Part of a PALB2-scaffolded HR complex containing BRCA2 and which is thought to play a role in DNA repair by HR. Protects RAD51 from ubiquitin-mediated degradation that is enhanced following DNA damage. Plays a role in regulating mitochondrial DNA copy number under conditions of oxidative stress in the presence of RAD51 and XRCC3. Contributes to DNA cross-link resistance, sister chromatid cohesion and genomic stability. Involved in maintaining centrosome number in mitosis.

NCBI and Uniprot Product Information

• NCBI GI #: 3914534
• NCBI GeneID: 5889
• UniProt Accession #: O43502; O43503; Q3B783
• Molecular Weight: 14,883 Da
• NCBI Official Full Name: DNA repair protein RAD51 homolog 3
• NCBI Official Synonym Full Names: RAD51 paralog C
• NCBI Official Symbol: RAD51C
• NCBI Official Synonym Symbols: FANCO; R51H3; BROVCA3; RAD51L2
• NCBI Protein Information: DNA repair protein RAD51 homolog 3
• UniProt Protein Name: DNA repair protein RAD51 homolog 3
• Protein Family: DNA repair protein
• UniProt Gene Name: RAD51C
• UniProt Synonym Gene Names: RAD51L2; R51H3
• UniProt Entry Name: RA51C_HUMAN

NCBI Description

This gene is a member of the RAD51 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 other RAD51 paralogs and is reported to be important for Holliday junction resolution. Mutations in this gene are associated with Fanconi anemia-like syndrome. This gene is one of four localized to a region of chromosome 17q23 where amplification occurs frequently in breast tumors. Overexpression of the four genes during amplification has been observed and suggests a possible role in tumor progression. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jul 2013]

Uniprot Description

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 induced by DNA-damaging agents. The RAD51B-RAD51C dimer exhibits single-stranded DNA-dependent ATPase activity. The BCDX2 complex binds single-stranded DNA, single-stranded gaps in duplex DNA and specifically to nicks in duplex DNA. Participates in branch migration and Holliday junction resolution and thus is important for processing HR intermediates late in the DNA repair process. Also has an early function in DNA repair in facilitating phosphorylation of the checkpoint kinase CHEK2 and thereby transduction of the damage signal, leading to cell cycle arrest and HR activation. Protects RAD51 from ubiquitin-mediated degradation that is enhanced following DNA damage. Plays a role in regulating mitochondrial DNA copy number under conditions of oxidative stress in the presence of RAD51 and XRCC3. Contributes to DNA cross-link resistance, sister chromatid cohesion and genomic stability. Involved in maintaining centrosome number in mitosis. Defects in RAD51C are the cause of Fanconi anemia complementation group O (FANCO). It is a disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair. Defects in RAD51C are the cause of familial breast- ovarian cancer type 3 (BROVCA3). It is a condition associated with familial predisposition to cancer of the breast and ovaries. Characteristic features in affected families are an early age of onset of breast cancer (often before age 50), increased chance of bilateral cancers (cancer that develop in both breasts, or both ovaries, independently), frequent occurrence of breast cancer among men, increased incidence of tumors of other specific organs, such as the prostate. Belongs to the RecA family. RAD51 subfamily. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: DNA repair, damage

Chromosomal Location of Human Ortholog: 17q22

Cellular Component: condensed nuclear chromosome; cytoplasm; mitochondrion; nucleoplasm; nucleus; perinuclear region of cytoplasm; replication fork

Molecular Function: crossover junction endodeoxyribonuclease activity; DNA binding; DNA-dependent ATPase activity; double-stranded DNA binding; four-way junction DNA binding; protein binding; recombinase activity; single-stranded DNA binding

Biological Process: blood coagulation; DNA recombinase assembly; DNA recombination; DNA repair; DNA synthesis during DNA repair; double-strand break repair via homologous recombination; meiotic recombination; mitotic recombination; response to ionizing radiation; sister chromatid cohesion; strand displacement; strand invasion

Disease: Breast-ovarian Cancer, Familial, Susceptibility To, 3; Fanconi Anemia, Complementation Group O; Tracheoesophageal Fistula With Or Without Esophageal Atresia