The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use at an assay dependent dilution.
Use at an assay dependent dilution. Predicted molecular weight: 37 kDa.
Plays an important role in homologous strand exchange, a key step in DNA repair through homologous recombination. Binds to single and double-stranded DNA and exhibits DNA-dependent ATPase activity. 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. Binds to single-stranded DNA in an ATP-dependent manner to form nucleoprotein filaments which are essential for the homology search and strand exchange (PubMed:26681308). Part of a PALB2-scaffolded HR complex containing BRCA2 and RAD51C and which is thought to play a role in DNA repair by HR. Plays a role in regulating mitochondrial DNA copy number under conditions of oxidative stress in the presence of RAD51C and XRCC3.
Highly expressed in testis and thymus, followed by small intestine, placenta, colon, pancreas and ovary. Weakly expressed in breast.
Breast cancer Mirror movements 2 Defects in RAD51 are found in a patient with microcephaly, mental retardation without bone marrow failure and pediatric cancers.
Belongs to the RecA family. RAD51 subfamily. Contains 1 HhH domain.
The nuclear localization may reside in the C-terminus (between 259 and 339 AA).
Ubiquitinated by the SCF(FBXO18) E3 ubiquitin ligase complex, regulating RAD51 subcellular location and preventing its association with DNA. Phosphorylated. Phosphorylation of Thr-309 by CHEK1 may enhance association with chromatin at sites of DNA damage and promote DNA repair by homologous recombination. Phosphorylation by ABL1 inhibits function.
Nucleus. Cytoplasm. Cytoplasm, perinuclear region. Mitochondrion matrix. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Colocalizes with RAD51AP1 and RPA2 to multiple nuclear foci upon induction of DNA damage. DNA damage induces an increase in nuclear levels. Together with FIGNL1, redistributed in discrete nuclear DNA damage-induced foci after ionizing radiation (IR) or camptothecin (CPT) treatment. Accumulated at sites of DNA damage in a SPIDR-dependent manner.