Rabbit anti-Human Rad50 Polyclonal Antibody

Uniprot Id

Q92878

Target Species

Human

Target Name

RAD50

Target Full Name

DNA repair protein RAD50

Target Function

Component of the MRN complex, which plays a central role in double-strand break (DSB) repair, DNA recombination, maintenance of telomere integrity and meiosis. The complex possesses single-strand endonuclease activity and double-strand-specific 3'-5' exonuclease activity, which are provided by MRE11. RAD50 may be required to bind DNA ends and hold them in close proximity. This could facilitate searches for short or long regions of sequence homology in the recombining DNA templates, and may also stimulate the activity of DNA ligases and/or restrict the nuclease activity of MRE11 to prevent nucleolytic degradation past a given point. The complex may also be required for DNA damage signaling via activation of the ATM kinase. In telomeres the MRN complex may modulate t-loop formation.

Target Involvement

Nijmegen breakage syndrome-like disorder (NBSLD)

Target Subcellular Location

Nucleus. Chromosome, telomere. Chromosome.

Target Protein Families

SMC family, RAD50 subfamily

Target Tissue Specificity

Expressed at very low level in most tissues, except in testis where it is expressed at higher level. Expressed in fibroblasts.

Target Research Area

Epigenetics and Nuclear Signaling

Target Synonyms

DNA repair protein RAD50; hRAD50; hsRAD50; Mrell; NBSLD; Rad 50; RAD50 2; rad50; RAD50 homolog (S cerevisiae); RAD50 homolog; RAD50 PEN; RAD50, S. cerevisiae, homolog of; RAD50_HUMAN; RAD502; Rad50l; Truncated RAD50 protein

Target Background

The protein encoded by this gene is highly similar to Saccharomyces cerevisiae Rad50, a protein involved in DNA double-strand break repair. This protein forms a complex with MRE11 and NBS1. The protein complex binds to DNA and displays numerous enzymatic activities that are required for nonhomologous joining of DNA ends. This protein, cooperating with its partners, is important for DNA double-strand break repair, cell cycle checkpoint activation, telomere maintenance, and meiotic recombination. Knockout studies of the mouse homolog suggest this gene is essential for cell growth and viability. Mutations in this gene are the cause of Nijmegen breakage syndrome-like disorder.