Anti-RAD9A Antibody, clone 5H8.1

Evaluated by Western Blotting in human skeletal muscle tissue lysate.

Western Blotting Analysis: 0.5 µg/mL of this antibody detected RAD9A in 10 µg of human skeletal muscle tissue lysate.

Detect RAD9A using this mouse monoclonal Anti-RAD9A Antibody, clone 5H8.1, Cat. No. MABS1758, validated for use in Immunohistochemistry (Paraffin) and Western Blotting.

Immunohistochemistry Analysis: A 1:50 dilution from a representative lot detected nuclear RAD9A immunoreactivity in human prostate cancer, pancreas, and small intestine tissue sections.

Research Category
Signaling

Clone 5H8.1 targeted epitope lies within RAD9A ABL1-interacting domain.

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Cell cycle checkpoint control protein RAD9A (EC 3.1.11.2; UniProt Q99638; also known as DNA repair exonuclease rad9 homolog A, hRAD9, Rad9-like protein) is encoded by the RAD9A (also known as RAD9A) gene (Gene ID 5883) in human. RAD9A is a component of the trimeric PCNA-like 9-1-1 complex (Rad9A, Rad1, and Hus1) and plays an important role in maintaining genomic integrity. RAD9A participates in both ATR and ATM signaling pathways-mediated cell cycle checkpoints in mitosis. Evidences indicate that RAD9A participates in DNA damage repair by interacting with proteins involved in base excision repair, mismatch repair and homologous recombination repair. RAD9A is shown to colocalize with γH2AX following DNA damage induction in an ATM-independent manner, and RAD9A inactivation delays the appearance of ionizing radiation-induced γH2AX foci. Rad9a-knockout causes embryonic lethality in mice due to increased apoptotic activity and reduced cellular proliferation, while mice heterozygous for Rad9a are prone to spontaneous and radiation-induced cataractogenesis. In addition, conditional knockout in keratinocytes causes enhanced susceptibility to carcinogen-induced skin tumors, while conditional Rad9a deletion in undifferentiated spermatogonia results in drastic effects on meiosis.

~42 kDa observed. 42.55 kDa calculated. Uncharacterized bands may be observed in some lysate(s).

GST-tagged recombinant human RAD9A ABL1-interacting domain fragment.

Concentration: Please refer to lot specific datasheet.

Format: Purified

Protein G purified

Purified mouse IgGκ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Stable for 1 year at 2-8°C from date of receipt.