MABS1758MI
MilliporeSigma™ RAD9A, Mouse, Unlabeled, Clone: 5H8.1,
Manufacturer: MilliporeSigma™
Select a Size
| Pack Size | SKU | Availability | Price |
|---|---|---|---|
| Each of 1 | MABS1758MI-Each-of-1 | In Stock | ₹ 41,813.98 |
MABS1758MI - Each of 1
In Stock
Quantity
1
Base Price: ₹ 41,813.98
GST (18%): ₹ 7,526.516
Total Price: ₹ 49,340.496
Antigen
RAD9A
Classification
Monoclonal
Concentration
Please refer to lot specific datasheet.
Formulation
Purified mouse IgGκ in buffer containing 0.1M Tris-Glycine (pH 7.4), 150mM NaCl with 0.05% Sodium Azide.
Gene Accession No.
Q99638
Immunogen
GST-tagged recombinant human RAD9A ABL1-interacting domain fragment.
Quantity
100 μg
Research Discipline
Signaling
Gene ID (Entrez)
NP_001230153
Target Species
Human
Form
Purified
Applications
Western Blot
Clone
5H8.1
Conjugate
Unconjugated
Gene
RAD9A, RAD9
Host Species
Mouse
Purification Method
Protein G Purified
Regulatory Status
RUO
Primary or Secondary
Primary
Test Specificity
Clone 5H8.1 targeted epitope lies within RAD9A ABL1-interacting domain.
Content And Storage
Stable for 1 year at 2°-8°C from date of receipt.
Isotype
IgG1 κ
Related Products
Description
- 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.