A synthetic peptide corresponding to the center region of the Human ARID3A
Preparation
Produced in rabbits immunized with a synthetic peptide corresponding to the center region of the Human ARID3A, and purified by antigen affinity chromatography.
Source
Polyclonal Rabbit IgG
Purification
Protein A & Antigen Affinity
Formulation
0.2 μm filtered solution in PBS
Conjugate
Unconjugated
Form
Liquid
Shipping
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Storage
This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free. Avoid repeated freeze-thaw cycles.
ARID3A/DRIL1/Bright is a family member of the AT rich interaction domain (ARID) DNA-binding proteins that are involved in diverse biological processes, and p53 activates ARID3A transcription, and ARID3A overexpression induces G1 arrest. Both cooperative and interdependent roles for ARID3A and p53 in the transcriptional activation of p21(WAF1) in response to DNA damage. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with severe defects in placental structural organization. ARID3A in mammalian placental development through regulation of both intrinsic and extrinsic developmental programs. AT-rich interactive domain 3A (ARID3A) is a member of the ARID family of DNA-binding proteins. Previous reports have shown that ARID3A controls cell growth in a p53-dependent manner. Recently, it has been reported that expression of the ARID3A protein was markedly increased in colon cancer tissue compared with matched normal colonic mucosa. ARID3A plays an important role in E2F-mediated transcriptional activation and cell growth. Bright/ARID3A is a nuclear matrix-associated transcription factor that stimulates immunoglobulin heavy chain (IgH) expression and Cyclin E1/E2F-dependent cell cycle progression. Bright positively activates IgH transcriptional initiation by binding to ATC-rich P sites within nuclear matrix attachment regions (MARs) flanking the IgH intronic enhancer (Emu).