Anti-UVRAG-FS mutant

Evaluated by Western Blotting in WT/ Mutant UVRAG-FS lysate.

Western Blotting Analysis: A 1:1,000 dilution of this antibody detected UV radiation resistance-associated gene protein in Wild-type (WT) and FS mutant UVRAG protein expression in microsatellite stable (MSS) and microsatellite instable (MSI) colorectal cancer cell lines.

Anti-UVRAG-FS mutant, Cat. No. ABC1434, detects FS mutant UV radiation resistance-associated gene protein. Validated for use in Immunoprecipitation and Western Blotting.

Research Category
Apoptosis & Cancer

Western Blotting Analysis: A representative lot detected UV radiation resistance-associated gene protein in Wild-type (WT) and FS mutant UVRAG protein expression in MSS and MSI CRC cell lines (Data courtesy of Dr Liang Laboratory).

Western Blotting Analysis: A representative lot detected Wild-type (WT) and FS mutant UVRAG protein expression in MSS and MSI CRC cell lines. (He, S., et. al. (2015). Nat Commun. 6:7839).

Immunoprecipitation Analysis: A representative lot detected Wild-type (WT) and FS mutant UVRAG protein expression in MSS and MSI CRC cell lines. (He, S., et. al. (2015). Nat Commun. 6:7839).

This polyclonal antibody targets an internal sequence in the N-terminal half and detects UVRAG-FS by Western blotting.

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.

UV radiation resistance-associated gene protein (UniProt: Q9P2Y5; also known as p63) is encoded by UVRAG gene (Gene ID: 7405) in human. UVRAG is a key autophagic tumor suppressor that is shown to be mutated in several common human cancers. UVRAG as a critical regulator of intracellular membrane trafficking, autophagy, and chromosomal stability. It contains four functional domains, a proline-rich domain, a lipid-binding C2 domain, a Beclin1-binding coiled-coil domain (CCD) and a C-terminal domain. UVRAG is truncated by a frameshift (FS) mutation in colorectal cancer cells. UVRAG-FS is shown to abolish the normal functions of UVRAG, including autophagy, in a dominant-negative manner. Ectopic expression of UVRAG-FS in both embryonic stem cells and cancer cells results in extensive centrosome amplification and concomitant aneuploidy. UVRAG-FS can also enhance the sensitivity to anticancer agents, such as 5-fluorouracil (5-FU), oxaliplatin, and irinotecan. Expression of UVRAG-FS is reported to trigger colorectal cancer metastatic spread through Rac1 activation and epithelial-to-mesenchymal transition, independently of autophagy. UVRAG-FS metastatic tumors display higher levels of p62 than primary tumors, which indicates suppressed autophagy. (Ref.: He, S., et al. (2015). Nat Commun. 6: 7839).

~32 kDa observed. Uncharacterized bands may be observed in some lysate(s).

A frameshift (FS)-UVRAG derived linear peptide.

Concentration: Please refer to lot specific datasheet.

Ammonium Sulfate

Format: Semi-Purified

Rabbit polyclonal antibody 1XPBS with 0.05% azide.

Stable for 1 year at -20°C from date of receipt. Handling Recommendations: Upon receipt and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.