ARC/NOL3 Antibody - BSA Free Summary
Immunogen |
Antibody was raised against a 17 amino acid peptide near the amino terminus of human ARC. The immunogen is located within the first 50 amino acids of ARC. Amino Acid Squence: GNAQERPSETIDRERKR |
Isotype |
IgG |
Clonality |
Polyclonal |
Host |
Rabbit |
Gene |
NOL3 |
Purity |
Peptide affinity purified |
Innovator's Reward |
Test in a species/application not listed above to receive a full credit towards a future purchase. |
Applications/Dilutions
Dilutions |
- ELISA 1:100-1:2000
- Western Blot 1:500
|
Application Notes |
An approximately 25 kDa band can be detected in Western Blot. |
Theoretical MW |
25 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors. |
Control Peptide |
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Packaging, Storage & Formulations
Storage |
Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles. |
Buffer |
PBS |
Preservative |
0.02% Sodium Azide |
Concentration |
1 mg/ml |
Purity |
Peptide affinity purified |
Alternate Names for ARC/NOL3 Antibody - BSA Free
Background
Apoptosis is regulated by death domain (DD) and/or caspase recruitment domain (CARD) containing molecules and a caspase family of proteases. CARD containing cell death regulators include RAIDD, RICK BCL10, Apaf-1, caspase-9, and caspase-2. A novel CARD domain containing protein was recently identified and designated ARC for apoptosis repressor with CARD. ARC interacts with caspase-2 and -8 and inhibits enzymatic activity of caspase-8. ARC suppresses apoptosis induced by cell death adapters FADD and TRADD and by cell death receptors Fas, TNFR-1, and DR3. The messenger RNA of ARC is primarily expressed in skeletal muscle and cardiac tissue.
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are
guaranteed for 1 year from date of receipt.
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