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ACMSD Antibody (N-term) Blocking PeptideSynthetic peptide
| Country | United States
Ordering Information
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| Catalog # | Size | Availability | Price | |
| BP8954a | 0.1 mg 400 ul | In Stock | $ 45.00 | DISCONTINED INQUIRE CLICK INQUIRE Add to cart |
- Specification
- Citiations : 0
- Reviews
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- Backgrounds
ACMSD Antibody (N-term) Blocking Peptide - Product info | |
| Primary Accession | Q8TDX5 |
| Clone Names | 90819032 |
| Calculated MW | 38035 Da |
ACMSD Antibody (N-term) Blocking Peptide - Additional info | |
| Gene ID 130013 | |
| Target/Specificity The synthetic peptide sequence used to generate the antibody AP8954a was selected from the N-term region of human ACMSD. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay. | |
| Format Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml. | |
| Storage Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. | |
| Precautions This product is for research use only. Not for use in diagnostic or therapeutic procedures. | |
ACMSD Antibody (N-term) Blocking Peptide - Protein Information | |
| Name ACMSD | |
| Function Converts alpha-amino-beta-carboxymuconate-epsilon- semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS) ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway | |
ACMSD Antibody (N-term) Blocking Peptide - Related products
AP8954a: ACMSD Antibody (N-term)
RI10060: ACMSD predesign siRNA
ACMSD Antibody (N-term) Blocking Peptide - Research Areas
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Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
ACMSD is an intermediate in the de novo synthesis pathway of NAD from tryptophan, and has been implicated in the pathogenesis of several neurodegenerative disorders. Quinolinate is derived from alpha-amino-beta-carboxy-muconate-epsilon-semialdehyde (ACMS).ACMSD (ACMS decarboxylase; EC 4.1.1.45) can divert ACMS to a benign catabolite and thus prevent the accumulation of quinolinate from ACMS.
REFERENCES
Garavaglia,S., et.al., FEBS J. 276 (22), 6615-6623 (2009)Fukuoka,S., et.al., J. Biol. Chem. 277 (38), 35162-35167 (2002)
