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Recombinant Human 2-amino-3-carboxymuconate-6-semialdehyde decarboxylase (ACMSD)

ACP13013

Number
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High Purity LevelsPrecision and ReliabilityCustomization Options

Specifications


Cat.No ACP13013 Target NameACMSD
FormLyophilized powderExpression SystemCustom Production. Please inquire and provide the desire expression system.
Expression Range1-336Protein LengthFull length protein
Purity>85% (SDS-PAGE)Storage Buffer5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0.

Immunogen Information


Target SpeciesHumanUniprot IDQ8TDX5
Background Information
  • Uniprot Id

    Q8TDX5

  • Target Species

    Human

  • Target Name

    ACMSD

  • Target Full Name

    2-amino-3-carboxymuconate-6-semialdehyde decarboxylase

  • Target 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.

  • Target Protein Families

    Metallo-dependent hydrolases superfamily, ACMSD family

  • Target Synonyms

    2 amino 3 carboxymuconate 6 semialdehyde decarboxylase; 2-amino-3-carboxymuconate-6-semialdehyde decarboxylase; acmsd; ACMSD_HUMAN; Aminocarboxymuconate semialdehyde decarboxylase; Picolinate carboxylase

  • Target Background

    The neuronal excitotoxin quinolinate 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.

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