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Recombinant Human ADSL/Adenylosuccinate Lyase Protein (His Tag)– MSE Supplies LLC

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Recombinant Human ADSL/Adenylosuccinate Lyase Protein (His Tag)

SKU: PKSH031168-100

  • $ 65895
  • Save $ 7400



Recombinant Human ADSL/Adenylosuccinate Lyase Protein (His Tag)

 

SKU # PKSH031168
Expression Host E.coli

 

Description

Synonyms AMPS, ASASE, ASL
Species Human
Expression Host E.coli
Sequence Met 1-Leu 484
Accession P30566-1
Calculated Molecular Weight 57.0 kDa
Observed Molecular Weight 53 kDa
Tag N-His
Bio-activity Not validated for activity
  

 

Properties

Purity > 95 % as determined by reducing SDS-PAGE.
Endotoxin Please contact us for more information.
Storage Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.
Shipping This product is provided as lyophilized powder which is shipped with ice packs.
Formulation Lyophilized from sterile PBS, 10% glycerol, pH 7.5
Normally 5% - 8% trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the printed manual.
Reconstitution Please refer to the printed manual for detailed information.


Background

Adenylosuccinate lyase, also known as adenylosuccinase, ADSL or ASL, is an enzyme implicated in the reaction of adenylosuccinat converting to AMP and fumarate as part of the purine nucleotide cycle. The two substates of adenylosuccinate lyase (ADSL) are dephosphorylated derivatives of SAICA ribotide (SAICAR) and adenylosuccinate (S-AMP), which catalyzes an important reaction in the de novo pathway of purine biosynthesis. ADSL catalyzes two distinct reactions in the synthesis of purine nucleotides, both of which involve the _-elimination of fumarate to produce either aminoimidazole carboxamide ribotide from SAICAR or AMP from S-AMP. The Adenylosuccinate lyase deficiency is a rare autosomal recessive metabolic disorder characterized by the present of SAICA riboside and succinyladenosine (S-Ado). ADSL defect in different patients is often caused by different mutations to the enzyme.