Recombinant Human ACLY/acly/ATP citrate lyase Protein (His Tag) | PKSH031004

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SKU:
575-PKSH031004
Weight:
1.00 KGS
€1,288.00
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Description

Recombinant Human ACLY/acly/ATP citrate lyase Protein (His Tag) | PKSH031004 | Gentaur US, UK & Europe Disrtribition

Synonyms: ACL;ATPCL;CLATP

Active Protein: N/A

Activity: A DNA sequence encoding the human ACLY (P53396) (Met 1-Met 1101) was expressed, with a polyhistidine tag at the N-terminus.

Protein Construction: A DNA sequence encoding the human ACLY (P53396) (Met 1-Met 1101) was expressed, with a polyhistidine tag at the N-terminus.

Fusion Tag: N-His

Species: Human

Expressed Host: Baculovirus-Insect Cells

Shipping: This product is provided as lyophilized powder which is shipped with ice packs.

Purity: > 90 % as determined by reducing SDS-PAGE.

Endotoxin: < 1.0 EU per µg as determined by the LAL method.

Stability and 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.

Molecular Mass: 123 kDa

Formulation: Lyophilized from sterile 20mM Tris, 500mM NaCl, pH 8.0, 10% gly

Reconstitution: Please refer to the printed manual for detailed information.

Background: ATP citrate lyase, also known as Acly or Acl, is the primary enzyme responsible for the synthesis of cytosolic acetyl-CoA in many tissues. The enzyme is composed of two polymer chains which are polypeptides in human. ATP citrate lyase is responsible for catalyzing the conversion of citrate and CoA into acetyl-CoA and oxaloacetate, along with the hydrolysis of ATP. A definitive role for ATP citrate lyase in tumorigenesis has emerged from ATP citrate lyase RNAi and chemical inhibitor studies, showing that ATP citrate lyase inhibition limits tumor cell proliferation and survival and induces differentiation in vitro. In vivo, it reduces tumor growth leading to a cytostatic effect and induces differentiation. 

Research Area: Signal Transduction, Cancer, metabolism,

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