Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

ATP Citrate Lyase Mouse anti-Human, Clone: OTI3G8, Invitrogen™

Mouse Monoclonal Antibody

Manufacturer:  Invitrogen MA525067

Catalog No. PIMA525067


Add to cart

Description

Description

ATP citrate lyase is the primary enzyme responsible for the synthesis of cytosolic acetyl-CoA in many tissues. The enzyme is a tetramer (relative molecular weight approximately 440,000) of apparently identical subunits. It catalyzes the formation of acetyl-CoA and oxaloacetate from citrate and CoA with a concomitant hydrolysis of ATP to ADP and phosphate. The product, acetyl-CoA, serves several important biosynthetic pathways, including lipogenesis and cholesterogenesis. In nervous tissue, ATP citrate-lyase may be involved in the biosynthesis of acetylcholine. Two transcript variants encoding distinct isoforms have been identified for this gene.
Specifications

Specifications

ATP Citrate Lyase
Monoclonal
0.6 mg/mL
PBS with 1% BSA, 50% glycerol and 0.02% sodium azide; pH 7.3
P53396
ACL, ATPCL, CLATP, ATP citrate synthase, ATP-citrate (pro-S-)-lyase, ATP-citrate synthase, citrate cleavage enzyme
Mouse
IgG1
100 μL
-20° C, Avoid Freeze/Thaw Cycles
Primary
47
Immunocytochemistry, Immunofluorescence, Immunohistochemistry (Paraffin), Western Blot
OTI3G8
Unconjugated
ACLY
Liquid
ACLY
Full length human recombit protein of ACLY produced in HEK293T cell
Affinity Chromatography
RUO
Antibody
Monoclonal
Human
Documents
Provide Content Correction

We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Cancel Submit