|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||265554 Da|
|Other Names||Acetyl-CoA carboxylase 1, ACC1, ACC-alpha, Biotin carboxylase, ACACA, ACAC, ACC1, ACCA|
|Target/Specificity||A synthetic peptide corresponding to residues in the human Acetyl-CoA carboxylase 1 was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Precautions||Acetyl-CoA1 (ACC1) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||ACAC, ACC1, ACCA|
|Function||Catalyzes the rate-limiting reaction in the biogenesis of long-chain fatty acids. Carries out three functions: biotin carboxyl carrier protein, biotin carboxylase and carboxyltransferase.|
|Tissue Location||Expressed in brain, placental, skeletal muscle, renal, pancreatic and adipose tissues; expressed at low level in pulmonary tissue; not detected in the liver|
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Provided below are standard protocols that you may find useful for product applications.
Acetyl-CoA carboxylase 1 (ACC1) is a biotin dependent lipogenic enzyme that is highly expressed during adipogenesis. ACC1 catalyzes acetyl-CoA carboxylation, producing malonyl-CoA, a metabolite involved in energy homeostasis regulation. Malonyl-CoA is a two carbon donor in the synthesis of long-chain fatty acids and the elongation of fatty acids found in the cystol (1). ACC1 is regulated short-term by citrate, CoA, and palmitoyl-CoA through allosteric interactions. Nutrients and hormones can be both short-term (inducing reversible phosphorylations by such as AMPK) and long-term (transcription level regulation) regulators of ACC1 (2). Highly expressed in lipogenic tissues, ACC1 is found in liver, adipose, and lactating mammary gland (3). ACC1 has been implicated as a target in the development of anti-obesity drugs (4).
1. Jianqiang M, et al. PNAS 100:7515-7520, 2003.
2. Girad J, et al. The FASEB Journal 8:36-42, 1994.
3. Wakil SJ, et al. Annu Rev Biochem 52:537-539
4. Abu-Elheiga L, et al. Science 291: 2613-2616. 2001.
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