A 16-aa peptide sequence mapping near the C-terminus of mouse CPT-2L (1) .
In cells, excess of metabolic fuel is converted into fatty acids in cytosol and oxidized later in mitochondria to generate ATP and acetyl-CoA. In fatty acid synthesis, catalytic formation of malonyl-CoA (precursor for long-chain fatty acyl-CoA, LCFA-CoA) from acetyl-CoA by Acetyl-CoA carboxylase (ACC-1) is the rate limiting step. The translocation of LCFA-CoA from cytosol to mitochondria is catalyzed by two carnitine palmitoyl transferases (CPT-1 & CPT-2) and regulated by ACC-2, the rate limiting step of mitochondrial fatty acid b-oxidation. Activities of ACC-1 and 2 are regulated by their phosphorylation by 5'-AMP-activated protein kinase (AMPK). Diabetes deranges AMPK master-switch and represses the ACC-1 gene-expression and stimulates excessive fatty acid oxidation which in turn interferes with glucose metabolism.
Mitochondrial oxidation of LC-FCA is initiated by the sequential action of CPT-1, which is located in the outer membrane, and CPT-2, which is located in the inner membrane together with a carnitine-acylcarnitine translocase. CPT-2 (mouse/rat/human 658-aa, ~74kD, chromosome 1p32, ~20% identity with CPT1) is a ubiquitous malonyl-CoA-insensitive transferase localized in the inner mitochondrial membrane. It catalyzes the re-synthesis of acyl-CoA from acyl-carnitines. CPT-2 deficiency leads to the most commonly inherited, lipid myopathy in adults characterized by exercise-induced pain, stiffness, and myoglobinuria. The aa sequences of the two isoforms are ~61% identical.
仕様
Size：100ug
Source Antigen：Mouse synthetic peptide
Grade：Highly Purified
Purity：Highly purified
Form：Supplied as a liquid in PBS, pH 7.2
Specificity：93% conserved in rat and 86% in human CPT-2. No significant sequence homology seen with any other protein
