Cell Signaling Technology

Product Pathways - Metabolism

CPT1A (D3B3) Rabbit mAb #12252

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H Endogenous 88 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

CPT1A (D3B3) Rabbit mAb recognizes endogenous levels of total CPT1A protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu213 of human CPT1A protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa, PANC-1, and MCF7 cells using CPT1A (D3B3) Rabbit mAb.

Background

Carnitine palmitoyltransferase-1 (CPT1), localized to the mitochondrial outer membrane, translocates fatty acids across the mitochondrial membranes and catalyzes the rate-limiting step of β-oxidation (1, 2). There are three isoforms of this enzyme: CPT1A (liver), CPT1B (muscle), and CPT1C (brain) (1, 2). Deficiency of CPT1A results in an autosomal recessive mitochondrial fatty acid oxidation disorder (3). Studies have shown that physiological high blood glucose and insulin levels inhibit CPT1B activity in human muscle and therefore divert long-chain fatty acids toward storage in human muscle as triglycerides (4). Furthermore, mice deficient in CPT1C show less food intake and reduced body weight (5). These findings suggest that CPT1 may play a role in metabolic syndromes.

  1. Wolfgang, M.J. et al. (2006) Proc Natl Acad Sci U S A 103, 7282-7.
  2. Bonnefont, J.P. et al. Mol Aspects Med 25, 495-520.
  3. Ogawa, E. et al. (2002) J Hum Genet 47, 342-7.
  4. Rasmussen, B.B. et al. (2002) J Clin Invest 110, 1687-93.
  5. Wolfgang, M.J. and Lane, M.D. (2011) FEBS J 278, 552-8.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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