2.3.1.21: carnitine O-palmitoyltransferase

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For detailed information about carnitine O-palmitoyltransferase, go to the full flat file.

Reaction

Synonyms

acylcarnitine transferase, carnitine O-palmitoyltransferase, carnitine O-palmitoyltransferase I, carnitine palmitoyl transferase 1, carnitine palmitoyl transferase 1A, carnitine palmitoyl transferase-1A, carnitine palmitoyl transferase-I, carnitine palmitoyl-transferase-1c, carnitine palmitoyltransferae 1A, carnitine palmitoyltransferase, carnitine palmitoyltransferase 1, carnitine palmitoyltransferase 1A, carnitine palmitoyltransferase 1B, carnitine palmitoyltransferase 2, carnitine palmitoyltransferase I, carnitine palmitoyltransferase IA, carnitine palmitoyltransferase II, carnitine palmitoyltransferase-1, carnitine palmitoyltransferase-1c, carnitine palmitoyltransferase-A, carnitine palmitoyltransferase-I, carnitine palmitoyltransferases 2, CPT, CPT I, CPT IA, CPT Ialpha1a, CPT Ialpha1b, CPT Ialpha2a, CPT Ibeta, CPT II, CPT-1, CPT-2, CPT-A, CPT-B, CPT-Ialpha, CPT-IL, CPT1, CPT1-A, CPT1-B, CPT1-C, CPT1A, CPT1B, CPT1c, CPT2, CPTi, CPTI beta, CPTII, CPTo, L-carnitine palmitoyltransferase, L-CPT 1, L-CPT1, M-CPT 1, M-CPTI, muscle carnitine palmitoyltransferase I, palmitoylcarnitine transferase, palmitoyltransferase, carnitine

ECTree

     2 Transferases

         2.3 Acyltransferases

             2.3.1 Transferring groups other than aminoacyl groups

                2.3.1.21 carnitine O-palmitoyltransferase

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Results	in table
29	Activating Compound
4324	AA Sequence
14	Application
1	CAS Registry Number
42	Cloned(Commentary)
1	Crystallization (Commentary)
3083	Disease/ Diagnostics
7	Expression
14	General Information
7	General Stability
63	IC50 Value
181	Inhibitors
22	Ki Value [mM]
200	KM Value [mM]
171	Localization
4	Metals/Ions
43	Molecular Weight [Da]
132	Natural Substrates/ Products (Substrates)
241	Organism
4	Pathway
13	PDB ID
33	pH Optimum
3	pH Range
1	pH Stability
2	pI Value
4	Posttranslational Modification
108	Protein Variants
28	Purification (Commentary)
10	Reaction
11	Reaction Type
169	Reference
3	Renatured (Commentary)
311	Source Tissue
95	Specific Activity [micromol/min/mg]
3	Storage Stability
293	Substrates and Products (Substrate)
28	Subunits
161	Synonyms
1	Systematic Name
29	Temperature Optimum [°C]
1	Temperature Stability [°C]

Application

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Application on EC 2.3.1.21 - carnitine O-palmitoyltransferase

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APPLICATION

ORGANISM

UNIPROT

COMMENTARY

LITERATURE

medicine

11 entries

pharmacology

2 entries

synthesis

Rattus norvegicus

Q63704

comparison of COS7 cell and yeast expression of isoform CPT1b. The mitochondrial fraction prepared from yeast cells expressing CPT1b shows 25% higher CPT1 activity than that obtained from COS7 cells. The expression level of CPT1b in the former is 3.8 times lower than that in the latter; and thus the specific activity of CPT1b expressed in yeast cells is estimated to be approximately five times higher than that expressed in COS7 cells

720974

medicine

Homo sapiens

P23786, P50416

treatment of CPT2 deficiency is based upon avoidance of fasting and/or exercise, a low fat diet enriched with medium chain triglycerides and carnitine

659899

medicine

Homo sapiens

-

enzyme inhibitors are used to shift the heart's reliance away from fatty acid oxidation to glucose as energy source to increase cardiac efficiency, overview

673216

medicine

Rattus norvegicus

-

hypertrophied myocardium displays a significant shift in the relative isoform distribution of CPT1 isoforms, L-CPT1 expression dramatically increases relative to M-CPT1 expression

686125

medicine

Rattus norvegicus

-

the data suggest that consuming a high-fat diet or inhibiting CPT-I do not result in cardiac hypertrophy or cardiac dysfunction in normal rats

686180

medicine

Homo sapiens

Q8TCG5

isoform CPT1C expression is frequently up-regulated in human lung tumors. Tumor cells constitutively expressing CPT1C show increased fatty acid oxidation, ATP production, and resistance to glucose deprivation or hypoxia. Conversely, cancer cells lacking CPT1C produce less ATP and are more sensitive to metabolic stress. CPT1Cdepletion via siRNA suppresses xenograft tumor growth and metformin responsiveness in vivo. CPT1C can be induced by hypoxia or glucose deprivation and is regulated by AMPKalpha

719554

medicine

Homo sapiens

P50416

overexpression of the enzyme correlates with a poor overall survival of ovarian cancer patients. CPT1A is a prognostic biomarker and rational target for therapeutic intervention of cancer

736916

medicine

Homo sapiens

P23786, Q8TCG5, Q92523

compared to isoforms CPT1A, CPT1B and CPT2, isoform CPT1C exerts the most significant effect on mitochondrial dysfunction-associated tumor cellular senescence among the members of the CPT family

757297

medicine

Homo sapiens

P23786

problems in CPT2 deficiency originating from the S113L mutation might be at least partially related to an impaired thermal stability of the protein

757810

medicine

Homo sapiens

P23786

triple-negative breast cancer cells resistant to glutaminase inhibitor CB-839 have increased CPT2 protein and CPT1 activity levels. CB-839-resistant triple-negative breast cancer cells mobilize more fatty acids into mitochondria for oxidation

757235

medicine

Homo sapiens

P23786

triple-negative breast cancer cells resistant to glutaminase inhibitor CB-839 have increased CPT2 protein and CPT1 activity levels. CB-839-resistant triple-negative breast cancer cells mobilize more fatty acids into mitochondria for oxidation. Inhibition of both glutaminase and CPT1 decreases cell proliferation and migration of CB-839-resistant cells compared with single inhibition of each enzyme

757235

medicine

Homo sapiens

P50416

when fatty acid oxidation is reduced approximately 90% by pharmacological inhibition of carnitine palmitoyltransferase I CPT1 with low concentrations of etomoxir, the proliferation rate of various cancer cells is unaffected. High concentrations of etomoxir (200 microM) have an off-target effect of inhibiting complex I of the electron transport chain. When fatty acid oxidation is reduced further by genetic knockdown of CPT1, the proliferation rate of these same cells decreases nearly 2fold and cannot be restored by acetate or octanoic acid supplementation. CPT1 knockdowns have altered mitochondrial morphology and impaired mitochondrial coupling, whereas cells in which CPT1 has been approximately 90% inhibited by etomoxir do not. Mitochondria isolated from CPT1 knockdowns show depleted concentrations of complex structural and signaling lipids. Expression of a catalytically dead CPT1 in CPT1 knockdowns does not restore mitochondrial coupling

758102

pharmacology

Rattus norvegicus

-

CPT I, model enzyme for studies of fatty acid-induced apoptosis in cancer therapy

486589

pharmacology

Rattus norvegicus

P18886, P32198

the data represent proof in principle that a pharmacological agent that stimulates hepatic fatty acid oxidation, perhaps acting on carnitine palmitoyltransferase 1a, could provide a novel approach to treatment of nonalcoholic fatty liver disease

684341