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CPT2Carnitine Palmitoyl Transferase 2
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A second graft biopsy showed an acute mixed rejection (t2 i2 ti2 g2 cpt2) without TMA lesions (Figure 3(b)).
These same genes (Gpx3, Echs1, and Cpt2) are regulated by AMP kinase (AMPK) and PPAR[alpha] [27-29], which are also downregulated in TauTKO muscle.
adipose [??]PPAR[gamma] INSIG1 Insulin induced gene 1 MAC-T [??]PPAR[gamma] SCD Stearoyl-CoA desaturase MDBK [??]PPAR[alpha] (delta-9-desaturase) SREBF1 Sterol regulatory element MAC-T [??]PPAR[gamma] binding factor 1 MDBK [??]PPAR[alpha] Fatty acid oxidation ACADVL Acyl-CoA dehydrogenase, MDBK [??]PPAR[alpha] very long chain Liver [??]PPAR[alpha] ACOX1 Acyl-coenzyme A oxidase 1 MDBK [??]PPAR[alpha] Liver ** [??]PPAR[alpha] CPT1A Carnitine MDBK [??]PPAR[alpha] palmitoyltransferase Liver ** [??]PPAR[alpha] 1A (liver) CPT2 Carnitine PAEC [??]PPAR[gamma] palmitoyltransferase 2 CRAT Carnitine O- PAEC [??]PPAR[gamma] acetyltransferase CYP4A11 Cytochrome P450, family Liver [??]PPAR[alpha] 4, subfam.
Deficiencies of both CPT1 and CPT2 have been described and leave patients unable to derive energy from fatty acid oxidation.
Normal muscle CPT1 and CPT2 activities in hepatic presentation with CPT1 deficiency in fibroblasts.
Lack of hepatic PPAR[alpha] prevented it from nuclear translocation and then reduced the transcriptional activation of multiple genes involved in lipid metabolism, including carnitine palmitoyltransferase 2 (CPT2) and acyl-CoA binding domain containing 3 (ACBD3) (Figures 4(a), 4(b), and 4(c)).
The expression levels of 10 genes: retinoid X receptor alpha (RXRA), peroxisome proliferator-activated receptor gamma (PPARG), phospholipid transfer protein (PLTP), stearoylCoA desaturase (SCD), nuclear receptor subfamily 1 group H member 3 (NR1H3), fatty acid binding protein 3 (FABP3), carnitine palmitoyltransferase II (CPT2), acyl-Coenzyme A dehydrogenase long chain (ACADL), acyl-Coenzyme A oxidase 2 branched chain (ACOX2), and fatty acid binding protein 4 (FABP4), showed significant differences in gene expression between the low- and high-marbled groups (p < 0.05) (Table 2).
Ligand activation of PPAR[alpha] induces transcription of many proteins and enzymes involved in fatty acid uptake (membrane fatty acid transporters (FATPs), liver fatty acid binding protein (LFABP)), intracellular fatty acid transport (L-FABP), and fatty acid oxidation (L-FABP, CPT1A, CPT2, ACOX1) (review in [17, 27-29]).
At least 15 mutations in CPT2 are associated with the adult and infantile disorders (7-9).
In the process of mitochondrial [beta]-oxidation, long-chain-fatty-acid-CoA ligase, carnitine palmitoyltransferase I (CPT1), and carnitine palmitoyltransferase 2 (CPT2) play critical roles in the transfer of free fatty acids into the mitochondrial matrix, with resultant production of fatty acyl-CoA which is the initial substrate for [beta]-oxidation [6, 7].
In addition, 5/7 PPAR signaling genes (solute carrier family 27 (fatty acid transporter), member 6 (SLC27A6), carnitine palmitoyltransferase 2 (CPT2), SORBS1, phosphoenolpyruvate carboxykinase 1 (PCK1) and SLC27A1) and 4 adipocytokine signaling pathway genes (OB, PRKAG2, PCK1, and PPARGC1A) were upregulated in the H group, which are significant to the development of marbling.