Publication for Cpt1a and Hmgcs2

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Cpt1a	carnitine palmitoyltransferase 1a, liver	12894			[link]
mmu	Hmgcs2	3-hydroxy-3-methylglutaryl-Coenzyme A synthase 2	15360

Pubmed ID	Priority	Text
24209497	0.99	Cpt1a, involved in beta-oxidation) and 3-hydroxy-3-methylglutarate-CoA synthase 2 (Hmgcs2, involved in ketogenesis), and PXR is able to directly bind Foxa2 and impair its ability to upregulate these genes .
27708682	0.98	CPTI, HMGCS2, BDH1, and UCP2).
	0.98	CPT1, and HMGCS2 through identified cAMP response elements (CRE) in the promoter region of these genes.
	0.97	CPT1 (Carnitine Palmitoyltransferase 1) and HMGCS2 (3-Hydroxy-3-Methylglutaryl-CoA Synthase 2) expression, respectively).
	0.95	CPT1 encourages flux of fatty acids through beta-oxidation, resulting in the production of acetyl-CoA. HMGCS2 is then required for the flux of acetyl-CoA into ketogenesis.
	0.94	CPT1 or HMGCS2 increases hepatic beta-oxidation and ketone synthesis, while HMGCS2 knockdown completely eliminates the fasting induced rise in serum beta-OH butyrate.
	0.94	CPT1 and HMGCS2 mRNA expression parallel the decline in beta-OH butyrate, yet the decline in hepatic ketogenesis is more robust and rapid than explained by changes in gene expression alone (Fig. 7d and e).
	0.93	CPTI, HMGCS2, BDH1, and BDH2 mRNA expression changes in response to refeeding.
	0.91	CPT1 and HMGCS2 mRNA decreased further after 2 h of food provision (P > 0.05).
24458359	0.98	CPT1a) and 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) genes was reduced in livers from control mice fed an HFD but not in LKO mice (Fig. 6H).
	0.98	CPT1a and HMGCS2 (Fig. 7C) and ketone body production (Fig. 7D).
	0.97	CPT1a and HMGCS2 gene expression as well as ketone body production (Fig. 7C and D).
	0.93	CPT1a and HMGCS2 expressions are dependent on PGC-1alpha and MED1.
	0.83	CPT1a and HMGCS2 genes in liver from HFD-fed control mice but not in LKO mice.
	0.64	CPT1a, HMGCS2, and ketone body formation in cells with PGC-1alpha or MED1 knockdown (Fig. 7C and D).
26838474	0.98	Cpt1a and indirectly also Hmgcs2, thereby increasing betaOHB production, which then serves as a signal to make the animal anticipate feeding time (Fig. 5).
	0.98	Cpt1a and Hmgcs2 expression, rate-limiting enzymes for betaOHB synthesis.
	0.97	Cpt1a and indirectly affecting Hmgcs2 expression.
	0.96	Cpt1a) and hydroxy-methlglutharyl-CoA synthase 2 (Hmgcs2), two mitochondrial enzymes that show reduced mRNA expression levels at ZT4 in L Per2-/- mice under RF conditions (Fig. 3c) but not under AL conditions although the diurnal expression is still maintained with peaks at ZT16 and ZT10, respectively (Supplementary Fig. 4a,b).
	0.96	Cpt1a and Hmgcs2 in the liver of L Per2-/- mice, we observed reduced acetyl-CoA as well as betaOHB levels in the plasma of these and T Per2-/- animals under RF but not under AL conditions (Fig. 3d,e).
	0.94	Cpt1a catalyses the rate-limiting step of the transfer of long-chain fatty acids from the outer to the inner mitochondrial membrane where they are liberated as acyl-CoA. beta-oxidation results in acetyl-CoA that can either enter the Krebs cycle or be used by Hmgcs2 for the production of ketone bodies such as betaOHB.
29482168	0.98	Cpt1a and Hmgcs2 (Fig. 4E).
	0.98	Cpt1a and Hmgcs2 (Fig. 5E).
	0.98	Cpt1a, Acox and Hmgcs2 (Fig. 6O).
	0.98	Cpt1a, Acox1 and Hmgcs2) in the livers of fasted mice (Fig. 3), as well as the mice with STZ-induced type 1 diabetes (Fig. 4).
	0.96	Cpt1a) and 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 2 (Hmgcs2) (Fig. 3G), but showed no impacts on expression levels of other genes involved in liver metabolism, such as lipogenesis, fatty acid uptake and vLDL secretion (Fig. 3H).
22338096	0.98	CPT1a) and 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) are FGF21 responsive genes and are required for ketogenesis by FGF21.
	0.97	HMGCS2, CPT1a, ACADVL, ACSL1, ACO, and L-FABP) mRNA expressions in the liver.
	0.94	HMGCS2 and CPT1a) mRNA expressions in the liver of obese mice.
	0.62	HMGCS2, CPT1a, very long-chain acyl-CoA dehydrogenase (ACADVL), acyl-CoA synthase long-chain family member 1 (ACSL1), acyl-CoA oxidase (ACO), and liver fatty acid-binding protein (L-FABP).
27982131	0.98	liver, including those encoding acyl-CoA oxidase (Acox1), which is involved in the peroxisomal beta-oxidation of fatty acids; Cpt1a, which transports fatty acids across the outer mitochondrial membrane; and HMGCS2.
	0.98	Hmgcs2, Hmgcl, and Bdh1 were significantly downregulated in the liver of Ppara-/- mice compared with WT mice (Fig. 5b).
	0.96	Cpt1a but did not affect the expression of any other beta-oxidation and ketogenesis genes, such as Acox1, Hmgcs2, and Hmgcl (Fig. 5a).
	0.95	Cpt1a, and the ketogenesis genes Hmgcs2, Bdh1, Fgf21, and Creb3l3 were also significantly upregulated in KD-fed WT mice compared with that in MF-fed WT mice (Fig. 7c) but significantly downregulated in KD-fed Creb3l3-/- mice compared with that in KD-fed WT mice.
29031725	0.98	Cpt1a and Lcad) and ketogenesis (Hmgcs2) in the duodenum, jejunum, and liver on HFD compared to CD.
	0.96	Hmgcs2 (P < 0.0001), carnitine palmitoyltransferase 1a (Cpt1a; P < 0.0001) and long chain acyl CoA dehydrogenase (Lcad; P < 0.001) mRNA and a downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (Pgc1a) mRNA (P < 0.001) in the duodenum of all animals on HFD compared to those on CD (Figure 4A).
	0.95	Hmgcs2, Cpt1a, ATP synthase (ATPsyn), and Lcad on HFD vs CD, with no genotypes differences.
	0.94	Hmgcs2, Cpt1a, and Lcad, as well as a downregulation of Pgc1a was seen in the jejunum of all the HFD fed mice compared to CD fed mice, irrespective of genotype (P < 0.0001) (Figure 4B).
30879920	0.98	Cpt1a, Acox1, Pgc1alpha, Hmgcs2, etc.) and secretion (Mttp) were significantly reduced in the Arid1aLKO mice with HFD administration.
	0.98	Cpt1alpha, and Hmgcs2, in the primary mouse hepatocytes (Fig. 6a) and immortalized hepatocytes with SV40 expression (Supplementary Fig. 6).
	0.98	Cpt1a, Hmgcs2, Peci and Pgc1alpha in the mouse hepatocytes with Arid1a deletion (Fig. 6b).
	0.98	Cpt1a, and Hmgcs2 in Arid1a-/- hepatocytes (Fig. 6e and Supplementary information, Fig. 8).
22988513	0.98	Cpt1a (i.e., via provision of acetyl-CoA) and directly by the activity of the mitochondrial key regulatory enzyme 3-hydroxy-3-methylglutaryl-CoA synthase 2 (Hmgcs2), which is a Ppara target.
	0.94	Cpt1a did not differ due to CLA but the expression of the ketogenic regulator Hmgcs2 (CLA = 0.13 versus control = -0.16 and enzyme Bdh1 (CLA = 0.13 versus control = -0.20) was upregulated with CLA.
24944901	0.98	Cpt1a, no other PPARalpha-regulated genes were down regulated and both Pdk4 and Hmgcs2 were upregulated in liver tissue from LDKO mice compared to controls (Figure 3A).
	0.97	CPT1a was decreased in LKDO liver tissue compared to flox controls, while five other PPARalpha regulated genes were unaltered or upregulated (Pdk4 and Hmgcs2).
26541158	0.98	3-hydroxy-3-methylglutarate-CoA synthase 2 (Hmgcs2) and carnitine palmitoyltransferase 1a (Cpt1a) in the liver.
	0.98	Hmgcs2 and Cpt1a are downstream genes of PPARalpha.
26924429	0.98	HMGCS2) and carnitine palmitoyltransferase 1A (CPT1A) during fasting or after prolonged exercise.
	0.98	HMGCS2 and CPT1A.
28249286	0.98	CPT1a and HMGCS2, both transcriptionally regulated by PPARalpha, were increased in FGF21 transgenic mice suggesting a posttranslational effect by which FGF21 regulates ketogenesis.
	0.97	CPT1a and are rapidly oxidized to produce acetyl-CoA, which can be converted to ketone bodies including aceto-acetate, beta-hydroxybutyrate, and acetone by HMGCS2.
19865483	0.98	CPT1A (2.5-fold decrease from E11.5 to E14.5), HMGCS2, and ACOX1 as well as control hydrogen peroxide production in peroxisomal oxidation.
22394543	0.98	Cpt1a), and the 3-hydroxy-3-methylglutaryl-coenzyme A synthase 2 (Hmgcs2), with an 8-fold increase in mRNA levels, were identified.
22441164	0.98	CPT-1a), which has a pivotal role in the regulation of mitochondrial beta-oxidation, CYP4A10, a microsomal omega-oxidation enzyme, and mitochondrial HMG-CoA synthase (HMGCS2), which is a key control site of ketogenesis.
22698140	0.98	Cpt-1a, Acox1, Hmgcs2, Acot1, Acot2, Mcad, and Lcad, were significantly upregulated in the duodenum of the Mgat2-deficient mice (Figure 7).
23996730	0.98	Cpt1 and Hmgcs2, increased in Tgfbr2DeltaHEP mice, but not in WT mice (Figure 6B).
27346353	0.98	Cpt1 and Hmgcs2 were lower in in Tsc1LKO livers (Figure 5C).
27932985	0.98	Cpt1a and Hmgcs2 genes transactivation.
28082426	0.98	3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2), and the mitochondrial FA transporter (carnitine palmitoyltransferase 1a and carnitine O-acetyltransferase (CPT1A and CRAT)) (Fig. 3A, Table S2).
31916705	0.98	Hmgcs2, Slc25a20, Cpt1a, and other genes involved in beta-oxidation are indeed significantly upregulated by GW7647 in sham mice, unresponsive to GW7647 after CLP and downregulated by CLP (Fig 1D).
25383754	0.97	Cpt1a, Acat1, Acad1 and Hmgcs2) were increased 2-3 fold.
	0.93	Cpt1a, and/or Acat1, Acadm, Hmgcs2 as a mechanism of their lipid-lowering effects, thus, up-regulation of mitochondrial FA beta-oxidation could be a mechanism for lipid lowering effects of icariin.
	0.76	Cpt1a 2.8-fold, Acat1 2.5-fold, Acadm 2.4-fold, and Hmgcs2 2.9-fold.
30018405	0.97	Cpt1mtfl/fl mice after 20 weeks on CD and HFD revealed increased expression of genes involved in fatty acid uptake (Fat/cd36) (P < 0.001), fatty acid binding (Fabp1), FAO (Lcad), ketogenesis (Hmgcs2) (P < 0.0001) and malonyl-CoA synthesis (Acc2) (P < 0.0001) in all HFD-fed mice compared to CD-fed mice (Fig. 7, Sup Fig. 2 and Sup Table 1).
	0.96	HMGCS2 protein levels were also downregulated in the jejunal enterocytes (P < 0.05), but not in the duodenal enterocytes or in the liver, of HFD-fed iCPT1mt mice compared to Cpt1mtfl/fl controls (Sup Fig. 4).
	0.95	Cpt1mtfl/fl mainly showed an upregulation of all the genes tested in HFD-fed mice, compared to those fed CD (P < 0.05 for Hmgcs2, P < 0.01 for Fasn and P < 0.0001 for the other genes), except for Pgc1a and Pepck1, which showed no differences between the genotypes or diets (Sup Fig. 3).
22682225	0.97	Cpt1a and Hmgcs2 mRNA levels and blood ketone levels are decreased two- to three-fold relative to the livers of fasted mice (Fig. 2C-E).
	0.96	Cpt1a and Hmgcs2, two genes required for ketone synthesis, are suppressed, and blood ketone levels fall.
27301791	0.97	Hmgcs2, Hadh, Acadm, and Acadl were similar between WT and Creb3l3-/- livers, except Cpt1a which appeared to be regulated by both CREBH and PPARalpha (Fig. 2C).
	0.97	Hmgcs2 and Cpt1a in Creb3l3-/- mice (Supplementary Fig. 4B,C), which might have helped to improve the hepatic steatosis.
21295138	0.97	Cpt1a and Hmgcs2 in wild-type, but not in PXR knockout mice.
28337174	0.97	Cpt1a and Hmgcs2 expression, two rate-limiting enzymes for beta-hydroxybutyrate synthesis.
32121253	0.97	HMGCS2, CPT1A, PPARA, and PPARGC1A, suggesting that these beneficial effects of genistein on NAFLD may occur by virtue of its ability to be an ESRRA agonist.
27038664	0.96	Cpt1a and Hmgcs2 can lead to increased ketone bodies synthesis.
	0.73	Cpt1a and Hmgcs2 induction at ZT4 in the FA protocol is lost in LPer2-/- mice.
23226270	0.96	HMGCS2, HSD17B10, UCP3, EHHADH, CPT1A, DCTN6, PIGL, SULT1A1, SLC27A2, MLYCD and ACOT1 were increased; LPCAT1 and CD74 were repressed.
26846427	0.96	CPT I and II were increased by TTP treatment (Fig. 4c, d), as was the HMG-CoA synthase activity (Fig. 4e).
26931208	0.96	CPT-1a) and hydroxymethyl glutaryl-CoA synthase-2 (HMGCS2) are rate-limiting enzymes in ketogenesis.
30181250	0.96	Hmgcs2, Cpt1a) and TG biosynthesis (Dgat2) was downregulated compared to control mice on a HFD (Fig. 7J and K), suggesting decreased FA intracellular levels; this, along with the results of LD fluorescence imaging, which did not show modifications of intracellular LD in comparison to CD, supports the idea of decreased dietary fat absorption by enterocytes in L. paracasei mice.
23343123	0.95	Cpt1a and Hmgcs2 were down-regulated when compared with IVF group (Figure 9B).
	0.90	Cpt1a and Hmgcs2 were higher in old NC liver than those in adult liver.
27576532	0.94	Cpt1a and Hmgcs2, which are rate-limiting enzymes for FA oxidation and ketogenesis, respectively (Supplementary Figure S7A).
27445980	0.92	CPT1a, ACADS, ACADM, ACADL, ACADVL, HADH), fatty acid import (CD36), gluconeogenesis (G6PC, PCK1), and ketone body production (HMGCS2, BDH1) were measured.
	0.56	CPT1a, ACADS, ACADM, ACADL, ACADVL, HADH), fatty acid import (CD36), gluconeogenesis (G6PC, PCK1), and ketone body production (HMGCS2, BDH1) were measured.
30405056	0.91	Cpt1, Ppara, Hmgcs2, Acc2).
24184811	0.88	CPT1alpha and MCAD) in the fasted SIRT1 LKO mice were normalized by reconstitution of FGF21, and the impairment of the transcription of ketogenic genes (HMGCS2 and HMGCL) in SIRT1 LKO mice was also restored.
27624175	0.86	Cpt1a), acyl-Coenzyme A dehydrogenase, medium chain (Acadm) and 3-hydroxy-3-methylglutaryl-CoA synthase 2 (mitochondrial) (Hmgcs2) and fibroblast growth factor 21 (Fgf21).
27462273	0.69	CPT-1a, MCAD, LCAD, HMGCS2, PPARalpha, and PPARgamma were not significantly changed in the livers of either Lrpprc transgenic mice or Lrpprc knockdown mice (data not shown).
23539345	0.68	CPT1A, outer mitochondrial membrane, rate limiting in mitochondrial LCFA beta-oxidation); carnitine palmitoyl transferase-2 (CPT2, inner mitochondrial membrane); 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase.