Research Article

Molecular Characterization of the Tumor Suppressor Candidate 5 Gene: Regulation by PPAR and Identification of TUSC5 Coding Variants in Lean and Obese Humans

Table 1

Relative transcript abundances of PPAR target genes in HepG2 cells experimentally-expressing different PPAR isoforms, in the presence or absence of isoform-selective agonists.

PPAR isoform expressedPPAR agonist treatment
+Treatment effect
*
**
***

PPAR
 Tusc5, adiponectin (adipoQ), leptin (ob)n.d.n.d.
 PEPCK1 (Pck1) **
 ACOX1 ***
 CPT1b *
 ADFP ***

PPAR
 Tusc5, adiponectin (adipoQ), leptin (ob)n.d.n.d.
 PEPCK1 (Pck1) **
 ACOX1 ***
 CPT1b *
 ADFP ***

PPAR 1
 Tusc5, adiponectin (adipoQ), leptin (ob)n.d.n.d.
 PEPCK1 (Pck1) **
 ACOX1 **
 CPT1b
 ADFP ***

PPAR 2
 Tusc5, adiponectin (adipoQ), leptin (ob)n.d.n.d.
 PEPCK1 (Pck1) *
 ACOX1 *
 CPT1b
 ADFP

Using HepG2 Tet-off human PPAR isoform-specific overexpressing stable cell lines [14] (see Methods); /treatment.
PPAR isoform-selective agonists used for PPAR , , 1, 2 experiments were, respectively, GW7647 (1  M), GW501516 (100 nM), and rosiglitazone (1  M); cells were treated for 24 hours prior to mRNA collection.
n.d.: not detectable (note that Tusc5, adiponectin, and leptin transcripts were readily detected in a human WAT sample run in parallel).