Publication for Fabp4 and Cd36

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Fabp4	fatty acid binding protein 4, adipocyte	11770			[link]
mmu	Cd36	CD36 molecule	12491

Pubmed ID	Priority	Text
23473036	0.99	aP2, an adipocyte marker highly induced in both white and brown fat differentiation (Fig. 1B).
	0.98	aP2-TLE3 Tg mice showed histological features of white fat and impaired adaptive thermogenesis, and these changes correlated with an impaired capacity to induce thermogenic gene expression during cold challenge.
22142492	0.98	fat accumulation in the aP2Spry-KO was associated with increased expression of adipogenic markers PPAR-gamma and FABP4 (Fig. 1D).
	0.98	FABP4 (Fig. 1H) both on a normal and a high fat diet.
	0.97	aP2-Spry1 mice, body fat was 35% (p<0.05) lower compared to the single transgenic controls on a high fat diet (Fig. 1F) indicating that mice expressing Spry1 in the fat tissue were protected from excessive fat accumulation.
	0.97	fat tissue showed significantly lower vessel area (p<0.05) in aP2-Spry1 mice compared to the controls on a high fat diet (Fig. 4E), indicating decrease in angiogenesis in the fat tissue.
	0.94	aP2 promoter (aP2-Spry1) suppressed fat development and improved bone health.
	0.93	aP2-Spry1 transgenics after high fat feeding (Fig. 4D).
	0.90	fat diet had markedly elevated insulin plasma levels (5.08ng/mul) that were completely suppressed (70% decrease, p<0.005) in the aP2-Spry1 mice (1.45ng/mul) fed a high fat diet (Fig. 3E).
	0.80	fat diet occurred in the aP2-Spry1 transgenics compared to single transgenics (Fig. 2C).
	0.80	fat diet model, aP2Spry-KO gained more weight and accumulated more body fat compared aP2-Spry1 transgenics.
	0.74	aP2-Spry1 transgenics, the control mice on the high fat diet alone developed glucose intolerance (p<0.05, Fig. 3B).
	0.72	fat diet-fed aP2Spry-KO, their respective controls, and the controls for the aP2-Spry1, all of which had elevated serum insulin, while in the aP2-Spry1 transgenic mice there was no relationship between insulin levels and bone mineral density.
	0.63	aP2-Spry1 transgenics (8.11ng/mul) on a high fat diet (p<0.005, Fig. 3F).
29383825	0.98	fat gene targets such as Agt, Retn/Resistin, Slc2a4/Glut4, Cfd/Adiposin, Adipoq/Adiponectin, and Fabp4/aP2 (Figure 6a,b), while downregulation of PPARgamma in aging mice affects specifically brown fat genes such as Dio2, Pparalpha, Prdm16, and Ucp1 (Figure 6a,c).
	0.95	fat tissue generated by crossing PPARgamma-LoxP mice with either aP2- or adiponectin-Cre mice revealed impaired fat development and reduced fat mass (He et al., 2003; Jones et al., 2005; Wang et al., 2013).
	0.95	fat during aging is associated with increased adiposity are surprising given that they are sharply in contrast with the lipodystrophic phenotype and the impairment in adipose tissue expansion previously reported in aP2- and adiponectin-driven fat-specific PPARgamma KO mice (He et al., 2003; Jones et al., 2005; Wang et al., 2013) and in young mice with decreased PPARgamma levels selectively in iWAT (Figure 5).
	0.94	fat tissue reported in published aP2- and adiponectin-driven knockout models and in our study of young mice may be due to the differences in the spatiotemporal conditions of PPARgamma ablation, given that PPARgamma deletion was previously achieved in every fat depot during development and in adult mice (He et al., 2003; Jones et al., 2005; Wang et al., 2013), while here PPARgamma levels are selectively reduced in subcutaneous fat tissue in mid-aged mice.
	0.90	aP2 and Ucp1 occurring in aging, given that those genes represent markers of white and brown fat programs, respectively.
30275401	0.98	aP2-Cre/Ghsrf/f mice (15-17 months) showed more pronounced body weight and body fat decreases compared with the age-matched controls (Figure 3B), underscoring the importance of GHS-R expression in tissues where aP2 gene is expressed during aging.
	0.96	aP2-Cre/Ghsrf/f mice of both age groups, with greater RMR increase during day time resting state in young mice (Figure 3K,L), indicating that the aP2-Cre/Ghsrf/f mice favor carbohydrates as a fuel substrate (as fat reserves in these mice were likely limited due to their leanness).
	0.93	aP2-Cre/Ghsrf/f mice indicates that the mice favor carbohydrate as a fuel substrate; the reduced fat reserves in the lean aP2-Cre/Ghsrf/f mice may obligate them to utilize carbohydrates instead of fat.
	0.77	aP2-Cre-Mediated GHS-R Knockdown Improves Thermogenesis in Brown Fat, and Enhances Glucose Uptake and Lipolysis in White Fat
	0.52	aP2-Cre/Ghsrf/f mice had normal body weight but reduced fat; old mice showed pronounced reductions of both body weight and body fat.
21480322	0.98	fat diet in MED1fl/fl mice was not associated with induction of PPARgamma target gene aP2 but this protein was detected in PPARgamma-induced hepatic adiposis (Fig. 1C).
	0.98	fat differentiation gene markers, such as aP2 were noted in mice expressing MED1 but not in MED1 null livers (Fig. 4A).
	0.97	fat diet feeding as evidenced by the failure of induction of aP2 expression in such livers and yet high-fat diet induced steatosis appears to be dependent on MED1.
21695273	0.98	FAT/CD36, aP2, LPL), and lipolysis (MGL) (Figure 5).
	0.96	fat mass development, body weight gain, cholesterolemia, insulinoresistance index, and expression of several genes that mediate differentiation and/or fatty acid uptake (PPARgamma, aP2, FAT/CD36, LPL, FIAF), fatty acid oxidation (CPT-1, ACO), short-chain fatty acid response (GPR43), and inflammation (IL6, F4/80) in the subcutaneous adipose tissue.
	0.68	fat mass development) to a lower fatty acid synthesis (FAS expression and activity) or fatty acid uptake in white adipose tissue (downregulation of lipoprotein lipase, fatty acid translocase/CD36 and fatty acid binding protein (aP2)), we may not exclude an effect of AX on lipid absorption through either its intrinsic capacity of fat binding or modulation of pancreatic lipase activity.
26085100	0.98	fat accumulation in CBA mice was paralleled by an increase in the hepatic expression of Ppargamma and the Ppargamma target genes Cd36, Fabp4, and Mogat1, i.e. genes involved in FA uptake and TG synthesis.
	0.97	Fabp4) and monoacylglycerol acetyltransferase (Mogat1), which enhances hepatic fat accumulation by stimulating incorporation of FAs into TG via a FA biosynthesis-independent pathway, was also increased in livers of CBA mice at 3w of SRD (Fig. 5, C and D), whereas hepatic Mogat1 and Fabp4 expression was unaltered in 3w SRD B6 mice (Fig. 5E).
	0.75	fat accumulation, and dysglycemia in B6 mice, and hepatic expression of Ppargamma, Cd36, Fabp4, and Mogat1 was not increased SRD B6 mice.
27448965	0.98	fat pad, gene expression of the mature adipocyte markers, Fabp4 and Adipoq (adiponectin), in the mammary fat pads of knock-out mice were reduced compared to wild-type mice.
	0.91	fat pads for the preadipocyte and mature adipocyte markers, pref-1 (Dlk1) and Fabp4, as well as the adipogenesis marker, Pparg, was similar despite clear differences in fat pad weights.
	0.67	fatty acid binding protein-4 (Fabp4) and adiponectin (Adipoq) as markers of fully mature adipocytes, pref-1 (Dlk1) as a preadipocyte marker, and peroxisome proliferator activated receptor gamma (Pparg) as an indicator of adipogenesis, we found no overall difference in the omental fat pads obtained from wild-type and BP3KO mice on either chow or HFD (Figure 3a).
24120574	0.98	CD36), fatty acid binding protein (FABP), and members of the fatty acid transport protein/very long-chain acyl-CoA synthetase (FATP/ACSVL) family.
	0.96	FAT/CD36, FABP is a cytosolic non-enzymatic protein of low molecular weight.
25008181	0.98	fat and mitochondrial marker genes such as Ucp1, Cebpbeta, Cidea, Pparalpha, Cox4, Cox7, and Cox8, and, to a lesser extent, common adipocyte marker genes such as Ppargamma, Fabp4, and Glut4 (Fig. 2A).
	0.96	fat marker mRNAs, such as Ucp1, Pgc1alpha, Cidea, and Pparalpha, and mitochondrial markers, such as Cox 7 and Cox8, but not the common adipogenic markers, including Ppargamma, Fabp4, and AdipoQ (Fig. 6C).
26525534	0.98	fat-selective genes, such as Cidea, Cited1, Cox8b, and Elov3, without affecting the expression of Fabp4 (Figure 2D).
	0.97	fat-selective genes, including Pgc1alpha, Cidea, Elov3, and Cited1, without affecting Fabp4 expression (Figures 3G and 3H).
26973598	0.98	fat driven by the promoter of the fatty acid binding protein, aP2, demonstrated that PRDM16 is also involved in the development of beige adipocytes in subcutaneous fat and that it induces thermogenic genes, such as Ucp1, Cidea, Cox8b, and Elovl3, in these cells.
	0.98	fat depots of mice with overexpression of Zfp516 driven by the -5.4 aP2 promoter kept at room temperatures showed increased clusters of cells containing multilocular lipid droplets, elevated UCP1 staining, consistent with increased amounts of beige fat cells.
30186237	0.98	aP2 and adiponectin, as well as brown fat-selective gene program, including Ucp1 and Cidea.
	0.96	aP2- and adiponectin-driven loss of PPARgamma in adipose tissues consistently lead to impaired adipocyte differentiation and reduced fat weights or lipodystrophy, though different animal models show improved or worsen insulin sensitivity depend on the extent of PPARgamma deficiency.
32169116	0.98	fat cells dramatically reduced browning-specific proteins (FABP4, PGC1alpha, PPARgamma, PRDM16 and UCP1), while increasing white-fat-related proteins (ACC, PAST1, LEPTIN, and FASN).
	0.96	fat marker genes showed that Acc, Asc1, Past1, Leptin, Fasn, and Scd expression decreased, while Cidea, Fabp4, Pgc1alpha, Ppargamma, Prdm16, and Ucp1were upregulated (Fig. 4c).
18719582	0.98	aP2 and adiponectin as well as brown fat cell-specific markers, UCP1 and CIDEA in a ligand-dependent manner (Fig. S5b).
25128964	0.98	fat cells, including peroxisome proliferator-activated receptor gamma (PPARgamma), CCAAT/enhancer binding protein (C/EBP, which includes C/EBP alpha, C/EBP beta, and C/EBP delta), adipocyte lipid binding protein (ALBP), and adipocyte determination and differentiation factor 1 (ADD1).
28186086	0.98	FABP4 and brown fat genes PRDM16 and Cox7a1 were also increased in shHOXC10-expressing cells (Figure 1k).
29626089	0.98	A-FABP is preferentially expressed in the CD11c-CD36+ subset, suggesting unique roles of individual FABPs in macrophages.
31847305	0.98	Ap2 (adipocyte protein 2 or Fabp4, Fatty acid binding protein) (Figure 5C), which is a lipid transport protein in adipocytes and is involved in brown and white fat cell differentiation, cholesterol homeostasis and positive regulation of inflammatory response, implying a possible role of increased expression of Ap2 underlying the increase of WAT weight and the elevation of serum pro-inflammatory cytokines in mice on HFD.
31964951	0.98	Fat accumulation in the liver is generally caused by increased lipotoxicity resulting from high levels of free fatty acids, free cholesterol, and lipid metabolites, and these, in turn, are regulated by lipogenic genes, such as PPARgamma, C/EBPalpha, FAS, and FABP4.
28128199	0.97	A-FABP KO mice exhibited a similar cold-induced expression of UCP-1 and thermogenic genes in the subcutaneous fat as that in the WT littermates (Supplementary Fig. 3).
	0.96	A-FABP knockout mice have reduced thermogenesis and whole-body energy expenditure after cold stress or after feeding a high-fat diet, which can be reversed by infusion of recombinant A-FABP.
	0.96	A-FABP enhances thermogenesis by promoting the conversion of thyroxine T4 to the bioactive form, T3, in brown adipocytes, and by enhancing fatty acid uptake of brown fat.
	0.94	A-FABP knockout (KO) mice are protected against high-fat diet (HFD)-induced metabolic dysfunction but exhibit increased adiposity comparing with their wild-type (WT) littermates.
	0.90	A-FABP KO mice exhibited a significantly less fat loss compared with WT controls after cold exposure for 8 h (Fig. 1g).
	0.78	fat mass in HFD-fed A-FABP KO mice was 1.6-folds higher than the WT littermates (Supplementary Fig. 1b).
26260145	0.97	Fabp4-5-/- mice were protected from high-fat diet-induced hepatic steatosis, with increased muscle AMP kinase activity and reduced hepatic expression of the key fatty acid metabolism enzyme Scd1 (encoding acyl-CoA desaturase 1), which could in part underlie the reduced lipid accumulation in this model.
	0.89	FABP4 is recruited to multivesicular bodies, and secreted in vesicles that have exosome markers including CD36, calveolin, lactadherin (also known as milk fat globule factor 8 protein), TSG101, and ALIX, as shown on the right.
	0.88	Fabp4-Fabp5 double mutant (Fabp4-5-/-) mice were protected from high fat diet-induced weight gain and had a more dramatic improvement in insulin sensitivity and glucose homeostasis than either of the single FABP4 or FABP5 deficiency models.
	0.78	FABP4 inhibitor also significantly limited atherosclerotic lesion formation and improved endothelial function in ApoE-/- mice, and reduced acute liver injury and high fat high cholesterol diet-induced non-alcoholic fatty liver disease.
23525438	0.97	FABP4) and fatty acid translocase (FAT)/CD36 in capillary endothelial cells (ECs) to promote FA transport into the heart.
	0.95	FABP4 and FAT/CD36.
	0.91	Fabp4 (also called aP2) has long been considered to be an adipocyte- and macrophage-specific gene, and its promoter has been widely used to generate "fat-specific" expression and disruption in transgenic mouse studies.
26310911	0.97	FAT expression level was decreased in respond to FABP4 overexpression.
	0.97	FABP4 increased the expression of FATP1 and reduced FAT expression, indicating that FABP4 enhanced the fatty acids transportation.
	0.84	FABP4 also reduced the levels of FAT, CPT-1 and AOX1, and decreased fatty acid mobilization and oxygenolysis (p < 0.05).
30158592	0.97	aP2-Prdm4) protect from obesity and fat expansion in HFD feeding.
	0.97	aP2 promoter can direct transgenic expression of Prdm4 in fat tissue.
	0.96	fat-specific aP2 gene promoter could direct Prdm4 expression in adipose tissues.
29187824	0.97	FABP4) reduced the potency of HFD for the increase in PGC-1alpha in BAT, while FAT/CD36 and FATP1 gene expression was upregulated to a similar extent as in a wild type mice (Shu et al.,).
28824548	0.96	fat volume in proximal tibia the expression of Fabp4 and Adip was significantly increased, whereas expression of Ucp1, Prdm16, Tbx1, and Dio2 was decreased after adjustment to Fabp4 expression.
	0.93	Fabp4 and Adiponectin expression and relative decrease in beige fat gene markers.
21723971	0.94	FABP4/aP2 is not changed in WAT and BAT of C57BL6 and Avy/a mice indicating that in adult animals rosiglitazone did not induce de novo adipogenesis in these fat depots.
28915325	0.94	fat mass in aP2-UCP1 transgenic mice.
26625958	0.93	fat genes Fabp4 (also known as aP2) and Adipoq (also known as Adiponectin) and the master adipogenic regulator Ppargamma were devoid of this mark
	0.91	fat genes Fabp4, Adipoq and Ppargamma (Figure 3B), entirely consistent with our observation that these common fat genes did not possess H3K27me3.
28242620	0.90	fat-specific knockout of Rheb had no significant effects on the levels of FABP4 and perilipin (Fig. 6E), indicating that Rheb deficiency had no major effect on adipogenesis.
25055851	0.87	fat PPARgamma and FABP4 expression in HFD fed older mice
21569430	0.85	fat metabolism (Glut4, LPL, FAS, ACC1 and CPT-1beta) and of adipocyte differentiation markers (PPARgamma, C/EBPalpha, PPARalpha, aP2 and adiponectin) were determined in maturing C3H10 T1/2 cells.
25578880	0.85	aP2-Zfp516 transgenic mice to high-fat diet (HFD) to test whether the increase in thermogenesis results in protection from diet-induced obesity.
23968980	0.83	FABP4 and FAT/CD36 by measuring the uptake of 14C-palmitic acid in cultured capillary EC in the presence or absence of siRNA for FABP4 or FAT/CD36.
	0.64	FAT/CD36 alone or in combination with FABP4/5 on transendothelial FA transport are now in progress.
22666778	0.79	ALBP genes in the periepididymal fat pad, both markers of triglyceride hydrolysis, did not change after physical training.