Publication for Creb3l3 and Apob

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Creb3l3	cAMP responsive element binding protein 3-like 3	208677			[link]
mmu	Apob	apolipoprotein B	238055

Pubmed ID	Priority	Text
28455595	0.98	CREBH expression, which in turn enhanced hepatic apoB biosynthesis and VLDL secretion.
	0.98	CREBH as the first transcription factor that regulates apoB expression on the transcriptional level and the subsequent VLDL biosynthesis in response to metabolic inflammation.
	0.98	apoB mRNA in the fetal livers of CREBH-depleted mice (CREBH-null) as compared to their wildtype (WT) littermates.
	0.98	CREBH is a transcription factor that positively regulates mRNA and protein expression of apoB and contributes to the metabolic inflammation-induced VLDL overproduction in chronic metabolic disorders.
	0.98	CREBH to upregulate expression of apoB, which subsequently leads to the abnormal lipoprotein biogenesis that contributes to the hyperlipoproteinemia associated with metabolic syndrome.
	0.98	apoB mRNA in mouse fetal liver was previously reported to be significantly reduced upon depletion of CREBH.
	0.98	CREBH positively regulates apoB mRNA and protein expression.
	0.98	apoB100 and B48 in the WT mice but not the CREBH-null mice, indicated by the significantly lessened secretion of both apoB100 and B48 (Figure 2C).
	0.98	CREBH activity inhibits apoB mRNA expression and compromises the assembly and secretion of VLDL and chylomicrons in the fasting state and in response to acute fat challenge.
	0.98	CREBH by TNFalpha was accompanied by a significant upregulation of apoB mRNA and protein in the WT mice (Figures C and D).
	0.98	apoB expression in CREBH-null mice (Figures 4C and D), suggesting that CREBH is integral in mediating the regulatory effect of TNFalpha on apoB mRNA transcription.
	0.98	CREBH compromises hepatic apoB mRNA and protein expression, leading to defective VLDL assembly and secretion in response to pro-inflammatory cytokine TNFalpha treatment.
	0.98	CREBH showed that LPS treatment induced CREBH mRNA and protein expression, which was associated with a significant upregulation of apoB mRNA in WT mice (Figures 5B and C).
	0.98	CREBH-null mice, apoB mRNA expression was not induced by LPS (Figure 5C), indicating that an intact CREBH is essential for hepatic apoB mRNA expression in response to LPS treatment.
	0.98	apoB biosynthesis and the subsequent defective VLDL-apoB secretion in CREBH-null mice were associated with downregulation of plasma CRP in response to nutritional lipid overload.
	0.98	CREBH as the first cellular transcription factor that enhances apoB mRNA expression and translation via association with the CRE binding element in the promoter region of the apoB gene.
	0.98	CREBH is constantly hyperactivated, such as during insulin resistance and metabolic inflammation, it enhances transcription and translation of hepatic apoB, leading to pathologic overproduction of VLDL and hyperlipidemia.
	0.98	CREBH-null mice, which showed that genetic depletion of CREBH significantly diminished the secretion of VLDL-apoB from hepatocytes in response to the inflammatory stimuli induced by TNFalpha and high-fat feeding, leading to lipid accumulation in the liver.
	0.98	CREBH-apoB axis is the signaling pathway that, at least partially, mediated upregulation of VLDL in APR induced by TNFalpha and LPS.
	0.97	CREBH), an acute-phase transcription factor, enhances very-low-density lipoprotein (VLDL) assembly and secretion by upregulating apolipoprotein B (apoB) expression, and contributes to metabolic inflammation-associated hyperlipoproteinemia induced by TNFalpha, lipopolysaccharides (LPS), and a high-fat diet (HFD) in mice.
	0.97	CREBH significantly induced mRNA and protein expression of apoB in McA-7777 cells.
	0.97	CREBH could significantly increase the activities of the apoB gene promoter.
	0.97	CREBH in mice resulted in significant reduction in expression of hepatic apoB mRNA.
	0.97	apoB, CREBH is dominantly expressed in the liver and small intestine.
	0.97	CREBH did not increase mRNA expression of the microsomal triglyceride transfer protein (MTP), an important chaperone involved in apoB lipidation during VLDL assembly (Figure 1A).
	0.97	apoB mRNA was significantly reduced in CREBH-null mice compared to their WT littermates (Figure 2A).
	0.97	CREBH may mediate the inflammatory cytokine signaling to overexpression of VLDL-apoB in metabolic inflammation.
	0.97	CREBH-apoB signaling pathway mediates metabolic inflammation induced by LPS and HFD to VLDL overproduction
	0.97	CREBH mRNA and apoB protein expression in the WT but not the CREBH-null mice (Figures 6B and C).
	0.97	CREBH is essential for VLDL-apoB biosynthesis and the subsequent transportation of hepatic lipids from hepatocytes to the circulation under physiological conditions.
	0.96	apoB and hyperlipoproteinemia in wildtype mice, but not in CREBH-null mice.
	0.96	CREBH upregulates apoB mRNA expression which facilitates apoB secretion
	0.96	CREBH exerts a regulatory effect on cellular apoB expression.
	0.96	CREBH activity and the abundance of cellular apoB mRNA and the secretion of VLDL-apoB protein.
	0.96	CREBH by TNFalpha at 6h post-treatment was followed by a marked increase in cellular apoB mRNA at 12 h post-treatment (Figures 3A and B).
	0.96	apoB reporter compared to the mock treated cells (Figure 3D), indicating that TNFalpha-CREBH signaling stimulates apoB expression.
	0.96	CREBH upregulates apoB mRNA expression which facilitates apoB secretion
	0.96	CREBH-apoB signaling pathway mediates metabolic inflammation induced by HFD to VLDL overproduction
	0.95	apoB in CREBH-null mice did not parallel the increase of secreted lipids at 3h, but instead was significantly reduced compared to WT controls (Figure 2B, lower panels), indicating defective VLDL-apoB biosynthesis in the CREBH-null mice.
	0.95	CREBH diminishes TNFalpha induced VLDL-apoB overproduction in vivo
	0.94	CREBH directly regulates apoB biosynthesis and how CREBH and apoB contribute to the hyperlipidemia induced by metabolic inflammation remains unclear.
	0.94	CREBH diminishes TNFalpha-induced VLDL-apoB overproduction in vivo
	0.94	CREBH-apoB signaling.
	0.93	apoB was significantly increased in the CREBH-WT-expressing cells compared to the mock transfected cells (Figure 1B).
	0.93	apoB and lipid substrates resulted in increased secretion of plasma VLDL-apoB in the WT but not the CREBH-null mice (Suppl.
	0.93	CREBH-null mice, despite the higher lipid levels in the hepatocytes, plasma VLDL-apoB was not increased in parallel (Figure 6E), suggesting a lack of proper VLDL assembly and secretion.
	0.92	CREBH-apoB axis may be effective in preventing and treating hyperlipidemia in metabolic syndrome.
	0.89	CREBH is the missing link between metabolic inflammation, hepatic VLDL-apoB overproduction, and hyperlipidemia.
	0.87	CREBH regulates expression of Stat3 and whether Stat3 plays a role in VLDL-apoB metabolism during metabolic inflammation requires further investigation.
	0.86	CREBH-DN inhibited VLDL-apoB secretion (Figure 1B).
	0.85	CREBH-apoB signaling pathway mediates
	0.73	CREBH has been reported to enhance expression of APR genes, such as CRP and SAP, we then tested the association between CREBH, apoB, and CRP in HFD-induced chronic metabolic inflammation.
	0.72	CREBH-WT stimulated apoB-luciferase expression.
	0.63	apoB protein levels revealed that expression of apoB protein was comparable between the WT and CREBH-null mice at the baseline (0h) (Figure 2B, upper panels).
	0.62	CREBH-apoB axis and found that Stat3 is downstream of CREBH in the context of this work.
29738435	0.98	ApoB expression is reduced in the fetal livers of CREBH KO mice, and CREBH binds to the ApoB promoter region, resulting in an increased ApoB expression.
	0.98	CrebH expression and increases ApoB biosynthesis and VLDL secretion in the liver.
	0.98	ApoB and MTP deficiencies block CREBH processing suggests that lipid movement into the ER, or another related function of these proteins, initiates vesicular trafficking of CREBH to the Golgi and CREBH processing to release the active form of CREBH.
	0.97	CREBH is reported to activate ApoB expression.
	0.97	ApoB production, resulting in hyperlipoproteinemia in WT mice but not in CREBH KO mice.
	0.97	ApoB or microsomal triglyceride-transfer protein (MTP) activity attenuates VLDL particle assembly, which attenuates CREBH processing and Apoa4 expression, despite a dramatic increase in liver TG content.
27417587	0.97	Creb3l3-/- compared with WT littermates, resulting in a 2.2-fold increase in apoB/apoA-I ratio in Creb3l3-/- mice (Figure 1A).
	0.94	apoB/apoA-I ratio (2.8-fold) in CREBH-deficient mice were maintained during 2 weeks of WD feeding (Figure 1B).
	0.50	CREBH deficiency increased plasma apoB/apoA-I ratio
22095841	0.94	ApoB48, the key indicator of chylomicron, detected in the CrebH null and wild-type mice (Supplemental S6D).
21666694	0.89	Creb3l3-/- mice versus WT, Apob level was also higher in Creb3l3-/- than in WT mice (Fig. 1e).