Publication for Apoa5 and Creb3l3

Species Symbol Function* Entrez Gene ID* Other ID Gene
coexpression
CoexViewer
mmu Apoa5 apolipoprotein A-V 66113 [link]
mmu Creb3l3 cAMP responsive element binding protein 3-like 3 208677

Pubmed ID Priority Text
21666694 0.98 Creb3l3-/- than in WT liver of Fads1, Fads2, Elovl2, Cidec, Apoc2 and Apoa5, which have been associated with human TG metabolism (Fig. 2a) .
0.98 Apoa5, Apoc2 and Fgf21 were induced in WT liver by fasting, an effect which was abrogated in Creb3l3-/- mice (Fig. 2b).
0.98 CREB-H is induced by fasting in the liver and required for the expression of a series of genes that play important roles in TG metabolism, which include Apoa4, Apoa5, Apoc2, Cidec, Elovl2, Elovl5, Fads1, Fads2, Fgf21, and G0s2.
0.98 CREB-H is also functionally related to PPARalpha which plays an important role in FA oxidation in the liver , as both genes are induced by fasting and have common targets such as Fgf21, Apoa5 and G0s2.
0.97 CREB-H deficient mice displayed hypertriglyceridemia (HTG) secondary to inefficient TG clearance catalyzed by lipoprotein lipase (Lpl), partly due to defective expression of the Lpl coactivators, Apoc2, Apoa4, and Apoa5 and concurrent augmentation of the Lpl inhibitor, Apoc3.
0.97 Creb3l3-/- mice displayed HTG and a defect in Lpl-mediated TG clearance, which might be ascribed to defective expression of Apoc2, Apoa4 and Apoa5 coupled with the augmentation of VLDL-associated Apoc3 with contributions from other yet-to-be-identified CREB-H targets.
0.93 Creb3l3-/- than in WT mice, its mRNA levels were not significantly different between these two groups (Supplementary Fig. 2e), suggesting post-transcriptional control of Apoc3 by CREB-H. We postulated that the concomitant reduction of Lpl activators, Apoa4, Apoa5, and Apoc2, and induction of Lpl inhibitor, Apoc3 impaired TG clearance, resulting in higher plasma TG levels in Creb3l3-/- than in WT mice.
0.83 CREB3L3 are significantly associated with the polygenic trait of HTG, similar to other established HTG-associated genes such as LPL and APOA5 .
22262056 0.98 CREB-H is transcriptionally activated by fasting, and induces lipid metabolism genes, such as Apoa4, Apoa5, and Apoc2 apolipoproteins which exhibit stimulatory effects on lipoprotein lipase (LPL).
0.98 CREB-H induces LPL coactivators, Apoa4, Apoa5, and Apoc2 that facilitate TG clearance from plasma.
0.97 Apoa5 (apoA-V), and Apoc2 (apoC-II) in CREB-H knockout mice was notable.
0.96 Apoa5 and Apoc2 as CREB-H target genes suggested that CREB-H might be involved in TG catabolism.
27417587 0.98 CREBH regulates plasma triglyceride clearance by inducing lipoprotein lipase (LPL) co-factors such as apolipoprotein A-IV (apoA-IV), apoA-V, and apoC-II.
0.98 CREBH reduces plasma TG by facilitating LPL-mediated TG clearance, which is attributed, in part, to the transcriptional activation of apolipoprotein genes such as Apoa1, Apoa4, Apoa5 and Apoc2 .
0.97 CREBH knockout mice exhibit hypertriglyceridemia in association with decreased production of apoA-IV, apoA-V, and apoC-II apolipoproteins .
0.97 Creb3l3-/- mice have hypertriglyceridemia due to a defect in VLDL-TG clearance, which is associated with the decreased expression of LPL coactivators, such as apoA-IV, apoA-V and apoC-II .
22123668 0.98 cyclic AMP-responsive element-binding protein H (CREB-H) as a regulator of several proteins affecting lipolysis, including apo-AV, apo-CII, and apo-CIII.
0.87 CREB-H in the liver, they observed decreased plasma triglyceride levels and increased expression of Apoc2 and Apoa5.
29738435 0.98 CREBH regulates the gene expression of lipoprotein lipase modulators such as Apoa4, Apoa5, Apoc2, and Apoc3, resulting in the activation of LPL activity.
0.98 CREBH overexpression in the liver reduces plasma TG by activating LPL-mediated TG clearance by the transcriptional activation of apolipoprotein genes, such as Apoa1, Apoa4, Apoa5, and Apoc2.
30866796 0.98 CREB3L3 deficiency leads to significant downregulation of genes involved in lipoprotein metabolism (Apoc2, Apoa5, Apoa1, Scarb1), lipid storage (Cidec), fatty acid binding (Fabp2), fatty acid desaturation and elongation (Fads1, Fads2, Elovl2, Elovl5), gluconeogenesis (Pck1, G6pc), and fatty acid oxidation (Cpt1a).
0.98 Apoa5, and of Fgf21, which at pharmacological doses has been shown to stimulate plasma triglyceride clearance, likely explains the elevated plasma triglyceride levels in CREB3L3-/- mice via reduced plasma triglyceride clearance.
23957007 0.98 CrebH null mice showed partial repression of APOA5 mRNA, we can speculate that not only CREBH but also USF is involved in APOA5 gene regulation at the transcriptional level.
27291420 0.97 CREB3L3 reduces plasma TG levels by increasing hepatic gene expression of apolipoproteins such as apolipoprotein A-IV (Apoa4), Apoa5, and Apoc2.
27301791 0.97 CREBH also induces apoA-IV, apoA-V and apoC-II that stimulate LPL-mediated TG clearance.
27982131 0.97 Creb3l3 deletion causes a defect in TG lipolysis in the blood, with Creb3l3-/- mice exhibiting hypertriglyceridaemia as a result of inefficient catalysis of TG clearance by lipoprotein lipase (LPL); this is due to a reduction in the expression of the LPL coactivators Apolipoprotein c2 (Apoc2), Apoa4, and Apoa5, and upregulation of the LPL inhibitor Apoc3.



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