Search results for APOC2

Showing 14 results out of 16

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Species

Types

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Reaction types

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Protein (3 results from a total of 3)

Identifier: R-HSA-2429686
Species: Homo sapiens
Compartment: early endosome
Primary external reference: UniProt: APOC2: P02655
Identifier: R-HSA-2404145
Species: Homo sapiens
Compartment: cytosol
Primary external reference: UniProt: APOC2: P02655
Identifier: R-HSA-174699
Species: Homo sapiens
Compartment: extracellular region
Primary external reference: UniProt: P02655

DNA Sequence (1 results from a total of 1)

Identifier: R-HSA-6784670
Species: Homo sapiens
Compartment: nucleoplasm
Primary external reference: ENSEMBL: ENSG00000234906

Reaction (6 results from a total of 8)

Identifier: R-HSA-9031521
Species: Homo sapiens
Compartment: nucleoplasm
Natural and synthetic ligands of liver X receptors (LXRα, NR1H3 and LXRβ, NR1H2) induced expression of a cluster of apolipoprotein genes APOE, APOC1, APOC2 and APOC4 in both human and mouse macrophages (Mak PA et al. 2002). The induction of all four mRNAs was greatly attenuated in peritoneal macrophages derived from LXR α/β-/- mice (Mak PA et al. 2002). Cell reporter assays suggest that the LXR response elements (LXRE) in the multienhancer regions ME.1 and ME.2, which confer tissue-specific expression in macrophages and adipocytes (Shih SJ et al. 2000), are necessary for the expression of this gene cluster (Mak PA et al. 2002). These secreted apolipoproteins regulate lipid transport and catabolism. APOC2 is recognized as an activator of lipoprotein lipase (reviewed in Wolska A et al. 2017). Thus the genetic deficiency of APOC2 results in a phenotype that resembles lipoprotein lipase deficiency, and is aptly called hyperlipoproteinemia type IB. Individuals lacking APOC2 exhibit hyperchylomicronemia and hypertriglyceridemia (reviewed in Wolska A et al. 2017).
Identifier: R-HSA-9031527
Species: Homo sapiens
Compartment: nucleoplasm
The APOC2 gene is transcribed to yield mRNA and the mRNA is translated to yield protein.

Ligand-activated liver X receptors (LXRα, NR1H3 and LXRβ NR1H2) induce expression of a cluster of apolipoprotein genes APOE, APOC1, APOC2 and APOC4 in both human and mouse macrophages (Mak PA et al. 2002). The induction of all four mRNAs was greatly attenuated in peritoneal macrophages derived from LXR α/β-/- mice (Mak PA et al. 2002). Cel reporter assays suggest that the LXR response elements (LXRE) in the multienhancer regions ME.1 and ME.2, which confer tissue-specific expression in macrophages and adipocytes (Shih SJ et al. 2000), are necessary for the expression of this gene cluster (Mak PA et al. 2002). These secreted apolipoproteins regulate lipid transport and catabolism.

Identifier: R-HSA-6784622
Species: Homo sapiens
Compartment: nucleoplasm, cytosol
Crebh(1-?) enters the nucleoplasm and induces the expression of APOA4, APOA5, APOC2, CIDEC and FGF21 (Lee et al. 2011). APOA4, APOA5 and APOC2 are known to augment lipoprotein lipase (LPL) activity. LPL is bound to the vascular endothelium, and hydrolyzes chylomicron and VLDL- associated TG to facilitate the transport of hydrolyzed fatty acids to peripheral cells. Patients with genetic defects in AOPC2, APOA5 or LPL display high circulating TG levels due to impaired TG clearance. Identification of APOA4, APOA5 and APOC2 as CREB-H target genes suggests that CREB-H might be involved in TG catabolism. CREB-H also strongly induces FGF21, a liver expressed hormone that has antidiabetic and TG- lowering effects, and CIDEC which encodes a lipid droplet-associated protein (Lee 2012).
Identifier: R-HSA-9031510
Species: Homo sapiens
Compartment: nucleoplasm
The APOC1 gene is transcribed to yield mRNA and the mRNA is translated to yield protein.

Ligand-activated liver X receptors (LXRα, NR1H3 and LXRβ NR1H2) induce expression of a cluster of apolipoprotein genes APOE, APOC1, APOC2 and APOC4 in both human and mouse macrophages (Mak PA et al. 2002). Induction of APOC2 mRNA was attenuated or abolished in macrophages derived from LXR α/β-/- mice (Mak PA et al. 2002).

Identifier: R-HSA-6784648
Species: Homo sapiens
Compartment: cytosol, nucleoplasm
The N-terminal fragment of CREB3L3 is released to the cytosol and translocates to the nucleus (Chan et al. 2010, Chin et al. 2005) to induce the transcriptional activation of different genes such as Apoa4, Apoa5, and Apoc2 apolipoproteins which exhibit stimulatory effects on lipoprotein lipase (LPL). Consistent with the essential role of LPL in TG clearance, CREB3L3-deficient mice showed hypertriglyceridemia, associated with defective production of these apolipoproteins and decreased LPL activity.
Identifier: R-HSA-9035279
Species: Homo sapiens
Compartment: nucleoplasm
The APOC4 gene is transcribed to yield mRNA and the mRNA is translated to yield protein.

Ligand-activated liver X receptors (LXRα, NR1H3 and LXRβ NR1H2) induce expression of a cluster of apolipoprotein genes APOE, APOC1, APOC2 and APOC4 in both human and mouse macrophages (Mak PA et al. 2002). The induction of all four mRNAs was greatly attenuated in peritoneal macrophages derived from LXR α/β-/- mice (Mak PA et al. 2002). Cel reporter assays suggest that the LXR response elements (LXRE) in the multienhancer regions ME.1 and ME.2, which confer tissue-specific expression in macrophages and adipocytes (Shih SJ et al. 2000), are necessary for the expression of this gene cluster (Mak PA et al. 2002). These secreted apolipoproteins regulate lipid transport and catabolism.

Set (2 results from a total of 2)

Identifier: R-HSA-6784718
Species: Homo sapiens
Compartment: cytosol
Identifier: R-HSA-6784668
Species: Homo sapiens
Compartment: nucleoplasm

Pathway (2 results from a total of 2)

Identifier: R-HSA-8963889
Species: Homo sapiens
Lipoprotein lipase (LPL) and hepatic triacylglycerol lipase (LIPC) enzymes on the lumenal surfaces of capillary endothelia mediate the hydrolysis of triglyceride molecules in circulating lipoprotein particles.
LPL is widely expressed in the body and is especially abundant in adipocytes and skeletal and cardiac myocytes. Activation of the protein requires glycosylation, dimerization, and glycosylphosphatidylinositol-anchored high density lipoprotein-binding protein 1 (GPIHBP1), which delivers it to heparan sulfate proteoglycan (HSPG) associated with the plasma membrane. It is inactivated by proteolytic cleavage (Berryman & Bensadoun 1995; Sukonina et al. 2006; Young et al. 2011).
Expression of the LPL gene is transcriptionally regulated by Cyclic AMP-responsive element-binding protein 3-like protein 3 (CREB3L3), which also regulates the expression of APOA4, APOA5, APOC2, CIDEC and FGF21 (Lee et al. 2011).
Maturation of LIPC enzyme requires association with LMF1 protein (or possibly, inferred from sequence similarity, LMF2). Heparin binding stabilizes LIPC in its active dimeric form (Babilonia-Rosa & Neher 2014; Ben-Zeev et al. 2011).
Identifier: R-HSA-9029569
Species: Homo sapiens
Compartment: nucleoplasm
The liver X receptors (LXRs), LXRα (NR1H3) and LXRβ (NR1H2), are nuclear receptors that are activated by endogenous oxysterols, oxidized derivatives of cholesterol (Janowski BA et al. 1996). When cellular oxysterols accumulate as a result of increasing concentrations of cholesterol, NR1H2,3 induce the transcription of genes that protect cells from cholesterol overload (Zhao C & Dahlman‑Wright K 2010; Ma Z et al. 2017). In peripheral cells such as macrophages, NR1H2 and NR1H3 increase cholesterol efflux by inducing expression of ATP-binding cassette subfamily A type 1 (ABCA1), ABCG1, and apolipoprotein APOE (Jakobsson T et al. 2009; Laffitte BA et al. 2001; Mak PA et al. 2002). In the intestine, LXR agonists decrease cholesterol absorption through induction of ABCA1, ABCG5, and ABCG8 (Repa JJ et al. 2000; Back SS et al. 2013). Cholesterol removal from non-hepatic peripheral cells, such as lipid-laden macrophages, and its delivery back to the liver for catabolism and excretion are processes collectively known as reverse cholesterol transport (RCT) (Francis GA 2010; Rosenson RS et al. 2012). This Reactome module describes the activation of several direct NR1H2,3 target genes that are closely associated with the RCT pathway, including genes encoding membrane lipid transporters, such ABCA1, ABCG1, ABCG5, ABCG8 and a cluster of apolipoprotein genes APOE, APOC1, APOC2 and APOC4 (Jakobsson T et al. 2009; Back SS et al. 2013; Mak PA et al. 2002).
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