bp(GO:"lipid metabolic process")

Entity

Name

lipid metabolic process

Namespace

go

Namespace Version

20180921

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

The apolipoprotein E type 4 allele (APOE-epsilon4) encodes the APOE lipoprotein, which through its lipid transport function plays a role in lipid metabolism. APOE-epsilon4 has been found to be a major risk factor for late familial or sporadic AD, with a strong gene-dosage effect such that the number of APOE-epsilon4 alleles correlated positively with the risk of developing AD and the age of onset (Corder et al., 1993). PubMed:19293145

The loss of alpha4 subunits was suggested to be related to lipid peroxidation, because the loss correlated with the level of peroxidation in the temporal cortex of brains from patients with AD, suggesting that receptor loss may be caused by oxidation of proteins (Yu et al., 2003). PubMed:19293145

They act as dominant regulators of lipid metabolism through their ability to transactivate genes encoding enzymes of lipid metabolism, providing a key linkage between the diet and the genome. PubMed:21718217

PP2A is an important player in many cellular functions. It controls cell metabolism by regulating the activity of the enzymes involved in glycolysis, lipid metabolism and catecholamine synthesis [8]. It also regulates various biological processes such as the cell cycle (by mediating cdc2 kinase activation), DNA replication, transcription and translation, signal transduction, cell proliferation, cytoskeleton dynamics and cell mobility and apoptosis. It has also been shown to play a role in cell transformation and cancer [9-12]. PubMed:23454242

In the 3-month-old hippocampi (Figure 4B), we found significant sex-dependent changes for Adnp+/– gene regulation and NAP rescue in the following genes in male mice: (a) apolipoprotein E (Apoe), the lead gene for Alzheimer’s disease risk, which was shown before to be a major gene regulated by ADNP (10, 13); (b) Gm21949, which is suggested to play a role in calcium-mediated responses, action potential conduction in myelinated cells, and axonal outgrowth and guidance (6); (c) lipase A (Lipa), which is related to lipid metabolism and was previously shown to be regulated by the Adnp genotype in mice (3); (d) autism-associated neuroligin 2 (Nlgn2), a postsynaptic membrane cell adhesion protein that mediates the formation and maintenance of synapses between neurons (12); (e) paired box protein 6 (Pax6), a key regulator in glutamatergic neuronal differentiation (38) and cortical development (39), which was shown before by us to be regulated by ADNP (complete knockout of Adnp rendered Pax6 expression undetectable in the brain primordium, contrasting with increased expression in Adnp+/– embryos [ref. 1] and in subcortical brain domains of 2-month-old male Adnp+/– mice [ref. 3]); and (f) Wolframin endoplasmic reticulum transmembrane glycoprotein (Wfs1), which is associated with neurodegeneration and cellular calcium homeostasis regulation and was previously shown to be regulated by NAP (34). PubMed:30106381

The apolipoprotein E type 4 allele (APOE-epsilon4) encodes the APOE lipoprotein, which through its lipid transport function plays a role in lipid metabolism. APOE-epsilon4 has been found to be a major risk factor for late familial or sporadic AD, with a strong gene-dosage effect such that the number of APOE-epsilon4 alleles correlated positively with the risk of developing AD and the age of onset (Corder et al., 1993). PubMed:19293145

The loss of alpha4 subunits was suggested to be related to lipid peroxidation, because the loss correlated with the level of peroxidation in the temporal cortex of brains from patients with AD, suggesting that receptor loss may be caused by oxidation of proteins (Yu et al., 2003). PubMed:19293145