Apolipoprotein D.
Apolipoprotein D
Arachidonic acid
Lipid metabolism
Lipid transport
Lipocalin
Neuroprotection
Journal
Gene
ISSN: 1879-0038
Titre abrégé: Gene
Pays: Netherlands
ID NLM: 7706761
Informations de publication
Date de publication:
25 Sep 2020
25 Sep 2020
Historique:
received:
11
03
2020
revised:
03
06
2020
accepted:
05
06
2020
pubmed:
20
6
2020
medline:
7
8
2020
entrez:
20
6
2020
Statut:
ppublish
Résumé
ApoD is a 25 to 30 kDa glycosylated protein, member of the lipocalin superfamily. As a transporter of several small hydrophobic molecules, its known biological functions are mostly associated to lipid metabolism and neuroprotection. ApoD is a multi-ligand, multi-function protein that is involved lipid trafficking, food intake, inflammation, antioxidative response and development and in different types of cancers. An important aspect of ApoD's role in lipid metabolism appears to involve the transport of arachidonic acid, and the modulation of eicosanoid production and delivery in metabolic tissues. ApoD expression in metabolic tissues has been associated positively and negatively with insulin sensitivity and glucose homeostasis in a tissue dependent manner. ApoD levels rise considerably in association with aging and neuropathologies such as Alzheimer's disease, stroke, meningoencephalitis, moto-neuron disease, multiple sclerosis, schizophrenia and Parkinson's disease. ApoD is also modulated in several animal models of nervous system injury/pathology.
Identifiants
pubmed: 32554047
pii: S0378-1119(20)30543-6
doi: 10.1016/j.gene.2020.144874
pmc: PMC8011330
mid: NIHMS1672253
pii:
doi:
Substances chimiques
APOD protein, human
0
Apolipoproteins D
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
144874Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM089820
Pays : United States
Informations de copyright
Crown Copyright © 2020. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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