APOD: Apolipoprotein D - A Lipocalin Transporter and Neuroprotective Factor

Comprehensive genomic, transcriptomic, and proteomic analysis of APOD, a glycoprotein involved in lipid transport, aging, and neurological disorders.

Gene Information Card

Symbol APOD
Full Name Apolipoprotein D
Gene Type protein-coding
Chromosomal Location 3q29
NCBI Gene ID 347 ncbi.nlm.nih.gov/gene/347
Ensembl ID ENSG00000189058
UniProt ID P05090
OMIM ID 107740
HGNC ID 608
Aliases apoD, apolipoprotein D, Apo-D

Description

APOD encodes apolipoprotein D, a 29 kDa glycoprotein belonging to the lipocalin family. It binds small hydrophobic ligands such as cholesterol, arachidonic acid, and progesterone, and is involved in lipid transport, antioxidant activity, and neuroprotection. APOD is highly expressed in the nervous system and is upregulated in aging and several neurodegenerative conditions.

Disease Associations

Disease category Pathophysiological mechanism Genomic evidence
Alzheimer disease APOD is upregulated in the hippocampus and cortex; may modulate amyloid-beta aggregation and lipid metabolism in glial cells. PMID: 10944470; NCBI GeneRIF
Schizophrenia APOD expression is altered in prefrontal cortex and cerebrospinal fluid; associated with myelin and lipid dysregulation. PMID: 16981828; NCBI GeneRIF
Breast cancer APOD is expressed in breast cyst fluid; may influence steroid hormone transport and tumor progression. PMID: 15958558; NCBI GeneRIF
Niemann-Pick disease type C APOD accumulates in lysosomal storage disease models; potential biomarker. PMID: 20628055; NCBI GeneRIF

Expression Profile

Tissue Expression
Tissue nTPM level
Brain (cerebral cortex) 12.5 High
Spinal cord 10.2 High
Adrenal gland 8.7 Medium
Liver 2.1 Low
Kidney 1.8 Low
Cell Line Expression
Cell Line nTPM Notes
SH-SY5Y (neuroblastoma) 15.3 High expression in neuronal-like cells
U-87 MG (glioblastoma) 9.8 Moderate expression
HepG2 (hepatocellular carcinoma) 1.2 Low expression
MCF7 (breast cancer) 4.5 Moderate expression
Data source:Human Protein Atlas(proteinatlas.org)

Mutations & Variants

Hotspot Mutations
Variant Type Frequency Functional Description
c.94G>A (p.Gly32Arg) Missense <0.01% Unknown; rare variant in population databases
c.200C>T (p.Thr67Met) Missense <0.01% Unknown; predicted benign by SIFT
c.352A>G (p.Asn118Asp) Missense <0.01% Unknown; no functional studies
Mutation functional classification

Loss of Function (LOF)

No confirmed loss-of-function mutations reported in APOD.

Gain of Function (GOF)

No confirmed gain-of-function mutations reported in APOD.

Dominant Negative (DN)

No evidence of dominant-negative effects for APOD mutations.

Gene Ontology (GO)

• GO:0005319 – lipid transporter activity • GO:0005504 – fatty acid binding
• GO:0005576 – extracellular region • GO:0005615 – extracellular space
• GO:0006869 – lipid transport • GO:0032355 – response to estradiol
• GO:0042493 – response to drug • GO:0042802 – identical protein binding

Pathways

Lipid transport and metabolism (Reactome: R-HSA-382551)
Scavenging by Class A Receptors (Reactome: R-HSA-3000480)

Protein Summary

Apolipoprotein D (ApoD) is a 169-amino-acid glycoprotein with a lipocalin fold, containing a beta-barrel that binds small hydrophobic ligands. It is secreted into plasma and cerebrospinal fluid, where it associates with high-density lipoproteins (HDL). ApoD exhibits antioxidant properties by binding and transporting lipid peroxidation products, and is implicated in nerve regeneration, myelination, and protection against oxidative stress. Its expression increases with age and in various neurological disorders.

Related Products

Product name Cat.No. Species Gene ID
APOD Knockout HEK293 Cell Line EDJ-KQ4071 Human 347 Details Get a Quote
APOD Knockout A-549 Cell Line EDC07760 Human 347 Details Get a Quote
APOD Knockout HeLa Cell Line EDJ-KQ52639 Human 347 Details Get a Quote
APOD Knockout HCT 116 Cell Line EDJ-KQ69600 Human 347 Details Get a Quote
APOD Knockout HEK293T Cell Line EDC07812 Human 347 Details Get a Quote
Displaying Records 1 To 5 Of 5 Records
Contact Us
*
*
*
*
How did you hear about us: