OMIA:002490-9986 : Hyperlipidaemia/atherosclerosis, APOC3-related in Oryctolagus cuniculus (rabbit)

Categories: Cardiovascular system phene

Possibly relevant human trait(s) and/or gene(s)s (MIM numbers): 107720 (gene) , 614028 (trait)

Links to MONDO diseases: No links.

Mendelian trait/disorder: yes

Considered a defect: no

Key variant known: no

Species-specific description: Zha et al. (2021): "High levels of apolipoprotein C3 (APOC3) can lead to hypertriglyceridemia, which increases the risk of cardiovascular disease. ... An APOC3-KO rabbit model was constructed using CRISPR/Cas9 gene editing technology. APOC3 deficiency alleviated cholesterol-induced hyperlipidemia and reduced atherosclerotic plaque formation." This phene includes references to studies involving genetically modified organisms (GMO).

Genetic engineering: Yes - variants have been created artificially, e.g. by genetic engineering or gene editing
Have human generated variants been created, e.g. through genetic engineering and gene editing

Associated gene:

Symbol Description Species Chr Location OMIA gene details page Other Links
APOC3 apolipoprotein C-III Oryctolagus cuniculus 1 NC_067374.1 (113568671..113567203) APOC3 Homologene, Ensembl , NCBI gene

Cite this entry

Nicholas, F. W., Tammen, I., & Sydney Informatics Hub. (2023). OMIA:002490-9986: Online Mendelian Inheritance in Animals (OMIA) [dataset].


2021 Zha, Y., Lu, Y., Zhang, T., Yan, K., Zhuang, W., Liang, J., Cheng, Y., Wang, Y. :
CRISPR/Cas9-mediated knockout of APOC3 stabilizes plasma lipids and inhibits atherosclerosis in rabbits. Lipids Health Dis 20:180, 2021. Pubmed reference: 34922545. DOI: 10.1186/s12944-021-01605-7.

Edit History

  • Created by Imke Tammen2 on 09 Jan 2022
  • Changed by Imke Tammen2 on 09 Jan 2022
  • Changed by Imke Tammen2 on 18 Dec 2023