Generation of Cerebral Cavernous Malformation in Neonatal Mouse Models Using Inducible Cre-LoxP Strategy

Jaesung P Choi; Xiangjian Zheng

doi:10.1007/978-1-0716-0640-7_18

Generation of Cerebral Cavernous Malformation in Neonatal Mouse Models Using Inducible Cre-LoxP Strategy

Methods Mol Biol. 2020:2152:253-258. doi: 10.1007/978-1-0716-0640-7_18.

Authors

Jaesung P Choi^{1

2}, Xiangjian Zheng^{3

4}

Affiliations

¹ Centre for Inflammation, Centenary Institute, and Faculty of Science, University of Technology Sydney, Sydney, New South Wales, Australia. j.choi@centenary.org.au.
² Laboratory of Cardiovascular Signalling, Centenary Institute, and Sydney Medical School, University of Sydney, University of Sydney, Sydney, New South Wales, Australia. j.choi@centenary.org.au.
³ Laboratory of Cardiovascular Signalling, Centenary Institute, and Sydney Medical School, University of Sydney, University of Sydney, Sydney, New South Wales, Australia.
⁴ Department of Pharmacology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.

PMID: 32524557
DOI: 10.1007/978-1-0716-0640-7_18

Abstract

Mutations in the CCM1 (aka KRIT1), CCM2, or CCM3 (aka PDCD10) gene cause cerebral cavernous malformation (CCM) in humans. Neonatal mouse models of CCM disease have been established by deleting any one of the Ccm genes. These mouse models provide invaluable in vivo disease model to investigate molecular mechanisms and therapeutic approaches for the disease. Here, we describe detailed methodology to generate CCM disease in mouse models (Ccm1 and Ccm2-deficient) using inducible Cre/loxP recombination strategy.

Keywords: CCM; CCM1; CCM2; Cerebral cavernous malformation; Cre/loxP; Endothelial cells; KRIT1; Mouse model; OSM; Vascular malformation.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Alleles
Animals
Apoptosis Regulatory Proteins / genetics*
Disease Models, Animal
Genotype
Hemangioma, Cavernous, Central Nervous System / genetics*
Hemangioma, Cavernous, Central Nervous System / metabolism
Homologous Recombination*
Integrases*
Mice
Mice, Knockout
Mice, Transgenic*
Phenotype

Substances

Apoptosis Regulatory Proteins
Cre recombinase
Integrases