Our Gene Editing Platform
MAGEC is a leading facility specialising in advanced CRISPR gene-editing technologies to generate pre-clinical models of human disease.
To date, the Melbourne Advanced Genome Editing Centre (MAGEC) has successfully created over 400 unique gene-edited pre-clinical models, playing a critical role in advancing both fundamental biological research and translational studies.
Using advanced CRISPR/Cas technology alongside precise microinjection techniques to deliver gene-targeting reagents directly into the pronucleus of one-cell stage embryos, MAGEC enables the rapid and efficient generation of gene-modified models for basic research and pre-clinical models of human disease.
Our team has developed sophisticated gene-editing methods to produce highly complex models, including gene reporters, humanised mice, and conditional alleles – contributing to more than 50 high-impact publications in leading research journals such as Nature, Nature Medicine, and Immunity.
Our Services
MAGEC is supported by Phenomics Australia. Phenomics Australia is supported by the Australian Government through the National Collaborative Research Infrastructure Strategy (NCRIS) program.
Contact
If you would like to discuss opportunities to use our MAGEC services, please contact:
Dr Andrew Kueh
CRISPR Platform Lead
Knockout Models
We generate knockout models by targeting a single gene exon or an entire gene sequence with two guide RNAs that direct CRISPR/Cas proteins to delete these regions. This approach allows for the deletion of sequences up to 300–400 kb in size.
Point-Mutant Models
We generate precise point-mutant models by co-injecting CRISPR/Cas proteins and single-stranded DNA templates into targeted exons, replicating disease-causing human mutations via homology-directed repair.
Complex Knock-In Models
We generate complex knock-in models by co-injecting CRISPR/Cas proteins and large double-stranded DNA templates into targeted exons, enabling the creation of gene reporters, conditional alleles, and humanised gene constructs.
Recent Publications
The kinase domain of RIPK3 tunes its scaffolding functions. Cell Death Differ. Feb 6 2026.
doi: 10.1038/s41418-026-01677-x.
Mbd4 and MutSα protect cells from spontaneous deamination of 5-methylcytosine. Nucleic Acids Res. Jan 14 2026. doi: 10.1093/nar/gkaf1493.
Resident phagocytes promote non-cell-autonomous fragmentation of apoptotic cells. Sci Adv. Dec 19 2025. doi: 10.1126/sciadv.adz5264.
ARAP2 regulates responses to interferon-gamma by restricting SOCS1. Cell Rep. Dec 23 2025. doi: 10.1016/j.celrep.2025.116667.
PA2G4 Functions as a Cofactor for MYC Family Oncoproteins in MYC-Driven Malignancies. Cells. Sep 11 2025. doi: 10.3390/cells14181422.
Genome-wide in vivo CRISPR screens identify GATOR1 complex as a tumor suppressor in Myc-driven lymphoma. Nat Commun. Aug 21 2025. doi: 10.1038/s41467-025-62615-y.
Rapid and Robust Generation of Homozygous Fluorescent Reporter Knock-In Cell Pools by CRISPR-Cas9. Cells. Jul 29 2025. doi: 10.3390/cells14151165.
Lymph-node-derived stem-like but not tumor-tissue-resident CD8+ T cells fuel anticancer immunity. Nat Immunol. August 26 2025. doi: 10.1038/s41590-025-02219-2.
NLRP3 inflammasome-driven hemophagocytic lymphohistiocytosis occurs independent of IL-1β and IL-18 and is targetable by BET inhibitors. Sci Adv. Jul 11 2025. doi: 10.1126/sciadv.adv0079.
Relative importance of the anti-apoptotic versus apoptosis-unrelated functions of MCL-1 in vivo. Science. Sep 4 2025. doi: 10.1126/science.adw1836.