Dr Gabriel Balmus, DVM

Postdoctoral associate

 

Alumni

This person is a member of Sanger Institute Alumni.

As part of Steve Jackson's laboratory, Gabi is interested in the DNA damage response (DDR) and its connection to inborn disease, cancer and ageing.

1. Gabi is interested in the mechanisms of ageing and their connection to DDR. Together with Dr. Delphine Larrieu in the lab, Gabi is exploring the possibility of ameliorating Hutchinson-Gilford progeria phenotypes.

2. Within the “CRISPR-Cas9 revolution” together with Dr. Josep Forment in the lab, Gabi is exploring the mechanism governing genetic interactions within the DDR, including synthetic lethality and viability, via the use of whole genome CRISPR libraries.

3. Together with Dr. Andrew Blackford in the lab, Gabi is exploring the roles of a newly identified non-homologous end joining factor, PAXX, in physiology and disease.

4. A particular area of interest is the roles of the deubiquitinating enzymes (DUBs) in DDR. To this extent, Gabi is investigating the roles of specific DUBs in physiology and disease.

5. Together with Dr. David Adams’s group, Gabi is performing a screen for genes involved in the formation of micronuclei, in vivo markers of genomic instability.

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Alcian blue- and Alizarin red-stained skulls from Hus1+/neoAtm-/- (top) and Hus1neo/neoAtm-/- (bottom) mouse embryos at E18.5. In these preparations, cartilage is stained blue and bone is stained red. The skull from the Hus1neo/neoAtm-/- embryo is smaller and presents an array of fenestrations in the parietal bone, highlighting the craniofacial defects present in Atm/Hus1 double mutant mice. For further detail, see the article by Balmus et al., pp. 3408–3420.

Alcian blue- and Alizarin red-stained skulls from Hus1+/neoAtm-/- (top) and Hus1neo/neoAtm-/- (bottom) mouse embryos at E18.5. In these preparations, cartilage is stained blue and bone is stained red. The skull from the Hus1neo/neoAtm-/- embryo is smaller and presents an array of fenestrations in the parietal bone, highlighting the craniofacial defects present in Atm/Hus1 double mutant mice. For further detail, see the article by Balmus et al., pp. 3408–3420.