` Genetic Mutant Models
CMCR_logoclick for homepagee-mail

Genetic Mutant Models

Previous research on mutant mouse models focused on the effects of mutations in key DNA repair pathways to the metabolome, in urine and blood. Parp1-/- mice are deficient in base excision repair, ATM-/- in double strand break repair and radiation signaling, and Prkdc-/- (Scid) deficient in non-homologous end joining. While Parp1-/- show delayed responses and a general equal number of metabolites of high and low levels of metabolites between irradiated wild type and mutant, Scid mice are characterized by an overall decreased level of metabolites, whereas Atm mice by high levels of excretion. New research will focus on pro- and anti-inflammatory mouse models to identify the contribution of immune responses and signaling in the metabolic signature.

Delayed response of small molecule excretion in Parp1-/- mice.

Laiakis EC, Pannkuk EL, Diaz-Rubio ME, Wang YW, Mak TD, Simbulan-Rosenthal CM, Brenner DJ, Fornace AJ. Implications of genotypic differences in the generation of a urinary metabolomics radiation signature. Mutat Res 2016.

Links

CRR

RARAF

Columbia University

Georgetown

NIAID

 



tel: (212) 305-5660
fax: (212) 305-3220
Center for High-Throughput Minimally-Invasive Radiation Biodosimetry