Related Experiment Video
Updated: May 7, 2026

Mouse Genome Engineering Using Designer Nucleases
Published on: April 2, 2014
Prostaglandin synthase 2 gene disruption causes severe renal pathology in the mouse
S G Morham1, R Langenbach, C D Loftin
1Department of Pathology, University of North Carolina at Chapel Hill 27599-7525, USA.
Abstract:
The prostaglandin endoperoxide H synthase isoform 2, cyclooxygenase 2 (COX-2), is induced at high levels in migratory and other responding cells by pro-inflammatory stimuli. COX-2 is generally considered to be a mediator of inflammation. Its isoform, COX-1, is constitutively expressed in most tissues and is thought to mediate "housekeeping" functions. These two enzymes are therapeutic targets of the widely used nonsteroidal anti-inflammatory drugs (NSAIDs). To investigate further the different physiologic roles of these isoforms, we have used homologous recombination to disrupt the mouse gene encoding COX-2 (Ptgs2). Mice lacking COX-2 have normal inflammatory responses to treatments with tetradecanoyl phorbol acetate or with arachidonic acid. However, they develop severe nephropathy and are susceptible to peritonitis.
Related Concept Videos
Mismatch Repair
In-vitro Mutagenesis
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Overview of Protein Metabolism
Amino acids play various roles in the body once they are absorbed into cells. They are restructured...
Inborn Errors of Metabolism
Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

