The Iqgap1 gene encodes a Ras GTPase-activating-like protein that acts as a cytoskeletal adaptor scaffold protein and regulates dendritic spine number and cognitive processes. These mice carry a knock out mutation of the Iqgap1 gene in which a 233 bp exon encoding amino acids 1186-1263 of the 1657 residue IQGAP1 protein is replaced by a PGK-neo cassette. 
Homozygotes exhibit gastric hyperplasia, delayed differentiation of neural progenitors into neuronal precursor cells, and increased pulmonary vascular leak. Prolonged cardiac pressure overload in homozygotes results in impaired cardiomyocyte hypertrophy and increased cardiomyocyte apoptosis. Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (protein) is detected by Western blot analysis of lung, liver, kidney, spleen or stomach from homozygous animals.

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This Iqgap1 knockout strain exhibits gastric hyperplasia, delayed differentiation of neural progenitors, increased pulmonary vascular leak and higher levels of cardiomyocyte apoptosis.

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