The present invention relates to new NOS variants or mutants which contain structural
alterations in the site of Akt dependent phosphorylation. The altered NOS proteins
or peptides, especially the human eNOS proteins or peptides, Akt proteins or polypeptides
and their encoding nucleic acid molecules are useful as gene therapy agents for
the treatment of diseases including post angioplasty restenosis, hypertension,
atherosclerosis, heart failure, diabetes and diseases with defective angiogenesis.
NOS proteins and peptides are also useful in methods of screening for agents which
modulate NOS activity.
