This suggested that shn might be a new mutation, identifying a novel gene. To identify potential alleles or hornologues of shn , we set out to genetically map the mutation. To locate the position of shn among the 20 rat autosomes, an intraspecific backcross was conducted and molecular analysis of the backcross progeny for inheritance of polymorphic DNA markers allowed us to eliminate the majority of the chromosomes as possible locations for shn . By contrast, shn is closely linked with markers from the distal tip of chromosome 7, where no prior hypotrichotic mutations exist. Intracellularly, one of the effects of Angiotensin II is the activation of cytoplasmic tyrosine kinases.
Previous research indicates that tyrosine phosphorylation can prolong sodium current.
It has also been shown to affect potassium current. Electrocardiograms of rats treated with Angiotensin II show a prolonged action potential, and a longer repolarization period, which proved to be arrhythmogenic. Our goal was to demonstrate, using immunoprecipitation and Western blotting, that Angiotensin II activates tyrosine kinase in the myocardium and causes phosphorylation of cardiac ion channels. Krakowiak and C. Watson Department of Biological Sciences, Central Connecticut State University Heart failure or hypertrophy affects many Americans. During hypertrophy there is an increase in intracellular tyrosine kinase, which increases cell growth and phosphorylates intracellular proteins.