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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

A novel genetic pathway for sudden cardiac death via defects in the transition between ventricular and conduction system cell lineages.

HF-1 b, an SP1 -related transcription factor, is preferentially expressed in the cardiac conduction system and ventricular myocytes in the heart. Mice deficient for HF-1 b survive to term and exhibit normal cardiac structure and function but display sudden cardiac death and a complete penetrance of conduction system defects, including spontaneous ventricular tachycardia and a high incidence of AV block. Continuous electrocardiographic recordings clearly documented cardiac arrhythmogenesis as the cause of death. Single-cell analysis revealed an anatomic substrate for arrhythmogenesis, including a decrease and mislocalization of connexins and a marked increase in action potential heterogeneity. Two independent markers reveal defects in the formation of ventricular Purkinje fibers. These studies identify a novel genetic pathway for sudden cardiac death via defects in the transition between ventricular and conduction system cell lineages.[1]

References

  1. A novel genetic pathway for sudden cardiac death via defects in the transition between ventricular and conduction system cell lineages. Nguyên-Trân, V.T., Kubalak, S.W., Minamisawa, S., Fiset, C., Wollert, K.C., Brown, A.B., Ruiz-Lozano, P., Barrere-Lemaire, S., Kondo, R., Norman, L.W., Gourdie, R.G., Rahme, M.M., Feld, G.K., Clark, R.B., Giles, W.R., Chien, K.R. Cell (2000) [Pubmed]
 
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