Background#R##N#Pathological cardiac development is precipitated by dysregulation of calreticulin, an endoplasmic reticulum (ER)-resident calcium binding chaperone and critical contributor to cardiogenesis and embryonic viability. However, pleiotropic phenotype derangements induced by calreticulin deficiency challenge the identification of specific downstream transcriptome elements that direct proper cardiac formation. Here, differential transcriptome navigation was used to diagnose high priority calreticulin domain-specific gene expression changes and decrypt complex cardiac-specific molecular responses elicited by discrete functional regions of calreticulin.
['Randolph S. Faustino', 'Saranya P. Wyles', 'Jody Groenendyk', 'Marek Michalak', 'Andre Terzic', 'Carmen Perez-Terzic']
Systems biology surveillance decrypts pathological transcriptome remodeling.